PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
21660956-6	2011	Moreover, sphingosine activated caspase-9 and the effector caspase-3 in a PKC-delta-dependent manner.	Sphingosine	10-21	caspase 9	Rattus norvegicus	32-41
21726175-6	2011	KV treatment also demonstrates significant restoration in ATZ-induced alterations in the expression of apoptosis markers viz., p53, Bax, Bcl2, caspase-3, caspase-9, cyclooxygenase-2 (COX-2), c-Jun and c-fos.	kolaviron	0-2	caspase 9	Rattus norvegicus	154-163
21726175-6	2011	KV treatment also demonstrates significant restoration in ATZ-induced alterations in the expression of apoptosis markers viz., p53, Bax, Bcl2, caspase-3, caspase-9, cyclooxygenase-2 (COX-2), c-Jun and c-fos.	atz	58-61	caspase 9	Rattus norvegicus	154-163
21336971-10	2011	In addition, specific inhibitor of caspase-12 (Z-ATAD-FMK) and caspase-9 (Z-LEHD-FMK) partly suppressed cyclic stretch-induced AF cell apoptosis and the anti-apoptotic effects of the caspase inhibitors were additive.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	74-84	caspase 9	Rattus norvegicus	63-72
22013807-13	2011	One of the mechanisms of ZDD in treating UU infection and improving the sperm quality is through regulating the expressions of the apoptosis effect factors Caspase-3 and Caspase-9.	zdd	25-28	caspase 9	Rattus norvegicus	170-179
22097342-6	2011	Puerarin can enhance the expression of Caspase-9 and Bax protein, decrease the expression of Bcl-2 protein.	puerarin	0-8	caspase 9	Rattus norvegicus	39-48
20963815-4	2011	The results showed that PTZ and ethanol produced extensive Bax-dependent caspase-9 and caspase-3 activation and caused neuronal apoptosis.	Pentylenetetrazole	24-27	caspase 9	Rattus norvegicus	73-82
21377855-8	2011	Also, at the same concentration, becatamide inhibited H(2)O(2)-induced caspase-9 activation and caspase-independent chromatin condensation by 68% (P<0.05) and 73% (P<0.05), respectively.	becatamide	33-43	caspase 9	Rattus norvegicus	71-80
21377855-8	2011	Also, at the same concentration, becatamide inhibited H(2)O(2)-induced caspase-9 activation and caspase-independent chromatin condensation by 68% (P<0.05) and 73% (P<0.05), respectively.	Hydrogen Peroxide	54-62	caspase 9	Rattus norvegicus	71-80
21377855-9	2011	This is the first report about the chemical synthesis of becatamide and its potential biological activity to inhibit H(2)O(2)-induced apoptosis of PC-12 cells via protecting mitochondrial membrane integrity, thereby suppressing caspase-9 activation and chromatin condensation.	becatamide	57-67	caspase 9	Rattus norvegicus	228-237
20859773-8	2011	Mefloquine-treated utricles were positive for the extrinsic initiator caspase-8 and intrinsic initiator caspase-9 and downstream executioner caspase-3.	Mefloquine	0-10	caspase 9	Rattus norvegicus	104-113
20859773-9	2011	These results indicate that mefloquine can induce significant hair cell degeneration in the postnatal rat utricle and that mefloquine-induced hair cell death is initiated by both caspase-8 and caspase-9.	Mefloquine	123-133	caspase 9	Rattus norvegicus	193-202
20963815-4	2011	The results showed that PTZ and ethanol produced extensive Bax-dependent caspase-9 and caspase-3 activation and caused neuronal apoptosis.	Ethanol	32-39	caspase 9	Rattus norvegicus	73-82
20963815-5	2011	Furthermore, the cotreatment of vit-C along with ethanol and PTZ showed significantly decreased expression of Bax, caspase-9, caspase-3, cytochrome-c, and significantly increased expression of antiapoptotic Bcl-2 protein when compared with control group.	Ascorbic Acid	32-37	caspase 9	Rattus norvegicus	115-124
20963815-5	2011	Furthermore, the cotreatment of vit-C along with ethanol and PTZ showed significantly decreased expression of Bax, caspase-9, caspase-3, cytochrome-c, and significantly increased expression of antiapoptotic Bcl-2 protein when compared with control group.	Ethanol	49-56	caspase 9	Rattus norvegicus	115-124
20963815-5	2011	Furthermore, the cotreatment of vit-C along with ethanol and PTZ showed significantly decreased expression of Bax, caspase-9, caspase-3, cytochrome-c, and significantly increased expression of antiapoptotic Bcl-2 protein when compared with control group.	Pentylenetetrazole	61-64	caspase 9	Rattus norvegicus	115-124
21371463-9	2011	The treatment of wortmannin suppressed the leptin-induced phospho-Akt, Bcl-2, phospho-Bad as well as Bcl-x(L), and recovered the leptin-reduced cleaved caspase-3 and caspase-9.	Wortmannin	17-27	caspase 9	Rattus norvegicus	166-175
21377526-4	2011	When PC12 cells are exposed to dopamine in varying concentrations (100-400muM) for up to 24h, a pronounced impairment of mitochondrial bio-energetic functions at several levels is observed along with a significant (nearly 40%) loss of cell viability with features of apoptotic nuclear changes and increased activities of caspase 3 and caspase 9 and all these effects of dopamine are remarkably prevented by N-acetyl cysteine.	Dopamine	31-39	caspase 9	Rattus norvegicus	335-344
21377526-6	2011	Clorgyline, an inhibitor of MAO-A, markedly decreases the formation of reactive oxygen species in PC12 cells upon dopamine exposure but has only mild protective actions against quinoprotein adduct formation, mitochondrial dysfunctions, cell death and caspase activation induced by dopamine.	Clorgyline	0-10	caspase 9	Rattus norvegicus	251-258
21628957-11	2011	The effect of alpha-tocopherol/Se supplementation on transcriptional activity of three key stress and apoptosis-related genes (i.e., Tp53, CASP3 and CASP9), in response to MTN exposure in rats, was investigated.	alpha-Tocopherol	14-30	caspase 9	Rattus norvegicus	149-154
21628957-11	2011	The effect of alpha-tocopherol/Se supplementation on transcriptional activity of three key stress and apoptosis-related genes (i.e., Tp53, CASP3 and CASP9), in response to MTN exposure in rats, was investigated.	Malathion	172-175	caspase 9	Rattus norvegicus	149-154
21419148-6	2011	DEX treatment significantly down-regulated Bax, caspase 9 and caspase 3 expression induced by BDL at 24-72 h, but had little effect on the expression of caspase 8, Bcl(2,) Fas and Fas-FasL complex.	Dexamethasone	0-3	caspase 9	Rattus norvegicus	48-57
20060605-6	2011	In addition, ABL also induced apoptosis in proliferative VSMCs, as evidenced by the induction of a higher ratio of Bax/Bcl-2, activation of caspase-9, caspase-3, and the cleavage of endogenous substrate Poly (ADP-ribose) polymerase.	lauric acid	13-16	caspase 9	Rattus norvegicus	140-149
21296132-4	2011	The caspase activity was measured by cleavage of the caspase substrate (Ac-DEVD-pNA for caspase-3, Ac-LEHD- pNA for caspase-9).	acetyl-aspartyl-glutamyl-valyl-aspartic acid p-nitroanilide	72-83	caspase 9	Rattus norvegicus	4-11
21296132-4	2011	The caspase activity was measured by cleavage of the caspase substrate (Ac-DEVD-pNA for caspase-3, Ac-LEHD- pNA for caspase-9).	ac-lehd- pna	99-111	caspase 9	Rattus norvegicus	4-11
21295102-7	2011	Pretreatment with curcumin significantly increased DOX-induced apoptosis of cardiac muscle cells through down regulation of Bcl-2, up-regulation of caspase-8 and caspase-9.	Curcumin	18-26	caspase 9	Rattus norvegicus	162-171
21439976-9	2011	Low concentration of EGb761 (10-100mug/ml) aggravated hypoxia/SD-induced apoptosis via Akt inactivation and an enhancement of caspase-9 and caspase-3 expressions, whereas high concentration of EGb761 (500-2000mug/ml) significantly prevented hypoxia/SD-induced BMSC apoptosis via the activated Akt and the inactivated caspase-9 and caspase-3.	SD 0006	62-64	caspase 9	Rattus norvegicus	317-326
21295102-7	2011	Pretreatment with curcumin significantly increased DOX-induced apoptosis of cardiac muscle cells through down regulation of Bcl-2, up-regulation of caspase-8 and caspase-9.	Doxorubicin	51-54	caspase 9	Rattus norvegicus	162-171
21194528-9	2011	Moreover, ghrelin decreased H(2)O(2)-induced Bax production and caspase-9 activation, and increased Bcl-2 levels.	Hydrogen Peroxide	28-36	caspase 9	Rattus norvegicus	64-73
21237271-8	2011	We further found that curcumin can reduce mutant alpha- synuclein-induced intracellular reactive oxygen species (ROS) levels, mitochondrial depolarization, cytochrome c release, and caspase-9 and caspase-3 activation.	Curcumin	22-30	caspase 9	Rattus norvegicus	182-191
21295553-6	2011	Signal transduction studies showed that doxorubicin increased p53, JNK, p38 and NFkappaB phosphorylation; decreased the levels of phospho ERK and Akt; disturbed the Bcl-2 family protein balance; activated caspase 12, caspase 9 and caspase 3; and induced cleavage of the PARP protein.	Doxorubicin	40-51	caspase 9	Rattus norvegicus	217-226
20549303-3	2011	DMI induced typical apoptotic morphology of chromatin condensation in rat glioma C6 cells and activated intracellular caspase 9 and caspase 3 with no change in mitochondrial membrane potential.	Desipramine	0-3	caspase 9	Rattus norvegicus	118-127
21244221-9	2011	Finally, it might be concluded that lead acetate could induce cell toxicity and apoptosis in MSCs, causing instability in mitochondria and in turn activation of the intrinsic pathway including over-expression of Bax, caspase 9 and caspase 3, leading to DNA damage and activation of P53.	Acetates	41-48	caspase 9	Rattus norvegicus	217-226
20934486-5	2011	Moreover, puerarin inhibited the activation of caspase-9 and caspase-3 in MPP(+)-exposed PC12 cells.	puerarin	10-18	caspase 9	Rattus norvegicus	47-56
21468576-4	2011	Treatment with 25 microM propofol significantly protected against hypoxia/reoxygenation-induced cell death, as determined by the MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay and Western blot analysis using anti-apoptotic signal proteins, such as apoptotic protease activating factor 1 and caspase 9.	Propofol	25-33	caspase 9	Rattus norvegicus	317-326
21283687-7	2011	Acetaminophen, a drug recently shown to decrease apoptotic incidence, caspase-9 activation, and mitochondrial dysfunction during global I-R, significantly inhibited the increase in iOPN protein in the right cortex, suggesting a role for iOPN in the response to I-R injury in the right cortex.	Acetaminophen	0-13	caspase 9	Rattus norvegicus	70-79
20803313-8	2011	The expression of both caspase-9 and caspase-3 significantly increased 1 day after SPS stimulation, then gradually increased and peaked at SPS 7d.	Sodium phenolsulfonate	83-86	caspase 9	Rattus norvegicus	23-32
20803313-8	2011	The expression of both caspase-9 and caspase-3 significantly increased 1 day after SPS stimulation, then gradually increased and peaked at SPS 7d.	Sodium phenolsulfonate	139-142	caspase 9	Rattus norvegicus	23-32
22178941-7	2011	Sulphurous mineral water and NaHS treatment may have improved the level of testicular GSH by blocking the overexpression of some apoptosis-related regulatory proteins such as Bax/Bcl-2, cytochrome c, caspase-9 and -3, and p53.	Water	19-24	caspase 9	Rattus norvegicus	200-216
22178941-7	2011	Sulphurous mineral water and NaHS treatment may have improved the level of testicular GSH by blocking the overexpression of some apoptosis-related regulatory proteins such as Bax/Bcl-2, cytochrome c, caspase-9 and -3, and p53.	sodium bisulfide	29-33	caspase 9	Rattus norvegicus	200-216
21747724-12	2011	In addition, the levels of activated caspase-9 and activated caspase-3 were significantly decreased in rats treated with ESC than those in rats treated with CCl(4) alone.	Cefaclor	157-160	caspase 9	Rattus norvegicus	37-46
20807727-8	2010	We provide evidence that PRX III protects pancreatic beta cells from cell stress induced by accumulation of hydrogen peroxide, or the induction of inducible nitric oxide synthase or caspase-9 and -3 by pro-inflammatory cytokines or streptozotocin.	Streptozocin	232-246	caspase 9	Rattus norvegicus	182-198
20869986-10	2011	ONOO(-) induced cytochrome c release from the mitochondria of SGNs and subsequently activated Caspase-9, Caspase-3 and cell apoptosis.	onoo	0-4	caspase 9	Rattus norvegicus	94-103
21686277-6	2011	Moreover, inhibition of JNK by SP600125 rescued PC12 cells from Chp-triggered cell death and attenuated activation of caspases-9 and -3/7 suggesting that activation of JNK mediates pro-apoptotic effect of Chp.	pyrazolanthrone	31-39	caspase 9	Rattus norvegicus	118-135
20712052-8	2010	Furthermore, tectorigenin-induced apoptosis of HSC-T6 cells was associated with the generation of ROS, increased intracellular [Ca(2+)](i), loss of mitochondrial membrane potential, translocation of cytochrome c, and activation of caspase-9 and -3.	tectorigenin	13-25	caspase 9	Rattus norvegicus	231-247
20624456-10	2010	Our results showed apoptotic cells were significantly increased in hippocampus of SPS rats, accompanied by release of cytochrome c from the mitochondria into the cytosol, increase of caspase-9 and caspase-3 expression and decrease of the Bcl-2/Bax ratio.	Sodium phenolsulfonate	82-85	caspase 9	Rattus norvegicus	183-192
21241565-10	2010	Compared with the control group, the gene expression levels of cytochrome C, caspase-9 and caspase-3 in all ethylbenzene-treated groups were enhanced (P < 0.05, P < 0.05, respectively), while bcl-2 gene expression levels in all ethylbenzene-treated groups were decreased (P < 0.05).	ethylbenzene	108-120	caspase 9	Rattus norvegicus	77-86
20538053-11	2010	In addition, FC(EtOH) led to the activation of anti-apoptotic proteins, Bcl-2 and Bcl-xL, the stabilization of the mitochondria membrane and the down-regulation of extrinsic and intrinsic pro-apoptotic proteins, such as TNFalpha, active caspase-8, t-Bid, Bax, active caspases-9, and -3.	Ethanol	16-20	caspase 9	Rattus norvegicus	267-285
20803709-8	2010	17beta-estradiol (E2) decreased OVX-induced proapoptotic t-Bid, Bax, Bax-to-Bcl2 ratio, Bax-to-BclXL ratio, activated caspase 9, and activated caspase 3 as well as increased anti-apoptotic Bcl2 and Bcl-XL relative to OVX (mitochondria pathway).	Estradiol	0-16	caspase 9	Rattus norvegicus	118-127
21029650-7	2010	Furthermore Cytochrome c, caspase 9 and caspase 3 are involved in the regulation of apoptosis under oxidative DNA damage induced by 6-OHDA.	Oxidopamine	132-138	caspase 9	Rattus norvegicus	26-35
20803709-8	2010	17beta-estradiol (E2) decreased OVX-induced proapoptotic t-Bid, Bax, Bax-to-Bcl2 ratio, Bax-to-BclXL ratio, activated caspase 9, and activated caspase 3 as well as increased anti-apoptotic Bcl2 and Bcl-XL relative to OVX (mitochondria pathway).	ovx	32-35	caspase 9	Rattus norvegicus	118-127
20434464-5	2010	Administration of eugenol induced apoptosis via the mitochondrial pathway by modulating the Bcl-2 family proteins, Apaf-1, cytochrome C, and caspases and inhibiting invasion, and angiogenesis as evidenced by changes in the activities of MMPs and the expression of MMP-2 and -9, VEGF, VEGFR1, TIMP-2 and RECK.	Eugenol	18-25	caspase 9	Rattus norvegicus	141-149
20573599-11	2010	The decrease in the number of apoptotic cells in the HGM containing BDNF, NT-4, or citicoline is correlated with the suppression of the caspase-9 and -3 activities.	Cytidine Diphosphate Choline	83-93	caspase 9	Rattus norvegicus	136-152
20406680-9	2010	GA prevents NSAID-induced activation of caspase-9, a marker for the mitochondrial pathway of apoptosis, and restores NSAID-mediated collapse of the mitochondrial transmembrane potential and dehydrogenase activity.	Gallic Acid	0-2	caspase 9	Rattus norvegicus	40-49
20726227-3	2010	The activity and the expression of mRNA and protein of caspase-9 were detected at Oh, 3h, 6h, 24h, 3d and 7d after laser irradiation.	Tritium	86-88	caspase 9	Rattus norvegicus	55-64
19957244-7	2010	1 muM beta-carotene decreased oxidative stress and prevented ethanol-induced cell death by inhibiting caspase-9 and caspase-3 expression.	Ethanol	61-68	caspase 9	Rattus norvegicus	102-111
19960285-9	2010	Furthermore, NS3694 and Z-ATAD-FMK dramatically suppress annular cell apoptosis and caspase-9 activity.	z-atad-fmk	24-34	caspase 9	Rattus norvegicus	84-93
19957244-5	2010	In contrast, cell viability, GSH levels, and glutathione reductase (GRD) activity significantly increased while lipid peroxides and expressions of CYP2E1, casapse-3, and caspase-9 decreased in the EB group.	Eriochrome Blue SE	197-199	caspase 9	Rattus norvegicus	170-179
20493166-5	2010	In addition, nitroalkenes stimulate extrinsic caspase-8 and intrinsic caspase-9 activity to trigger the caspase-3 apoptotic signaling cascade, resulting in RASMCs death.	nitroalkenes	13-25	caspase 9	Rattus norvegicus	70-79
19957244-7	2010	1 muM beta-carotene decreased oxidative stress and prevented ethanol-induced cell death by inhibiting caspase-9 and caspase-3 expression.	beta Carotene	6-19	caspase 9	Rattus norvegicus	102-111
19883181-6	2010	Measurements of caspase-3/7 and caspase-9 showed a significant increase in cisplatin-treated rats.	Cisplatin	75-84	caspase 9	Rattus norvegicus	32-41
20171161-8	2010	Subsequent analysis of DNA degradation and caspase activation reveals that MG inhibits activation of caspase 9 and has a partial inhibitory effect on DNA degradation.	methyl gallate	75-77	caspase 9	Rattus norvegicus	101-110
19944120-5	2010	Moreover, acute L-Glu significantly induced mRNA expression of nNOS, iNOS, caspase-3 and caspase-9.	Glutamic Acid	16-21	caspase 9	Rattus norvegicus	89-98
20152804-3	2010	Brief CO pretreatment (10 min) or a caspase-9 inhibitor (Z-LEHD-FMK) attenuated these apoptotic changes.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	57-67	caspase 9	Rattus norvegicus	36-45
20079345-7	2010	Acetaminophen maintained mitochondrial cytochrome c content and reduced activation of caspase-9 and incidence of apoptosis.	Acetaminophen	0-13	caspase 9	Rattus norvegicus	86-95
19940077-6	2010	NAO treatment significantly reduced the cytosolic cytochrome c contents and caspase-9 activity in the ischemic region but did not affect caspase-8 activity.	10-N-nonylacridinium orange	0-3	caspase 9	Rattus norvegicus	76-85
20117987-6	2010	LY294002 treatment prior to rHuEPO injection significantly abolished the effects of rHuEPO on caspase-9 and p-Akt immunohistochemical positivity and caspase-9 mRNA and p-Akt protein expressions (P<0.05).	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	0-8	caspase 9	Rattus norvegicus	94-103
19922764-9	2010	Our experimental evidence suggests that APAP-induced nephro-toxicity is a caspase-dependent process that involves activation of caspase-9 and caspase-3 in the absence of cytosolic cytochrome C release.	Acetaminophen	40-44	caspase 9	Rattus norvegicus	128-137
20117987-6	2010	LY294002 treatment prior to rHuEPO injection significantly abolished the effects of rHuEPO on caspase-9 and p-Akt immunohistochemical positivity and caspase-9 mRNA and p-Akt protein expressions (P<0.05).	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	0-8	caspase 9	Rattus norvegicus	149-158
20092796-6	2009	RESULTS: Pretreatment with geniposide markedly improved the cells viability and morphology, decreased the expression of Bax, P53 and caspase-9, and increased the expression of Bcl-2 in PC12 cells challenged by CoCl(2)2.	geniposide	27-37	caspase 9	Rattus norvegicus	133-142
20110659-7	2010	These studies suggest that apoptosis induced by BC or DA is mediated through distinct and independent pathways that converge with activation of the terminal caspase, caspase-3.	Bromocriptine	48-50	caspase 9	Rattus norvegicus	157-164
20110659-7	2010	These studies suggest that apoptosis induced by BC or DA is mediated through distinct and independent pathways that converge with activation of the terminal caspase, caspase-3.	Dopamine	54-56	caspase 9	Rattus norvegicus	157-164
19995276-11	2009	Sivelestat also inhibited the elastase-induced caspase-3 and -9 activities and cytochrome c release from the mitochondria but did not inhibit the bleomycin-induced caspase activities in A549 cells.	sivelestat	0-10	caspase 9	Rattus norvegicus	47-63
19995276-12	2009	In conclusion, bleomycin caused the lung inflammatory cell apoptosis through the caspase-9 and -3 pathways in rats.	Bleomycin	15-24	caspase 9	Rattus norvegicus	81-97
20113661-8	2009	Caspase 8 and caspase 9 were activated in 20 microM of copper aceticum culture medium 4 hrs after incubation and peaked at 48 hrs in various concentrations of copper aceticum culture medium, presenting with a time and concentration dependent manner.	copper aceticum	55-70	caspase 9	Rattus norvegicus	14-23
19630065-7	2009	On the other hand, Tau or L-Gln significantly suppressed the release of cytochrome C from mitochondria and attenuated the activities of both caspases, which could be attributed to the maintenance of Bcl-2 expression.	Taurine	19-22	caspase 9	Rattus norvegicus	141-149
19630065-7	2009	On the other hand, Tau or L-Gln significantly suppressed the release of cytochrome C from mitochondria and attenuated the activities of both caspases, which could be attributed to the maintenance of Bcl-2 expression.	Glutamine	26-31	caspase 9	Rattus norvegicus	141-149
20113661-1	2009	OBJECTIVE: This study aimed to investigate the mechanism of primary cortical neuron injury induced by high concentrations of copper by observing the effect of aceticum culture medium on apoptosis of rat primary cortical neurons and expression of cleaved caspase 3, caspase 8 and caspase 9.	Copper	125-131	caspase 9	Rattus norvegicus	279-288
20113661-8	2009	Caspase 8 and caspase 9 were activated in 20 microM of copper aceticum culture medium 4 hrs after incubation and peaked at 48 hrs in various concentrations of copper aceticum culture medium, presenting with a time and concentration dependent manner.	copper aceticum	159-174	caspase 9	Rattus norvegicus	14-23
20137408-11	2009	Compared with the control group, the expression levels of cytochrome C and Caspase-9 were enhanced, while the expression levels of Bcl-2 were restrained in all ethylbenzene-treated groups (P < 0.05, P < 0.05, respectively).	ethylbenzene	160-172	caspase 9	Rattus norvegicus	75-84
20113661-12	2009	Caspase 3, caspase 8 and caspase 9 cascade reaction may involve in the apoptosis of copper induced rat primary cortical neurons.	Copper	84-90	caspase 9	Rattus norvegicus	25-34
19678761-9	2009	WST-8 and JC-1 assays were used to evaluate mitochondrial function, since a strong activation of caspase-9 by TBTC suggested mitochondrial involvement.	tbtc	110-114	caspase 9	Rattus norvegicus	97-106
19643096-8	2009	The anti-apoptotic effects of these compounds were confirmed by verifying their ability to inhibit the DNA fragmentation and caspase-9 activation induced by manganese.	Manganese	157-166	caspase 9	Rattus norvegicus	125-134
19467786-5	2009	The present study examined the involvement of caspase-3, the executioner, and two initiators of apoptosis, caspase-8 and caspase-9, during high glucose-induced apoptosis in PC12 cells, a neuronal cell line.	Glucose	144-151	caspase 9	Rattus norvegicus	121-130
19464431-9	2009	We show that calcium and Bax are responsible for the decrease in mitochondrial membrane potential (Deltapsi(m)), thereby leading to the release of cytochrome c and activation of caspase-9.	Calcium	13-20	caspase 9	Rattus norvegicus	178-187
19694182-5	2009	Schisandrin B also reduced the release of mitochondrial cytochrome c into cytosol and decreased caspase-9 and caspase-3 activities.	schizandrin B	0-13	caspase 9	Rattus norvegicus	96-105
19515844-7	2009	However, if mitochondria were prevented from loading with Ca2+ with 10 mum RU360, then caspase-9 activation did not occur irrespective of the content of other Ca2+ stores.	Ru 360	75-80	caspase 9	Rattus norvegicus	87-96
19641885-1	2009	The present study was designed to investigate the cardio-protective effect of Ac-LEDH-cmk a selective caspase-9 inhibitor and 5-aminoisoquinolinone a selective Poly (ADP-ribose) polymerase inhibitor on ischemia and reperfusion induced apoptotic and necrotic cell death in rats.	Actinium	78-80	caspase 9	Rattus norvegicus	102-111
19641885-1	2009	The present study was designed to investigate the cardio-protective effect of Ac-LEDH-cmk a selective caspase-9 inhibitor and 5-aminoisoquinolinone a selective Poly (ADP-ribose) polymerase inhibitor on ischemia and reperfusion induced apoptotic and necrotic cell death in rats.	ledh	81-85	caspase 9	Rattus norvegicus	102-111
19346530-4	2009	We found that one intratesticular injection of etoposide (1.2 microg/testis) induced a significant increase in spermatocytes undergoing apoptosis, along with activation of caspase-9, -8 and -3 after 24 h of treatment.	Etoposide	47-56	caspase 9	Rattus norvegicus	172-192
19221718-7	2009	Furthermore, treatment of hippocampal neurons with EGCG resulted in an elevation of caspase-3 and caspase-9 activities with no significant accompaniment of lactate dehydrogenase release, which provided further evidence that apoptosis was the dominant mode of EGCG-induced cell death in cultures of hippocampal neurons.	epigallocatechin gallate	51-55	caspase 9	Rattus norvegicus	98-107
19954022-8	2009	After streptomycin treatment, the nuclear shrinkage and fragmentation were found in most cochlear hair cells, and the caspase-8, caspase-9 and caspase-6 were greatly activated.	Streptomycin	6-18	caspase 9	Rattus norvegicus	129-138
19608010-11	2009	In accordance, U50488H treatment significantly inhibited I/R-induced elevated activities of caspase-3 and caspase-9.	3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer	15-22	caspase 9	Rattus norvegicus	106-115
19293697-10	2009	Isoflurane decreased caspase 9 activity, inhibited proliferation, and decreased the proportion of cells in s-phase.	Isoflurane	0-10	caspase 9	Rattus norvegicus	21-30
19009284-3	2009	The objectives of this study were to determine the effect of fluoride treatment on osteoblast proliferation, apoptosis and caspase-3 and caspase-9 mRNA expression in vitro.	Fluorides	61-69	caspase 9	Rattus norvegicus	137-146
19009284-7	2009	Increased-osteoblast caspase-3 and caspase-9 mRNA was also observed in response to sodium fluoride treatment (5 mg/l) for 72 h. Results indicate that negative effects of excess fluoride on skeletal health may be mediated in part by inhibition of osteoblast survival.	Sodium Fluoride	83-98	caspase 9	Rattus norvegicus	35-44
19009284-7	2009	Increased-osteoblast caspase-3 and caspase-9 mRNA was also observed in response to sodium fluoride treatment (5 mg/l) for 72 h. Results indicate that negative effects of excess fluoride on skeletal health may be mediated in part by inhibition of osteoblast survival.	Fluorides	90-98	caspase 9	Rattus norvegicus	35-44
19484960-16	2009	CONCLUSIONS: Curcumin can induce apoptosis of pulmonary fibroblasts in rats with bleomycin-induced pulmonary fibrosis and the mechanism may be related to the activation of Caspase-3, Caspase-8, and Caspase-9.	Curcumin	13-21	caspase 9	Rattus norvegicus	198-207
19095035-9	2009	Curcumin-induced apoptosis was mediated by caspase-9 in young but not older rats.	Curcumin	0-8	caspase 9	Rattus norvegicus	43-52
19049974-10	2009	The scavengers also restore indomethacin-induced activation of caspase-9 and caspase-3 to block mitochondrial pathway of apoptosis and gastric mucosal damage.	Indomethacin	28-40	caspase 9	Rattus norvegicus	63-72
19713707-10	2009	LA attenuated the translocation of mitochondrial bax, reduced the release of cytochrome c, and decreased the expression of caspase-3 and caspase-9 serially in cisplatin nephrotoxicity.	Cisplatin	159-168	caspase 9	Rattus norvegicus	137-146
19382457-10	2009	Cyt-C release and the expression of caspase-3 and caspase-9 proteins in groups of middle and high doses of dauricine were also inhibited compared with Model group (P<0.01).	dauricine	107-116	caspase 9	Rattus norvegicus	50-59
18926904-3	2008	Activation of caspase-9 and -3 was considerably lower in DOX-treated ARCM as compared with NRCM and H9c2 cardiomyoblasts.	Doxorubicin	57-60	caspase 9	Rattus norvegicus	14-30
18926904-7	2008	Adenoviral expression of Apaf1 exacerbated the activation of caspase-9 and -3 in DOX-treated NRCM, but did not increase their activities in DOX-treated ARCM.	Doxorubicin	81-84	caspase 9	Rattus norvegicus	61-77
18591962-6	2008	However, cells treated with Actinomycin D (ActD) become susceptible to TNF-alpha-induced cell death through the activation of caspase-8, generation of tBid and activation of caspase-9 and -3.	Dactinomycin	28-41	caspase 9	Rattus norvegicus	174-190
18706882-6	2008	These effects are strengthened by the activation of caspase-9 along with increased caspase-3 activity upon treatment of PC12 cells with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	136-141	caspase 9	Rattus norvegicus	52-61
18720870-6	2008	In addition, Fufang Haishe capsule inhibited the activity of caspase-9 and caspase-3 of PC-12 cells which was induced by Abeta.	UNII-042A8N37WH	121-126	caspase 9	Rattus norvegicus	61-70
18695920-10	2008	Results showed that in mammary tumours induced by NMU, the apoptotic death receptor-mediated pathway is activated through caspase-3 and -8, but the apoptotic mitochondrial pathway is suppressed through a non-activating process of caspase-9 activity, despite the release of cytochrome c. In conclusion, these findings have demonstrated a suppression of the apoptotic mitochondrial pathway through a non-activating process of caspase-9 activity, despite the release of cytochrome c in mammary tumours induced by NMU.	Methylnitrosourea	50-53	caspase 9	Rattus norvegicus	230-239
18695920-10	2008	Results showed that in mammary tumours induced by NMU, the apoptotic death receptor-mediated pathway is activated through caspase-3 and -8, but the apoptotic mitochondrial pathway is suppressed through a non-activating process of caspase-9 activity, despite the release of cytochrome c. In conclusion, these findings have demonstrated a suppression of the apoptotic mitochondrial pathway through a non-activating process of caspase-9 activity, despite the release of cytochrome c in mammary tumours induced by NMU.	Methylnitrosourea	50-53	caspase 9	Rattus norvegicus	424-433
18381230-3	2008	In this study, to determine the apoptotic pathway initiated by copper treatment, apoptotic factors such as Bax, Bad and Bcl-2, and the caspase family in PC12 cells treated with copper were measured by Western blot and RT-PCR analyses.	Copper	177-183	caspase 9	Rattus norvegicus	135-142
18490855-8	2008	As indicated by Western blotting, schizandrin attenuated the protein level changes of procaspase-9, caspase-9, and caspase-3 and cleaved poly(ADP-ribose) polymerase (PARP).	schizandrin	34-45	caspase 9	Rattus norvegicus	89-98
18569012-3	2008	25-OH-chol increased the production of reactive oxygen species and opened mitochondrial permeability transition pore, resulting in release of cytochrome c and subsequent activation of caspase-9 and -3.	25-oh-chol	0-10	caspase 9	Rattus norvegicus	184-200
18569012-3	2008	25-OH-chol increased the production of reactive oxygen species and opened mitochondrial permeability transition pore, resulting in release of cytochrome c and subsequent activation of caspase-9 and -3.	Reactive Oxygen Species	39-62	caspase 9	Rattus norvegicus	184-200
18569012-5	2008	The JNK inhibitor SP600125 attenuated the activation of caspase-9 and -3 and reduced 25-OH-chol-induced cell death.	pyrazolanthrone	18-26	caspase 9	Rattus norvegicus	56-72
18163394-2	2008	Staurosporine induced apparent cleavage of caspase-8, caspase-9, and caspase-3.	Staurosporine	0-13	caspase 9	Rattus norvegicus	54-63
18154951-7	2008	Furthermore, naringenin-7-O-glucoside increased the protein levels of heme oxygenase-1 (HO-1) and Bcl-2 in cardiomyocytes (as detected by Western blotting) and suppressed the mRNA expression of caspase-3 and caspase-9 (as detected by RT-PCR).	naringenin-7-O-glucoside	13-37	caspase 9	Rattus norvegicus	208-217
18339080-0	2008	Atorvastatin induces apoptosis by a caspase-9-dependent pathway: an in vitro study on activated rat hepatic stellate cells.	Atorvastatin	0-12	caspase 9	Rattus norvegicus	36-45
18339080-12	2008	Atorvastatin-induced apoptosis in activated HSCs is related to an increased protease activity of caspase-9 and -3.	Atorvastatin	0-12	caspase 9	Rattus norvegicus	97-113
18339080-16	2008	CONCLUSIONS: Atorvastatin induces apoptosis in activated HSCs acting through an ERK-dependent cleavage of Bid and a highly increased protease activity of caspase-9 and -3.	Atorvastatin	13-25	caspase 9	Rattus norvegicus	154-170
17894423-6	2008	The increased cellular sizes, DNA fragmentation, nuclear condensation, Bad, cyt c, and caspase-9 activities of H9c2 cells treated with P. gingivalis conditioned medium were all significantly reduced after pre-administration of SB203580.	SB 203580	227-235	caspase 9	Rattus norvegicus	87-96
18466417-5	2008	Moreover, treatment with vanadyl sulfate also significantly inhibited the apoptosis-related Caspase-3 and Caspase-9 processing, thereby elicited the antiapoptotic effect.	vanadyl sulfate	25-40	caspase 9	Rattus norvegicus	106-115
18202115-13	2008	The MEK1 and MEK2 inhibitors U-0126 and PD-98059 significantly attenuated the protection of IL-11 against caspase-3 and caspase-9 cleavage and cytoplasmic oligonucleosomal DNA accumulation.	U 0126	29-35	caspase 9	Rattus norvegicus	120-129
18202115-13	2008	The MEK1 and MEK2 inhibitors U-0126 and PD-98059 significantly attenuated the protection of IL-11 against caspase-3 and caspase-9 cleavage and cytoplasmic oligonucleosomal DNA accumulation.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	40-48	caspase 9	Rattus norvegicus	120-129
18093848-0	2008	Aqueous extract of the Chinese medicine, Danggui-Shaoyao-San, inhibits apoptosis in hydrogen peroxide-induced PC12 cells by preventing cytochrome c release and inactivating of caspase cascade.	Hydrogen Peroxide	84-101	caspase 9	Rattus norvegicus	176-183
18093848-3	2008	The apoptosis in H2O2-induced PC12 cells was accompanied by downregulation of Bcl-2, upregulation of Bax, the release of mitochondrial cytochrome c into cytosol, and sequential activation of caspase-9 and -3.	Hydrogen Peroxide	17-21	caspase 9	Rattus norvegicus	191-207
18321562-6	2008	The results showed that adriamycin administered to the mother rat before pregnancy subsequently induced changes in fetal kidneys involving both the mitochondrial pathway of apoptosis, with increased labeling of the proteins p53, Bax, Apaf-1 and caspase 9, and the endoplasmic reticulum pathway of apoptosis, with increased labeling of caspase 12.	Doxorubicin	24-34	caspase 9	Rattus norvegicus	245-254
18300051-3	2008	Asbestos exposure induced a dose-dependent increase of apoptotic cells, and both pretreatment with Z-LEHD-FMK (caspase-3 inhibitor) or Z-DEMK-FMK (caspase-9 inhibitor) significantly suppressed asbestos-induced apoptosis.	Asbestos	0-8	caspase 9	Rattus norvegicus	147-156
18300051-3	2008	Asbestos exposure induced a dose-dependent increase of apoptotic cells, and both pretreatment with Z-LEHD-FMK (caspase-3 inhibitor) or Z-DEMK-FMK (caspase-9 inhibitor) significantly suppressed asbestos-induced apoptosis.	z-demk-fmk	135-145	caspase 9	Rattus norvegicus	147-156
18300051-3	2008	Asbestos exposure induced a dose-dependent increase of apoptotic cells, and both pretreatment with Z-LEHD-FMK (caspase-3 inhibitor) or Z-DEMK-FMK (caspase-9 inhibitor) significantly suppressed asbestos-induced apoptosis.	Asbestos	193-201	caspase 9	Rattus norvegicus	147-156
18300051-6	2008	Asbestos exposure increased the number of apoptotic cells and the activation of cleaved caspase-3 and -9 most at 3 days in a dose dependent manner, and continued to increase them until at least 6 months after asbestos exposure.	Asbestos	0-8	caspase 9	Rattus norvegicus	88-104
21141559-13	2008	The expressions of Bax, caspase-9, 3 protein in 30, 60 micromol x L(-1) propofol were obviously lower than those of I/R group( P < 0.05).	Propofol	72-80	caspase 9	Rattus norvegicus	24-33
18207679-8	2008	DMSO treatment induced TUNEL-positive staining in many hair cells and activated both initiator caspase-9 and caspase-8 and executioner caspase-3; this suggests that apoptosis is initiated by both intrinsic mitochondrial and extrinsic membrane cell death signaling pathways.	Dimethyl Sulfoxide	0-4	caspase 9	Rattus norvegicus	95-104
18595259-15	2007	CONCLUSION: Early AT II apoptosis may be induced by bleomycin, which may be explained by the increase of intracellular free calcium concentration, depression of MMP, increased expressions of Fas and Bax, and increase of Caspase-3, Caspase-8, and Caspase-9 activities.	Bleomycin	52-61	caspase 9	Rattus norvegicus	246-255
17906689-7	2007	KEY RESULTS: CDDP significantly increased the levels of caspase-3/7 activity and active caspase-3 protein expression and caspase-3 immunofluorescence staining, caspase-9 activity, and Bax protein expression but decreased Bcl-2 protein expression within the rat cochleae.	Cisplatin	13-17	caspase 9	Rattus norvegicus	160-169
18974856-7	2008	In accordance, cocaine dose dependently increased activities of caspase-3, caspase-8, and caspase-9 (% of control) in the fetal brain by 177%, 155%, 174%, respectively, at 30 mg/kg/day, and by 191%, 176%, 274%, respectively, at 60 mg/kg/day.	Cocaine	15-22	caspase 9	Rattus norvegicus	90-99
17950707-6	2007	Kaempferol treatment efficiently protected against nitrosative-oxidative stress after ischemia/reperfusion, as shown by nearly complete protection against the increase of protein nitrotyrosines, and also afforded strong protection against the increase of apoptotic cell death (TUNEL) and biochemical markers of apoptosis, such as caspase-9 activity and poly-(ADP-ribose) polymerase degradation.	kaempferol	0-10	caspase 9	Rattus norvegicus	330-339
17592516-7	2007	CONCLUSIONS AND IMPLICATIONS: Amlodipine inhibition of Akt occurred prior to and during SMC apoptosis induction, a process mediated by the early activation of caspase-8 followed by caspase-9 and -3 and associated with MAP kinase inhibition.	Amlodipine	30-40	caspase 9	Rattus norvegicus	181-197
17426927-5	2007	Saturated fatty acids increased caspase-9 and caspase-3 activity, however increased caspase-12 activity was not observed.	Fatty Acids	0-21	caspase 9	Rattus norvegicus	32-41
17635674-2	2007	We previously showed that cocaine exposure in vitro activates pro-apoptotic Bax, caspase-9, and caspase-3 in LC neurons dissected from embryonic day 14 rats, implicating that apoptosis may be orchestrated via signal transduction events.	Cocaine	26-33	caspase 9	Rattus norvegicus	81-90
17636024-6	2007	Finally, we provide evidence that PHIP1 overexpression blocks free fatty acid-induced apoptosis in INS-1 cells, which is accompanied by marked activation of phosphoprotein kinase B (PKB)/AKT and the concomitant inhibition of caspase-9 and caspase-3 cleavage.	Fatty Acids, Nonesterified	62-77	caspase 9	Rattus norvegicus	225-234
17551980-3	2007	This study assesses whether ammonia intoxication in vivo leads to induction of apoptotic markers such as permeability transition pore (PTP) formation, caspase-3, and caspase-9 activation, changes in p53 protein, or cytochrome c release.	Ammonia	28-35	caspase 9	Rattus norvegicus	166-175
17204252-2	2007	We investigated whether the initiator caspase in the extrinsic pathway, caspase-8, or the intrinsic pathway, caspase-9, is activated during the first 24 h following lithium-pilocarpine-induced status epilepticus, when neuronal death is maximal and widespread.	Lithium	165-172	caspase 9	Rattus norvegicus	109-118
17420221-12	2007	In the styrene-induced apoptotic OHCs, histochemical staining detected activated caspases-9 and 8, indicating that both mitochondrial-dependent pathway and death receptor-dependent pathway were involved in the styrene-induced cell death.	Styrene	7-14	caspase 9	Rattus norvegicus	81-97
17420221-12	2007	In the styrene-induced apoptotic OHCs, histochemical staining detected activated caspases-9 and 8, indicating that both mitochondrial-dependent pathway and death receptor-dependent pathway were involved in the styrene-induced cell death.	Styrene	210-217	caspase 9	Rattus norvegicus	81-97
17240404-5	2007	Also, EGCG attenuated the CoCl(2)-induced disruption of mitochondrial membrane potential (DeltaPsim), release of cytochrome c from the mitochondria to cytosol and abolished the CoCl(2)-stimulated activities of the caspase cascades, caspase-9 and caspase-3.	epigallocatechin gallate	6-10	caspase 9	Rattus norvegicus	214-221
17240404-5	2007	Also, EGCG attenuated the CoCl(2)-induced disruption of mitochondrial membrane potential (DeltaPsim), release of cytochrome c from the mitochondria to cytosol and abolished the CoCl(2)-stimulated activities of the caspase cascades, caspase-9 and caspase-3.	epigallocatechin gallate	6-10	caspase 9	Rattus norvegicus	232-241
17240404-5	2007	Also, EGCG attenuated the CoCl(2)-induced disruption of mitochondrial membrane potential (DeltaPsim), release of cytochrome c from the mitochondria to cytosol and abolished the CoCl(2)-stimulated activities of the caspase cascades, caspase-9 and caspase-3.	cobaltous chloride	26-33	caspase 9	Rattus norvegicus	214-221
17531161-9	2007	In clipped kidneys from 2K1C rats, inhibition of HO activity by SnMP augmented caspase-3 and caspase-9 activity and decreased expression of the anti-apoptotic Bcl-2 protein, while induction of HO-1 with CoPP strongly inhibited the activity of both caspases and increased the induction of Bcl-2 and Bcl-xl proteins.	tin mesoporphyrin	64-68	caspase 9	Rattus norvegicus	93-102
17612592-6	2007	CONCLUSIONS: K(ATP) opener can significantly decrease the neuronal apoptosis and the expressions of caspase-3, caspase-8 and caspase-9 mRNAs following cerebral ischemia-reperfusion.	Adenosine Triphosphate	15-18	caspase 9	Rattus norvegicus	125-134
17448277-11	2007	CONCLUSION: K( ATP) opener can significantly mitigate neuronal apoptosis and inhibit the expressions of caspase-3 and caspase-9 mRNA and protein after cerebral I/R injury.	Adenosine Triphosphate	15-18	caspase 9	Rattus norvegicus	118-127
17240404-5	2007	Also, EGCG attenuated the CoCl(2)-induced disruption of mitochondrial membrane potential (DeltaPsim), release of cytochrome c from the mitochondria to cytosol and abolished the CoCl(2)-stimulated activities of the caspase cascades, caspase-9 and caspase-3.	cobaltous chloride	26-33	caspase 9	Rattus norvegicus	232-241
17240404-5	2007	Also, EGCG attenuated the CoCl(2)-induced disruption of mitochondrial membrane potential (DeltaPsim), release of cytochrome c from the mitochondria to cytosol and abolished the CoCl(2)-stimulated activities of the caspase cascades, caspase-9 and caspase-3.	cobaltous chloride	177-184	caspase 9	Rattus norvegicus	214-221
17240404-5	2007	Also, EGCG attenuated the CoCl(2)-induced disruption of mitochondrial membrane potential (DeltaPsim), release of cytochrome c from the mitochondria to cytosol and abolished the CoCl(2)-stimulated activities of the caspase cascades, caspase-9 and caspase-3.	cobaltous chloride	177-184	caspase 9	Rattus norvegicus	232-241
17204252-4	2007	Following methamphetamine treatment, caspase-9 but not caspase-8 was activated in thymocytes.	Methamphetamine	10-25	caspase 9	Rattus norvegicus	37-46
17301078-2	2007	Treatment of brefeldin A, an inhibitor of transport between the ER and Golgi complex, induced cell death during 24 h, which accompanied activation of caspase-2, caspase-3 and caspase-9, starting at 12 h and increasing time-dependently up to 28 h. Caspase-2 was expressed and activated in not only mitochondria and cytosol, but also in the microsomal fraction containing ER and Golgi.	Brefeldin A	13-24	caspase 9	Rattus norvegicus	175-184
17291986-9	2007	Vitamin E treatment abolished the large upregulation of caspases-9 and -12 and MuRF1 transcripts in unloaded muscle and greatly decreased the upregulation of mu-calpain, caspase-3, and MAFbx mRNA.	Vitamin E	0-9	caspase 9	Rattus norvegicus	56-74
17291991-7	2007	On the other hand, 6-OHDA-induced caspase-3 activation was inhibited in the presence of caspase-8, caspase-9, and calpain inhibitors.	Oxidopamine	19-25	caspase 9	Rattus norvegicus	99-108
17250636-13	2007	Dauricine (42 and 84 mg/kg) pretreatment improved histopathological recovery, diminished DNA fragmentation and reduced cytochrome c release and activation of caspase 9 and caspase 3 in the penumbra at 24 h. 4.	dauricine	0-9	caspase 9	Rattus norvegicus	158-167
17171702-8	2007	Pretreatment with a caspase-3 or caspase-9 inhibitor nearly completely prevented the morphologic, biochemical, and functional changes induced by methimazole.	Methimazole	145-156	caspase 9	Rattus norvegicus	33-42
17171702-9	2007	These findings suggest strongly that methimazole-induced cell death in rat ORNs is predominantly apoptosis; moreover, the majority of this apoptotic cell death is triggered through mitochondrial cytochrome c-mediated caspase-3 activation pathway, and both caspase-3 and caspase-9 inhibitors can prevent methimazole-induced cell death in the ORNs.	Methimazole	37-48	caspase 9	Rattus norvegicus	270-279
17086548-9	2007	Both BDNF and NMDA decreased caspase-9 activity and mRNA caspase-3 levels and activity induced by low potassium.	N-Methylaspartate	14-18	caspase 9	Rattus norvegicus	29-38
17018771-9	2007	Western blot analysis demonstrated that H(2)O(2)-induced cytochrome c release from mitochondrion to cytosol and the activation of caspase-9 and -3 were decreased by 17beta-estradiol.	Hydrogen Peroxide	40-48	caspase 9	Rattus norvegicus	130-146
17018771-9	2007	Western blot analysis demonstrated that H(2)O(2)-induced cytochrome c release from mitochondrion to cytosol and the activation of caspase-9 and -3 were decreased by 17beta-estradiol.	Estradiol	165-181	caspase 9	Rattus norvegicus	130-146
17018771-10	2007	These findings suggest that 17beta-estradiol attenuated H(2)O(2)-induced apoptosis via ER-dependent activation of caspase-9 and -3 in rat endothelial cells through mitochondria.	Estradiol	28-44	caspase 9	Rattus norvegicus	114-130
17018771-10	2007	These findings suggest that 17beta-estradiol attenuated H(2)O(2)-induced apoptosis via ER-dependent activation of caspase-9 and -3 in rat endothelial cells through mitochondria.	Hydrogen Peroxide	56-64	caspase 9	Rattus norvegicus	114-130
17086548-9	2007	Both BDNF and NMDA decreased caspase-9 activity and mRNA caspase-3 levels and activity induced by low potassium.	Potassium	102-111	caspase 9	Rattus norvegicus	29-38
17116366-8	2007	EGCG abrogated the activation of caspase-9, caspase-8 and caspase-3 induced by SNP.	epigallocatechin gallate	0-4	caspase 9	Rattus norvegicus	33-42
17084983-8	2007	Further, cocaine exposure significantly increased caspase-9 and caspase-3 activities at all time points, without changes in caspase-8 activity in LC neurons.	Cocaine	9-16	caspase 9	Rattus norvegicus	50-59
17046714-8	2006	GdCl(3) also activated caspase 9 and increased apoptosis in myocyte by increasing [Ca(2+)](i).	gdcl	0-4	caspase 9	Rattus norvegicus	23-32
17106869-0	2007	The water extract of Omija protects H9c2 cardiomyoblast cells from hydrogen peroxide through prevention of mitochondrial dysfunction and activation of caspases pathway.	Water	4-9	caspase 9	Rattus norvegicus	151-159
17106869-8	2007	Taken together, these data indicate that the water extract of Omija protects H9c2 cardiomyoblast cells from oxidative stress of H(2)O(2) through inhibition of mitochondrial dysfunction and activation of intrinsic caspase cascades, including caspase-3 and caspase-9.	Water	45-50	caspase 9	Rattus norvegicus	213-220
17106869-8	2007	Taken together, these data indicate that the water extract of Omija protects H9c2 cardiomyoblast cells from oxidative stress of H(2)O(2) through inhibition of mitochondrial dysfunction and activation of intrinsic caspase cascades, including caspase-3 and caspase-9.	Water	45-50	caspase 9	Rattus norvegicus	255-264
17007737-10	2006	In parallel with these findings, Abeta1-40-induced changes in activation of caspase-9, caspase-7, and caspase-3 were inhibited by pretreatment with SF.	ferulic acid	148-150	caspase 9	Rattus norvegicus	76-85
17076656-4	2006	Glutamate increased activation of caspase 9 followed by cleavage of caspase 7, which in turn fragmented poly(ADP-ribose) polymerase, terminating in cell death in both the hypothalamus and cerebellum.	Glutamic Acid	0-9	caspase 9	Rattus norvegicus	34-43
16514665-9	2006	The results showed that Hcy-mediated ROS production preceded the loss of MP, the release of cytochrome-c, and the activation of caspase-9 and -3.	Homocysteine	24-27	caspase 9	Rattus norvegicus	128-144
16781062-7	2006	MK-801 treatment did not modify the activity of caspase-8 at any age, but decreased caspase-9 activity at P8 and increased the activity of caspase-1 (76%) at P8, caspase-3 (160%) at P16 and caspase-9 (50%) at P12.	Dizocilpine Maleate	0-6	caspase 9	Rattus norvegicus	84-93
16781062-7	2006	MK-801 treatment did not modify the activity of caspase-8 at any age, but decreased caspase-9 activity at P8 and increased the activity of caspase-1 (76%) at P8, caspase-3 (160%) at P16 and caspase-9 (50%) at P12.	Dizocilpine Maleate	0-6	caspase 9	Rattus norvegicus	190-199
16597613-6	2006	Caspases-9 and -3 were activated only by 10 microM cadmium for 24 h, and accordingly apoptosis was significantly reduced by the respective inhibitors (z-LEHD-fmk, z-DEVD-fmk; 10 microg/ml) at 24 h, but not at 6 h, without affecting necrosis.	Cadmium	51-58	caspase 9	Rattus norvegicus	0-17
16597613-6	2006	Caspases-9 and -3 were activated only by 10 microM cadmium for 24 h, and accordingly apoptosis was significantly reduced by the respective inhibitors (z-LEHD-fmk, z-DEVD-fmk; 10 microg/ml) at 24 h, but not at 6 h, without affecting necrosis.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	151-161	caspase 9	Rattus norvegicus	0-17
16597613-6	2006	Caspases-9 and -3 were activated only by 10 microM cadmium for 24 h, and accordingly apoptosis was significantly reduced by the respective inhibitors (z-LEHD-fmk, z-DEVD-fmk; 10 microg/ml) at 24 h, but not at 6 h, without affecting necrosis.	benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone	163-173	caspase 9	Rattus norvegicus	0-17
16597613-8	2006	Thus cadmium-induced apoptosis of PT cells involves a complex and sensitive interplay of signaling cascades involving mitochondrial proapoptotic factors, calpains and caspases, whose activation is also determined by cadmium concentration and the duration of cadmium exposure.	Cadmium	5-12	caspase 9	Rattus norvegicus	167-175
16514665-9	2006	The results showed that Hcy-mediated ROS production preceded the loss of MP, the release of cytochrome-c, and the activation of caspase-9 and -3.	Reactive Oxygen Species	37-40	caspase 9	Rattus norvegicus	128-144
16514665-12	2006	The cytotoxic effect of Hcy was blocked by using small interfering RNA (siRNA)-mediated suppression of caspase-9 in MVEC.	Homocysteine	24-27	caspase 9	Rattus norvegicus	103-112
16514665-14	2006	Our data suggested that Hcy-mediated ROS production promotes endothelial cell death in part by disturbing MP, which results in subsequent release of cytochrome-c and activation of caspase-9 and 3, leading to cell death.	Homocysteine	24-27	caspase 9	Rattus norvegicus	180-195
16514665-14	2006	Our data suggested that Hcy-mediated ROS production promotes endothelial cell death in part by disturbing MP, which results in subsequent release of cytochrome-c and activation of caspase-9 and 3, leading to cell death.	Reactive Oxygen Species	37-40	caspase 9	Rattus norvegicus	180-195
16902863-8	2006	TMP was found to reduce the adriamycin-stimulated activities of caspase-3, caspase-8 and caspase-9, inhibit adriamycin-induced release of cytochrome C, and elevate the expression of Bcl-x (L).	tetramethylpyrazine	0-3	caspase 9	Rattus norvegicus	89-98
16902863-8	2006	TMP was found to reduce the adriamycin-stimulated activities of caspase-3, caspase-8 and caspase-9, inhibit adriamycin-induced release of cytochrome C, and elevate the expression of Bcl-x (L).	Doxorubicin	28-38	caspase 9	Rattus norvegicus	89-98
16709801-7	2006	The caspase-9 inhibitor can also inhibit apoptosis of alveolar macrophages in vivo when it is intranasally instilled into dexamethasone-immunosuppressed, Pneumocystis-infected rats or L3T4 cell-depleted, Pneumocystis-infected mice.	Dexamethasone	122-135	caspase 9	Rattus norvegicus	4-13
16774749-7	2006	The cleavage of caspase-8 and Bid increased at 0 h, cytosolic fraction of cytochrome c and Smac/DIABLO increased by 2 h, cleavage of caspase-9 was detected by 4 h, TUNEL-positive neurons appeared at 8 h and reached a maximum at 24 h following administration of diazepam in the ipsilateral CA3 subfield of hippocampus.	Diazepam	261-269	caspase 9	Rattus norvegicus	133-142
16542823-12	2006	Finally, we show that the caspase 8 inhibitor Ac-IETD-CHO was more effective at blocking seizure-induced cell death than the caspase 9 inhibitor Ac-LEHD-CHO.	acetyl-leucyl-glutamyl-histidyl-aspartal	145-156	caspase 9	Rattus norvegicus	125-134
16765055-8	2006	Moreover, inhibitors of GSK-3beta (IGF-I, lithium) and caspase-9 (LEHD-fmk) significantly protected CGNs from apoptosis induced by either ER stress or TFW.	lehd-fmk	66-74	caspase 9	Rattus norvegicus	55-64
16469385-12	2006	Extracellular adenosine, thus, appears to activate caspase-9 followed by the effector caspase, caspase-3, at least via two independent pathways linked to A(1) adenosine receptor-mediated adenylate cyclase inhibition and adenosine uptake into cells/conversion to AMP/activation of AMPK, possibly regardless of mitochondrial damage, thereby leading to RCR-1 cell death, dominantly by apoptosis.	Adenosine	14-23	caspase 9	Rattus norvegicus	51-60
16469385-12	2006	Extracellular adenosine, thus, appears to activate caspase-9 followed by the effector caspase, caspase-3, at least via two independent pathways linked to A(1) adenosine receptor-mediated adenylate cyclase inhibition and adenosine uptake into cells/conversion to AMP/activation of AMPK, possibly regardless of mitochondrial damage, thereby leading to RCR-1 cell death, dominantly by apoptosis.	Adenosine	159-168	caspase 9	Rattus norvegicus	51-60
16469385-12	2006	Extracellular adenosine, thus, appears to activate caspase-9 followed by the effector caspase, caspase-3, at least via two independent pathways linked to A(1) adenosine receptor-mediated adenylate cyclase inhibition and adenosine uptake into cells/conversion to AMP/activation of AMPK, possibly regardless of mitochondrial damage, thereby leading to RCR-1 cell death, dominantly by apoptosis.	Adenosine Monophosphate	262-265	caspase 9	Rattus norvegicus	51-60
16357363-4	2006	We show that inhibitors of p53-dependent transcriptional activation (pifithrin and type 16-E6 protein) block asbestos-induced AEC mitochondrial membrane potential change (DeltaPsim), caspase 9 activation, and apoptosis.	Asbestos	109-117	caspase 9	Rattus norvegicus	183-192
16263807-4	2006	Camptothecin initiated the intrinsic pathway with activation of caspase-9 and caspase-dependent cleavage of procaspase-3.	Camptothecin	0-12	caspase 9	Rattus norvegicus	64-73
16343480-6	2006	Ad-COX-1/PGIS transfection was found to reduce the adriamycin-stimulated activities of caspase-3 and caspase-9, inhibit adriamycin-induced release of cytochrome c, elevate the expression of Bcl-x(L), and suppress the activation and translocation of nuclear factor-kappaB (NF-kappaB) in adriamycin-treated renal tubular cells.	Doxorubicin	51-61	caspase 9	Rattus norvegicus	101-110
16236330-2	2006	When clofibrate (30 to 300 microM) was applied to L6 rat skeletal myoblasts, dose-dependently apoptosis was observed within 24 h. In the apoptotic myoblasts, a caspase-12 cleavage was observed at 2 h and with following caspases-9 and -3-related cascade activation.	Clofibrate	5-15	caspase 9	Rattus norvegicus	219-236
16365280-5	2006	NMDA increased the activity of caspases 2, 3, 6, 8, and 9 and reached the maximum after 8-h treatment.	N-Methylaspartate	0-4	caspase 9	Rattus norvegicus	31-39
16365280-6	2006	TABM and TABE abrogated NMDA-induced activation of caspases 2, 3, 6, and 8 by approximately 80 to 90% and 50 to 60%, respectively, and to a higher extent for caspase 9.	N-Methylaspartate	24-28	caspase 9	Rattus norvegicus	51-59
16365280-6	2006	TABM and TABE abrogated NMDA-induced activation of caspases 2, 3, 6, and 8 by approximately 80 to 90% and 50 to 60%, respectively, and to a higher extent for caspase 9.	N-Methylaspartate	24-28	caspase 9	Rattus norvegicus	158-167
16365280-13	2006	These events subsequently eliminated the accumulation of O2-* and blocked the activation of caspase cascade, thereby conferring their neuroprotective effects on NMDA-mediated excitotoxicity.	N-Methylaspartate	161-165	caspase 9	Rattus norvegicus	92-99
16502258-5	2006	Using primary rat hippocampal cultures, staurosporine (STS, 100 nM) induced a time-dependent apoptosis, accompanied by a marked production of reactive oxygen species (ROS), release of cytochrome c and activation of caspase 9 and 3.	Staurosporine	40-53	caspase 9	Rattus norvegicus	215-230
16502258-5	2006	Using primary rat hippocampal cultures, staurosporine (STS, 100 nM) induced a time-dependent apoptosis, accompanied by a marked production of reactive oxygen species (ROS), release of cytochrome c and activation of caspase 9 and 3.	Staurosporine	55-58	caspase 9	Rattus norvegicus	215-230
16316708-7	2006	Cerebral I/R-induced internucleosomal DNA fragmentation, caspase-8, caspase-9, and caspase-3 activation, and cytochrome c release were reduced by TMP treatment.	tetramethylpyrazine	146-149	caspase 9	Rattus norvegicus	68-77
16095815-5	2005	LY 294002 diminished the effect of NGF on the inactivation of all these caspases.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	0-9	caspase 9	Rattus norvegicus	72-80
16284628-5	2006	Piracetam also reduced caspase 9 activity after SNP treatment.	Piracetam	0-9	caspase 9	Rattus norvegicus	23-32
16477149-0	2005	Activation of the caspase cascade underlies the rat trigeminal primary neuronal apoptosis induced by neonatal capsaicin administration.	Capsaicin	110-119	caspase 9	Rattus norvegicus	18-25
16133124-2	2005	Recently, we have shown that water deprivation leads to the activation of vasopressin (VP) secretion and expression of Bcl-2 and caspase-9 apototic proteins in the hypothalamus of the rat brain.	Water	29-34	caspase 9	Rattus norvegicus	129-138
16477149-2	2005	Here we examined the trigeminal ganglion neurons immunohistochemically for the possible induction of activated forms of caspases-9 and -3 following a subcutaneous injection of capsaicin in newborn rats.	Capsaicin	176-185	caspase 9	Rattus norvegicus	120-137
16477149-5	2005	After the capsaicin injection, TUNEL-positive neurons began to increase by 12 h, reached a peak at 24 h (11.4%), and returned to the control level by 120 h. Vehicle control levels of caspase- 9-immunoreactive (ir) and caspase-3-ir neurons were low (< 0.5%).	Capsaicin	10-19	caspase 9	Rattus norvegicus	183-193
16477149-6	2005	Neonatal capsaicin administration induced caspase-9-immunoreactivity (ir) and -3-ir.	Capsaicin	9-18	caspase 9	Rattus norvegicus	42-51
16477149-11	2005	These results suggest that neonatal capsaicin triggers the caspase cascade and, thereby, induces trigeminal primary neuronal apoptosis.	Capsaicin	36-45	caspase 9	Rattus norvegicus	59-66
16206047-5	2005	Specific inhibitors of caspase-3 and caspase-9 prevented the apoptotic process induced by skullcapflavone I.	skullcapflavone	90-105	caspase 9	Rattus norvegicus	37-46
16164961-10	2005	The broad-spectrum caspase inhibitor (Boc-D-FMK) and the caspase-9-specific inhibitor (Z-LEHD-FMK) protect against paraoxon-mediated apoptosis, paraoxon-stimulated caspase-3 activity and neuronal cell death.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	87-97	caspase 9	Rattus norvegicus	57-66
16164961-10	2005	The broad-spectrum caspase inhibitor (Boc-D-FMK) and the caspase-9-specific inhibitor (Z-LEHD-FMK) protect against paraoxon-mediated apoptosis, paraoxon-stimulated caspase-3 activity and neuronal cell death.	Paraoxon	115-123	caspase 9	Rattus norvegicus	57-66
16164961-10	2005	The broad-spectrum caspase inhibitor (Boc-D-FMK) and the caspase-9-specific inhibitor (Z-LEHD-FMK) protect against paraoxon-mediated apoptosis, paraoxon-stimulated caspase-3 activity and neuronal cell death.	Paraoxon	144-152	caspase 9	Rattus norvegicus	57-66
16206047-6	2005	From these results, skullcapflavone I from S. baicalensis selectively induced apoptosis in T-HSC/Cl-6 cells via caspase-3 and caspase-9 activation.	skullcapflavone	20-35	caspase 9	Rattus norvegicus	126-135
16133867-4	2005	Pretreatment of polyamine-depleted cells with LY294002 increased caspase-9 and caspase-3 activation and decreased basal levels of GSK-3beta phosphorylation.	Polyamines	16-25	caspase 9	Rattus norvegicus	65-74
16133867-4	2005	Pretreatment of polyamine-depleted cells with LY294002 increased caspase-9 and caspase-3 activation and decreased basal levels of GSK-3beta phosphorylation.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	46-54	caspase 9	Rattus norvegicus	65-74
15796713-7	2005	Singlet oxygen inhibited caspase 9 and 3 activities directly and also suppressed the activation of the caspase cascade.	Singlet Oxygen	0-14	caspase 9	Rattus norvegicus	25-40
16179556-0	2005	Cocaine induces a differential dose-dependent alteration in the expression profile of immediate early genes, transcription factors, and caspases in PC12 cells: a possible mechanism of neurotoxic damage in cocaine addiction.	Cocaine	0-7	caspase 9	Rattus norvegicus	136-144
16179556-6	2005	A concentration-dependent increase in the expression of caspase-9 and -3 was observed up to 500 microM cocaine.	Cocaine	103-110	caspase 9	Rattus norvegicus	56-72
15928547-11	2005	CONCLUSIONS: Fas-mediated mitochondrial caspase 9 pathway is constitutively present in the rat notochordal cells.	ammonium ferrous sulfate	13-16	caspase 9	Rattus norvegicus	40-49
15926913-10	2005	Furthermore, A beta activation of caspases 9 and 3, which are signaling pathways implicated in apoptotic cell death, is blocked by pretreatment of cultures with Fucoidan.	fucoidan	161-169	caspase 9	Rattus norvegicus	34-50
15629764-0	2005	A tetracycline-regulated adenovirus encoding dominant-negative caspase-9 is regulated in rat brain and protects against neurotoxin-induced cell death in vitro, but not in vivo.	Tetracycline	2-14	caspase 9	Rattus norvegicus	63-72
15862175-3	2005	We and others have shown that caspase 9 is cleaved in the retina in other injury models and we hypothesized that the neuroprotection observed with FK506 was mediated by interference with caspase 9 activation.	Tacrolimus	147-152	caspase 9	Rattus norvegicus	30-39
15862175-3	2005	We and others have shown that caspase 9 is cleaved in the retina in other injury models and we hypothesized that the neuroprotection observed with FK506 was mediated by interference with caspase 9 activation.	Tacrolimus	147-152	caspase 9	Rattus norvegicus	187-196
15862175-8	2005	Furthermore, the oral administration of FK506 5 mg kg(-1) day(-1) blocks the cleavage of caspase 9 at both time points.	Tacrolimus	40-45	caspase 9	Rattus norvegicus	89-98
15862175-9	2005	These data suggest that caspase 9 activation may play an important role in retinal ganglion cell death following optic nerve crush and that the neuroprotection seen with FK506 may be mediated by interfering with the activation of caspase 9.	Tacrolimus	170-175	caspase 9	Rattus norvegicus	230-239
15796358-0	2005	Neuroprotection and functional recovery after application of the caspase-9 inhibitor z-LEHD-fmk in a rat model of traumatic spinal cord injury.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	85-95	caspase 9	Rattus norvegicus	65-74
15796358-3	2005	The aim of this study was to evaluate the neuroprotective effect of the caspase-9 inhibitor, z-LEHD-fmk, in a rat model of spinal cord trauma.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	93-103	caspase 9	Rattus norvegicus	72-81
15796358-15	2005	Furthermore, immediate treatment with the caspase-9 inhibitor z-LEHD-fmk blocked apoptosis effectively and was associated with better functional outcome.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	62-72	caspase 9	Rattus norvegicus	42-51
15842833-0	2005	[The effect on apoptosis in anterior pituitary induced by cadmium chloride and its relations with caspase-9 pathway].	Cadmium Chloride	58-74	caspase 9	Rattus norvegicus	98-107
15842833-7	2005	CONCLUSION: It was suggested that cadmium could induce apoptosis of anterior pituitary both in vivo and in vitro in the manner of dose-dependent, and caspase-9 might play a role during above processes.	Cadmium	34-41	caspase 9	Rattus norvegicus	150-159
15629764-1	2005	Caspase-9 is a critical downstream effector molecule involved in apoptosis, a cell death process thought to be involved in the demise of dopamine (DA) neurons in the substantia nigra (SN) affected by Parkinson"s disease (PD).	Dopamine	137-145	caspase 9	Rattus norvegicus	0-9
15629764-2	2005	In this study, we determined that a tetracycline-regulated adenovirus harboring a dominant-negative form of caspase-9 (Casp9DN) and the marker gene, enhanced green fluorescent protein (EGFP), under the control of a bidirectional promoter could each be regulated in vitro and in vivo by doxycycline.	Tetracycline	36-48	caspase 9	Rattus norvegicus	108-117
15629764-2	2005	In this study, we determined that a tetracycline-regulated adenovirus harboring a dominant-negative form of caspase-9 (Casp9DN) and the marker gene, enhanced green fluorescent protein (EGFP), under the control of a bidirectional promoter could each be regulated in vitro and in vivo by doxycycline.	Doxycycline	286-297	caspase 9	Rattus norvegicus	108-117
15382069-5	2004	The mechanism(s) by which bilirubin induces apoptosis was investigated by Western blotting for cytochrome c release, assaying for caspase-8 and caspase-9 activation and for mitochondrial depolarization by JC-1 staining.	Bilirubin	26-35	caspase 9	Rattus norvegicus	144-153
15365088-4	2005	Cocaine induced time-dependent, concurrent increases in cytochrome c release and activities of caspase-9 and caspase-3, which preceded apoptosis.	Cocaine	0-7	caspase 9	Rattus norvegicus	95-104
15596134-5	2005	Upregulation of Akt activity by overexpression of constitutively active Akt inhibited elevated glucose-induced apoptosis, whereas downregulation of Akt activity by overexpression of dominant negative Akt exacerbated elevated glucose-induced apoptosis, as assessed by caspase activity and nucleic acid staining.	Glucose	95-102	caspase 9	Rattus norvegicus	267-274
15365088-6	2005	In accordance, cyclosporin A and the inhibitors of caspase-9 and caspase-3 inhibited cocaine-induced caspase activation and apoptosis.	Cocaine	85-92	caspase 9	Rattus norvegicus	51-60
15365088-10	2005	Consistent with its inhibition of apoptosis, SB203580 inhibited cocaine-induced cytochrome c release and activation of caspase-9 and caspase-3.	SB 203580	45-53	caspase 9	Rattus norvegicus	119-128
15365088-10	2005	Consistent with its inhibition of apoptosis, SB203580 inhibited cocaine-induced cytochrome c release and activation of caspase-9 and caspase-3.	Cocaine	64-71	caspase 9	Rattus norvegicus	119-128
16213988-4	2005	Furthermore, melatonin treatment diminished cytochrome c release from mitochondria and reduced caspase 3 and caspase 9 activation induced by hyperhomocysteinemia.	Melatonin	13-22	caspase 9	Rattus norvegicus	109-118
15557468-5	2004	Specific pathway inhibition was performed with the caspase-9 inhibitor zLEHD.fmk or neutralizing antibodies against either the FAS-receptor or FAS-ligand.	zlehd	71-76	caspase 9	Rattus norvegicus	51-60
15557468-9	2004	Injection of zLEHD.fmk into the subretinal space of a detached retina resulted in decreased caspase-9 activity, as did injection of anti-FAS-receptor antibody into either the subretinal space or the vitreous.	zlehd	13-18	caspase 9	Rattus norvegicus	92-101
15569250-8	2004	In cerebellar granule neurons, vincristine and to a lesser extent topotecan induced caspase 3 and caspase 9 cleavage, and enhanced caspase activity and Akt-dependent expression of phosphorylated BAD.	Vincristine	31-42	caspase 9	Rattus norvegicus	98-107
15569250-8	2004	In cerebellar granule neurons, vincristine and to a lesser extent topotecan induced caspase 3 and caspase 9 cleavage, and enhanced caspase activity and Akt-dependent expression of phosphorylated BAD.	Vincristine	31-42	caspase 9	Rattus norvegicus	84-91
15569250-8	2004	In cerebellar granule neurons, vincristine and to a lesser extent topotecan induced caspase 3 and caspase 9 cleavage, and enhanced caspase activity and Akt-dependent expression of phosphorylated BAD.	Topotecan	66-75	caspase 9	Rattus norvegicus	98-107
15569250-8	2004	In cerebellar granule neurons, vincristine and to a lesser extent topotecan induced caspase 3 and caspase 9 cleavage, and enhanced caspase activity and Akt-dependent expression of phosphorylated BAD.	Topotecan	66-75	caspase 9	Rattus norvegicus	84-91
15569250-9	2004	zVAD-fmk, a caspase inhibitor and brain-derived neurotrophic factor (BDNF), but not MK-801, a non-competitive NMDA receptor antagonist, significantly reduced vincristine- or topotecan-induced cell death.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	0-8	caspase 9	Rattus norvegicus	12-19
15382069-9	2004	Bilirubin treatment evokes specific activation of caspase-9, enhances cytochrome c release into the cytoplasm and triggers the mitochondrial permeability transition in colon cancer monolayers.	Bilirubin	0-9	caspase 9	Rattus norvegicus	50-59
15253891-0	2004	Taurine inhibits apoptosis by preventing formation of the Apaf-1/caspase-9 apoptosome.	Taurine	0-7	caspase 9	Rattus norvegicus	65-74
15253891-6	2004	Taurine treatment had no effect on mitochondrial membrane potential and cytochrome c release; however, it inhibited ischemia-induced cleavage of caspase-9 and -3.	Taurine	0-7	caspase 9	Rattus norvegicus	145-161
15253891-7	2004	Taurine loading also suppressed the formation of the Apaf-1/caspase-9 apoptosome and the interaction of caspase-9 with Apaf-1.	Taurine	0-7	caspase 9	Rattus norvegicus	60-69
15253891-7	2004	Taurine loading also suppressed the formation of the Apaf-1/caspase-9 apoptosome and the interaction of caspase-9 with Apaf-1.	Taurine	0-7	caspase 9	Rattus norvegicus	104-113
15253891-8	2004	These findings demonstrate that taurine effectively prevents myocardial ischemia-induced apoptosis by inhibiting the assembly of the Apaf-1/caspase-9 apoptosome.	Taurine	32-39	caspase 9	Rattus norvegicus	140-149
15532535-6	2004	This results in the inhibition of caspase-9 and -3 and apoptotic cell death in PC12 cells by suppressing the toxic actions of reactive oxygen and nitrogen species, including the GSH depletion.	reactive oxygen and nitrogen species	126-162	caspase 9	Rattus norvegicus	34-50
15451339-9	2004	The apoptotic process involved fas system, bax and caspase family genes and the apoptotic extent and cell types were gossypol dose-dependent.	Gossypol	117-125	caspase 9	Rattus norvegicus	51-58
15532535-6	2004	This results in the inhibition of caspase-9 and -3 and apoptotic cell death in PC12 cells by suppressing the toxic actions of reactive oxygen and nitrogen species, including the GSH depletion.	Glutathione	178-181	caspase 9	Rattus norvegicus	34-50
15339981-7	2004	Azelnidipine administration ameliorated cellular and mitochondrial Ca(2+) accumulation, mitochondrial permeability transition, cytochrome c release, caspase-9 activation, and resultant apoptosis (15.8 +/- 0.8% versus 8.9 +/- 0.7%; P < 0.01).	azelnidipine	0-12	caspase 9	Rattus norvegicus	149-158
15135649-9	2004	These results suggest that BR931 can increase generation of ROS, leading to DNA damage and p53 phosphorylation, which, in turn, induces the activation of Bax, release of cytochrome-c from mitochondria and activation of caspases, culminating in cell death.	Reactive Oxygen Species	60-63	caspase 9	Rattus norvegicus	219-227
15159394-9	2004	Following Bax induction by hydrogen peroxide, mitochondrial membrane integrity was compromised, and caspase-9 became activated.	Hydrogen Peroxide	27-44	caspase 9	Rattus norvegicus	100-109
15241557-0	2004	Cytochrome c release and endoplasmic reticulum stress are involved in caspase-dependent apoptosis induced by G418.	antibiotic G 418	109-113	caspase 9	Rattus norvegicus	70-77
15241557-4	2004	The pan caspase inhibitor z-VAD-fmk completely inhibited this type of apoptosis, suggesting a caspase-dependent mechanism.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	26-35	caspase 9	Rattus norvegicus	8-15
15241557-7	2004	Inhibition of caspase-9 activity by z-LEHD-fmk prevented most of the cells from apoptosis, and E-64d, an inhibitor of calpain accentuated this block.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	36-46	caspase 9	Rattus norvegicus	14-23
15241557-8	2004	The cleavage of caspase-9 and caspase-12 was blocked only by simultaneous application of z-VAD-fmk and E-64d, but not by either alone.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	89-98	caspase 9	Rattus norvegicus	16-25
14976128-3	2004	On the other hand, our previous study has shown that Trp-P-1 exhibits cytotoxicity to primary cultured rat hepatocytes, via induction of caspase-9-dependent apoptosis without being metabolized by CYP 1A1.	Tryptophan	53-56	caspase 9	Rattus norvegicus	137-146
15172961-12	2004	Benidipine treatment significantly reduced mitochondrial cytochrome c release and caspase-9 activation, but had no effect on caspase-8 activation, suggesting that benidipine exerts its antiapoptotic effect by inhibiting the mitochondrial-mediated, but not death receptor-mediated, apoptotic pathway.	benidipine	0-10	caspase 9	Rattus norvegicus	82-91
15172961-12	2004	Benidipine treatment significantly reduced mitochondrial cytochrome c release and caspase-9 activation, but had no effect on caspase-8 activation, suggesting that benidipine exerts its antiapoptotic effect by inhibiting the mitochondrial-mediated, but not death receptor-mediated, apoptotic pathway.	benidipine	163-173	caspase 9	Rattus norvegicus	82-91
15172961-19	2004	Benidipine tilted the balance between ERK1/2 and p38 MAPK toward an antiapoptotic state, decreased mitochondrial cytochrome c release, reduced caspase-9 activation, and attenuated subsequent caspase-3 activation and postischemic myocardial apoptosis.	benidipine	0-10	caspase 9	Rattus norvegicus	143-152
15113843-3	2004	Detailed analysis of the mechanism underlying the NGF-mediated cell survival revealed that the activities of all seriate caspases were reduced through the phosphatidylinositol 3-kinase (PI3-K) signaling pathway induced by NGF.	seriate	113-120	caspase 9	Rattus norvegicus	121-129
15127126-6	2004	The expression of Smac increased at 2 h and the 37-kD cleaved fragment of caspase-9 was detected at 4 h, TUNEL-positive neurons appeared at 8 h and reached maximal at 24 h following seizure cessation within the ipsilateral (the same side as the intra-amygdaloid injection of kainic acid) CA3 subfield of the hippocampus.	Kainic Acid	275-286	caspase 9	Rattus norvegicus	74-83
15127126-7	2004	Intracerebroventricular infusion of caspase-9 inhibitor z-LEHD-fluoromethyl ketone (z-LEHD-fmk) significantly decreased TUNEL-positive neurons and increased the number of surviving cells.	z-lehd-fluoromethyl ketone	56-82	caspase 9	Rattus norvegicus	36-45
15127126-7	2004	Intracerebroventricular infusion of caspase-9 inhibitor z-LEHD-fluoromethyl ketone (z-LEHD-fmk) significantly decreased TUNEL-positive neurons and increased the number of surviving cells.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	84-94	caspase 9	Rattus norvegicus	36-45
15020243-0	2004	Taurine prevents the ischemia-induced apoptosis in cultured neonatal rat cardiomyocytes through Akt/caspase-9 pathway.	Taurine	0-7	caspase 9	Rattus norvegicus	100-109
15020243-4	2004	Although taurine treatment had no effect on the expression of Bcl-2 in mitochondria and the level of cytosolic cytochrome c, it inhibited ischemia-induced cleavage of caspases 9 and 3.	Taurine	9-16	caspase 9	Rattus norvegicus	167-183
15020243-5	2004	Moreover, adenovirus transfer of the dominant negative form of Akt objected taurine-mediated anti-apoptotic effects, cancelling the suppression of caspase-9 and caspase-3 activities by taurine.	Taurine	185-192	caspase 9	Rattus norvegicus	147-156
15020243-6	2004	These findings provide the first evidence that taurine inhibits ischemia-induced apoptosis in cardiac myocytes with the increase in Akt activities, by inactivating caspase-9.	Taurine	47-54	caspase 9	Rattus norvegicus	164-173
14713542-3	2004	By comparing liver sections from CPA-treated and control rats with high and low rates of apoptosis we observed a close correlation between the occurrence of cleaved caspase-positive apoptotic figures and H&E-stained apoptotic bodies when evaluated in parallel sections.	Cyproterone Acetate	33-36	caspase 9	Rattus norvegicus	165-172
14700529-8	2004	Pharmacological inhibition of caspase activity, p38 stress-responsive protein kinase activity, or oxidative stress prevented TMT-induced cell death.	trimethyltin	125-128	caspase 9	Rattus norvegicus	30-37
15114044-5	2004	Increased expression of p21 and Bax, decreased expression of Bcl-2, cytochrome C release from the mitochondria into the cytosol and subsequent activation of caspase-9 and -3 were identified in the cells treated with ammonia, although there was no apparent change in p53 expression.	Ammonia	216-223	caspase 9	Rattus norvegicus	157-173
14713542-6	2004	By use of this technique, inhibition of apoptosis by 2,3,7,8-tetrachlorodibenzo-p-dioxin as detected by counting of H&E-stained apoptotic bodies was found to correlate with a strong reduction of cleaved caspase-positive hepatocytes in GST-P-positive preneoplastic foci.	Polychlorinated Dibenzodioxins	53-88	caspase 9	Rattus norvegicus	207-214
12898128-5	2003	Magnolol increased caspase-3 and caspase-9 activities significantly and reduced the mitochondrial potential (Deltapsi(m)).	magnolol	0-8	caspase 9	Rattus norvegicus	33-42
12869386-10	2003	SP-600125, a specific inhibitor of JNK activation, prevented cytochrome c release from mitochondria, JNK activation, DNA fragmentation, and caspase-9 activation in response to TNF-alpha/CHX.	pyrazolanthrone	0-9	caspase 9	Rattus norvegicus	140-149
12869386-12	2003	Polyamine depletion prevented JNK activation, which may confer protection against apoptosis by modulation of upstream caspase-9 activation.	Polyamines	0-9	caspase 9	Rattus norvegicus	118-127
14599484-8	2003	It was found that CAPE did not interfere with the marked decrease in [Ca(2+)](i) induced by low K(+), whereas it completely blocked caspase-3, caspase-9, and NF-kappaB activation.	caffeic acid phenethyl ester	18-22	caspase 9	Rattus norvegicus	143-152
14599484-9	2003	It is concluded that CAPE could exert its anti-apoptotic effect in CGNs by blocking ROS formation and by inhibiting caspase activity.	caffeic acid phenethyl ester	21-25	caspase 9	Rattus norvegicus	116-123
12917435-0	2003	In vivo calpain/caspase cross-talk during 3-nitropropionic acid-induced striatal degeneration: implication of a calpain-mediated cleavage of active caspase-3.	3-nitropropionic acid	42-63	caspase 9	Rattus norvegicus	16-23
12917435-3	2003	Results showed that 3NP-induced death of striatal neurons was preceded by cytochrome c redistribution, transient caspase-9 processing, and activation of calpain, whereas levels of the active/processed form of caspase-3 remained low and were even reduced as compared with control animals.	3-nitropropionic acid	20-23	caspase 9	Rattus norvegicus	113-122
12917435-6	2003	1) Pharmacological blockade of calpain in 3NP-treated rats increased the levels of endogenous processed caspase-9 and caspase-3.	3-nitropropionic acid	42-45	caspase 9	Rattus norvegicus	104-113
12917435-7	2003	2) Cell-free extracts prepared from the striatum of 3NP-treated rats degraded in vitro the p34 and p20 subunits of active recombinant caspase-9 and caspase-3, respectively.	3-nitropropionic acid	52-55	caspase 9	Rattus norvegicus	134-143
15804062-7	2003	RESULTS: (1) H2O2 (0.5 mmol/L) resulted in a marked release of Smac from mitochondria to cytoplasm at 2 h after the treatment, the activation of caspase-9 and caspase-3 at 4 h after the treatment and specific morphological changes of apoptosis at 24 h after the treatment.	Hydrogen Peroxide	13-17	caspase 9	Rattus norvegicus	145-154
15804062-8	2003	(2) Heat shock pretreatment (42 degrees C, 1 h) could increase the expression of hsp90, hsp70 and betaB-crystallin, and inhibit the H2O2-induced release of Smac from mitochondria, the activity of caspase-9, caspase-3 and apoptosis of cardiomyocytes.	Hydrogen Peroxide	132-136	caspase 9	Rattus norvegicus	196-205
14535961-6	2003	Such activation of the caspases was again inhibited by CACA in a TPMPA-sensitive manner.	(1,2,5,6-tetrahydropyridin-4-yl)methylphosphinic acid	65-70	caspase 9	Rattus norvegicus	23-31
14511319-3	2003	MPP+ exposure in rat dopaminergic neuronal cells resulted in time-dependent increases in reactive oxygen species generation, cytochrome c release, and caspase-9 and caspase-3 activation.	mangion-purified polysaccharide (Candida albicans)	0-4	caspase 9	Rattus norvegicus	151-160
12657721-0	2003	Celecoxib acts in a cyclooxygenase-2-independent manner and in synergy with emodin to suppress rat cholangiocarcinoma growth in vitro through a mechanism involving enhanced Akt inactivation and increased activation of caspases-9 and -3.	Celecoxib	0-9	caspase 9	Rattus norvegicus	218-235
12812840-6	2003	LEHD-CHO is a specific cell permeable caspase-9 inhibitor.	Ac-Ala-Ala-Val-Ala-Leu-Leu-Pro-Ala-Val-Leu-Leu-Ala-Leu-Leu-Ala-Pro-Leu-Glu-His-Asp-Cho	0-8	caspase 9	Rattus norvegicus	38-47
12717106-7	2003	The peptide increased terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling (TUNEL) staining and caspase 9 activation more in the taurine-deficient than the normal cell.	Taurine	167-174	caspase 9	Rattus norvegicus	134-143
12675929-4	2003	MK-801/CNQX-induced neuronal apoptosis was prevented by zVAD-fmk, a broad inhibitor of caspases, but insensitive to inhibitors of calpain or cathepsin D.	Dizocilpine Maleate	0-6	caspase 9	Rattus norvegicus	87-95
12675929-4	2003	MK-801/CNQX-induced neuronal apoptosis was prevented by zVAD-fmk, a broad inhibitor of caspases, but insensitive to inhibitors of calpain or cathepsin D.	6-Cyano-7-nitroquinoxaline-2,3-dione	7-11	caspase 9	Rattus norvegicus	87-95
12675929-4	2003	MK-801/CNQX-induced neuronal apoptosis was prevented by zVAD-fmk, a broad inhibitor of caspases, but insensitive to inhibitors of calpain or cathepsin D.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	56-64	caspase 9	Rattus norvegicus	87-95
12675929-7	2003	Reducing extracellular Ca2+, but not Na+, activated caspase-3, suggesting an essential role of Ca2+ deficiency in MK-801/CNQX-induced activation of caspases.	Dizocilpine Maleate	114-120	caspase 9	Rattus norvegicus	148-156
12675929-7	2003	Reducing extracellular Ca2+, but not Na+, activated caspase-3, suggesting an essential role of Ca2+ deficiency in MK-801/CNQX-induced activation of caspases.	6-Cyano-7-nitroquinoxaline-2,3-dione	121-125	caspase 9	Rattus norvegicus	148-156
12675929-8	2003	Cortical neurons treated with MK-801/CNQX triggered activation of caspase-9, release of cytochrome c from mitochondria, and translocation of Bax into mitochondria.	Dizocilpine Maleate	30-36	caspase 9	Rattus norvegicus	66-75
12675929-8	2003	Cortical neurons treated with MK-801/CNQX triggered activation of caspase-9, release of cytochrome c from mitochondria, and translocation of Bax into mitochondria.	6-Cyano-7-nitroquinoxaline-2,3-dione	37-41	caspase 9	Rattus norvegicus	66-75
12684213-3	2003	Pretreatment of IEC-6 cells with LPA inhibited campothecin-induced caspase-9 and caspase-3 activation and DNA fragmentation.	lysophosphatidic acid	33-36	caspase 9	Rattus norvegicus	67-76
12684213-3	2003	Pretreatment of IEC-6 cells with LPA inhibited campothecin-induced caspase-9 and caspase-3 activation and DNA fragmentation.	campothecin	47-58	caspase 9	Rattus norvegicus	67-76
12684213-4	2003	A caspase-9 inhibitor peptide mimicked the LPA-elicited antiapoptotic activity.	lysophosphatidic acid	43-46	caspase 9	Rattus norvegicus	2-11
12684213-6	2003	The LPA-elicited antiapoptotic activity and inhibition of caspase-9 activity were abrogated by pertussis toxin, PD 98059, wortmannin, and LY 294002.	lysophosphatidic acid	4-7	caspase 9	Rattus norvegicus	58-67
12684213-6	2003	The LPA-elicited antiapoptotic activity and inhibition of caspase-9 activity were abrogated by pertussis toxin, PD 98059, wortmannin, and LY 294002.	Wortmannin	122-132	caspase 9	Rattus norvegicus	58-67
12684213-6	2003	The LPA-elicited antiapoptotic activity and inhibition of caspase-9 activity were abrogated by pertussis toxin, PD 98059, wortmannin, and LY 294002.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	138-147	caspase 9	Rattus norvegicus	58-67
12540492-9	2003	An iron chelator (phytic acid or deferoxamine) or a hydroxyl radical scavenger (sodium benzoate) each blocked asbestos-induced reductions in deltapsi(m) and caspase 9 activation, suggesting a role for iron-derived ROS.	Iron	3-7	caspase 9	Rattus norvegicus	157-166
12639677-13	2003	CONCLUSIONS: Our results suggest that the release of cytochrome c from mitochondria and its subsequent activation of caspase 9 and caspase 3 in testes play a key role in cocaine-induced germ cell apoptosis.	Cocaine	170-177	caspase 9	Rattus norvegicus	117-126
12540492-9	2003	An iron chelator (phytic acid or deferoxamine) or a hydroxyl radical scavenger (sodium benzoate) each blocked asbestos-induced reductions in deltapsi(m) and caspase 9 activation, suggesting a role for iron-derived ROS.	Phytic Acid	18-29	caspase 9	Rattus norvegicus	157-166
12540492-7	2003	Asbestos-induced deltapsi(m) was associated with the release of cytochrome c from the mitochondria to the cytoplasm as well as activation of caspase 9, a mitochondrial-activated caspase.	Asbestos	0-8	caspase 9	Rattus norvegicus	141-150
12540492-9	2003	An iron chelator (phytic acid or deferoxamine) or a hydroxyl radical scavenger (sodium benzoate) each blocked asbestos-induced reductions in deltapsi(m) and caspase 9 activation, suggesting a role for iron-derived ROS.	Sodium Benzoate	80-95	caspase 9	Rattus norvegicus	157-166
12540492-11	2003	We conclude that asbestos-induced AEC apoptosis results from mitochondrial dysfunction, in part due to iron-derived ROS, which is followed by the release of cytochrome c and caspase 9 activation.	Asbestos	17-25	caspase 9	Rattus norvegicus	174-183
17682315-4	2003	In this study, we hypothesize that PGF2alpha and staurosporine will induce apoptosis in the rat corpus luteum and this process is mediated through the mitochondrial phospholipid cardiolipin and activation of caspase-9.	Dinoprost	35-44	caspase 9	Rattus norvegicus	208-217
17682315-4	2003	In this study, we hypothesize that PGF2alpha and staurosporine will induce apoptosis in the rat corpus luteum and this process is mediated through the mitochondrial phospholipid cardiolipin and activation of caspase-9.	Staurosporine	49-62	caspase 9	Rattus norvegicus	208-217
12831855-3	2003	Exposure of PC12 cells to dieldrin (100-300 microM) results in the rapid release of cytochrome C, followed by the activation of caspase-9 and caspase-3 in a time- and dose-dependent manner.	Dieldrin	26-34	caspase 9	Rattus norvegicus	128-137
12426148-2	2002	In C6 rat glioma cells, cadmium caused externalization of phosphatidylserine, breakdown of the mitochondrial membrane potential, activation of caspase-9, internucleosomal DNA fragmentation, chromatin condensation, and nuclear fragmentation.	Cadmium	24-31	caspase 9	Rattus norvegicus	143-152
12181189-3	2002	Hepatocyte apoptosis induced by glycodeoxycholate (GCDC) was associated with mitochondrial depolarization, activation of caspases, the release of cytochrome c from the mitochondria, and translocation of BAX from the cytosol to the mitochondria.	Glycodeoxycholic Acid	32-49	caspase 9	Rattus norvegicus	121-129
12176737-5	2002	Treatment of rats with L-carnitine, known for its protective effect on muscle metabolism injuries, was found to inhibit caspases and to decrease the levels of TNF-alpha and sphingosine, as well as the number of apoptotic myonuclei.	Carnitine	23-34	caspase 9	Rattus norvegicus	120-128
12181189-3	2002	Hepatocyte apoptosis induced by glycodeoxycholate (GCDC) was associated with mitochondrial depolarization, activation of caspases, the release of cytochrome c from the mitochondria, and translocation of BAX from the cytosol to the mitochondria.	Glycodeoxycholic Acid	51-55	caspase 9	Rattus norvegicus	121-129
12181189-4	2002	cAMP inhibited GCDC-induced apoptosis, caspase 3 and caspase 9 activation, and cytochrome c release in a PI3K-dependent manner.	Cyclic AMP	0-4	caspase 9	Rattus norvegicus	53-62
12181189-4	2002	cAMP inhibited GCDC-induced apoptosis, caspase 3 and caspase 9 activation, and cytochrome c release in a PI3K-dependent manner.	Glycodeoxycholic Acid	15-19	caspase 9	Rattus norvegicus	53-62
12181189-8	2002	These results suggest that GCDC-induced apoptosis in cultured rat hepatocytes proceeds through a caspase-dependent intracellular stress pathway and that the survival effect of cAMP is mediated in part by PI3K-dependent Akt activation at the level of the mitochondria.	Glycodeoxycholic Acid	27-31	caspase 9	Rattus norvegicus	97-104
12063258-5	2002	Surprisingly, FADD-dn, as well as the specific caspase-8 inhibitor benzyloxycarbonyl-IETD-fluoromethylketone also inhibited the activation of caspase-9 and -3 in CMs subjected to hypoxia/SD.	benzyloxycarbonyl-ietd-fluoromethylketone	67-108	caspase 9	Rattus norvegicus	142-158
12322785-3	2002	The purpose of this report is to determine if the administration of a specific caspase-9 inhibitor, Z-Leu-Glu(Ome)-His-Asp(Ome)-FMK x TFA (Z-LEHD-FMK) would attenuate apoptosis and the resultant brain injury after ischemia.	z-leu-glu	100-109	caspase 9	Rattus norvegicus	79-88
12322785-3	2002	The purpose of this report is to determine if the administration of a specific caspase-9 inhibitor, Z-Leu-Glu(Ome)-His-Asp(Ome)-FMK x TFA (Z-LEHD-FMK) would attenuate apoptosis and the resultant brain injury after ischemia.	Histidine	115-118	caspase 9	Rattus norvegicus	79-88
12322785-3	2002	The purpose of this report is to determine if the administration of a specific caspase-9 inhibitor, Z-Leu-Glu(Ome)-His-Asp(Ome)-FMK x TFA (Z-LEHD-FMK) would attenuate apoptosis and the resultant brain injury after ischemia.	Aspartic Acid	119-122	caspase 9	Rattus norvegicus	79-88
12322785-3	2002	The purpose of this report is to determine if the administration of a specific caspase-9 inhibitor, Z-Leu-Glu(Ome)-His-Asp(Ome)-FMK x TFA (Z-LEHD-FMK) would attenuate apoptosis and the resultant brain injury after ischemia.	Trifluoroacetic Acid	134-137	caspase 9	Rattus norvegicus	79-88
12322785-3	2002	The purpose of this report is to determine if the administration of a specific caspase-9 inhibitor, Z-Leu-Glu(Ome)-His-Asp(Ome)-FMK x TFA (Z-LEHD-FMK) would attenuate apoptosis and the resultant brain injury after ischemia.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	139-149	caspase 9	Rattus norvegicus	79-88
12322785-6	2002	Administration of the caspase-9 inhibitor, Z-LEHD-FMK, to the experimental group (n = 12) reduced total infarction volume by 49% (p < 0.05) and improved neurological outcome by 63% (p < 0.01) as compared to the control group (n = 12).	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	43-53	caspase 9	Rattus norvegicus	22-31
12015210-4	2002	In addition, activated caspase-9 was detected at 4 h post-METH exposure.	Methamphetamine	58-62	caspase 9	Rattus norvegicus	23-32
12149481-3	2002	TMC specifically blocked tyrosine phosphorylation of intracellular signal mediators downstream of Src tyrosine kinases in a T cell-specific manner, leading to apoptosis due to cleavage of Bcl-2, caspase-9, caspase-3, and poly(ADP-ribose) polymerase, but not caspase-1.	tautomycetin	0-3	caspase 9	Rattus norvegicus	195-204
12149481-3	2002	TMC specifically blocked tyrosine phosphorylation of intracellular signal mediators downstream of Src tyrosine kinases in a T cell-specific manner, leading to apoptosis due to cleavage of Bcl-2, caspase-9, caspase-3, and poly(ADP-ribose) polymerase, but not caspase-1.	Tyrosine	25-33	caspase 9	Rattus norvegicus	195-204
11997243-7	2002	Depletion of polyamines prevented camptothecin-induced release of cytochrome c from mitochondria and decreased the activity of caspase-9 and caspase-3.	Polyamines	13-23	caspase 9	Rattus norvegicus	127-136
11997243-7	2002	Depletion of polyamines prevented camptothecin-induced release of cytochrome c from mitochondria and decreased the activity of caspase-9 and caspase-3.	Camptothecin	34-46	caspase 9	Rattus norvegicus	127-136
11973426-8	2002	Furthermore, intracerebral ventricular infusion of the relatively specific caspase-9 inhibitor N-benzyloxycarbonyl-Leu-Glu-His-Asp-fluoro-methylketone before ischemia attenuated caspase-3-like activity and significantly enhanced neuronal survival in the CA1 sector.	n-benzyloxycarbonyl-leu-glu	95-122	caspase 9	Rattus norvegicus	75-84
11973426-8	2002	Furthermore, intracerebral ventricular infusion of the relatively specific caspase-9 inhibitor N-benzyloxycarbonyl-Leu-Glu-His-Asp-fluoro-methylketone before ischemia attenuated caspase-3-like activity and significantly enhanced neuronal survival in the CA1 sector.	Histidine	123-126	caspase 9	Rattus norvegicus	75-84
11973426-8	2002	Furthermore, intracerebral ventricular infusion of the relatively specific caspase-9 inhibitor N-benzyloxycarbonyl-Leu-Glu-His-Asp-fluoro-methylketone before ischemia attenuated caspase-3-like activity and significantly enhanced neuronal survival in the CA1 sector.	asp-fluoro-methylketone	127-150	caspase 9	Rattus norvegicus	75-84
11903043-5	2002	The activation of all four caspases was inhibited by cyclosporin A, with the order of susceptibility caspase-8=caspase-9=caspase-6>caspase-3.	Cyclosporine	53-66	caspase 9	Rattus norvegicus	111-120
11934844-7	2002	Production of tBID then sustains mitochondrial injury and perpetuates caspase-9 activation.	tBID	14-18	caspase 9	Rattus norvegicus	70-79
11045015-0	2000	Activation of caspase-9 and -3 during H2O2-induced apoptosis of PC12 cells independent of ceramide formation.	Hydrogen Peroxide	38-42	caspase 9	Rattus norvegicus	14-30
11753565-4	2001	Cleavage of caspase-9 was detected approximately 4 h following seizure cessation within ipsilateral hippocampus and was accompanied by increased cleavage of the substrate Leu-Glu-His-Asp-p-nitroanilide (LEHDpNA) and subsequent strong caspase-9 immunoreactivity within neurons exhibiting DNA fragmentation.	Leucine	171-174	caspase 9	Rattus norvegicus	12-21
11753565-4	2001	Cleavage of caspase-9 was detected approximately 4 h following seizure cessation within ipsilateral hippocampus and was accompanied by increased cleavage of the substrate Leu-Glu-His-Asp-p-nitroanilide (LEHDpNA) and subsequent strong caspase-9 immunoreactivity within neurons exhibiting DNA fragmentation.	Leucine	171-174	caspase 9	Rattus norvegicus	234-243
11753565-4	2001	Cleavage of caspase-9 was detected approximately 4 h following seizure cessation within ipsilateral hippocampus and was accompanied by increased cleavage of the substrate Leu-Glu-His-Asp-p-nitroanilide (LEHDpNA) and subsequent strong caspase-9 immunoreactivity within neurons exhibiting DNA fragmentation.	Glutamic Acid	175-178	caspase 9	Rattus norvegicus	12-21
11753565-4	2001	Cleavage of caspase-9 was detected approximately 4 h following seizure cessation within ipsilateral hippocampus and was accompanied by increased cleavage of the substrate Leu-Glu-His-Asp-p-nitroanilide (LEHDpNA) and subsequent strong caspase-9 immunoreactivity within neurons exhibiting DNA fragmentation.	Histidine	179-182	caspase 9	Rattus norvegicus	12-21
11753565-4	2001	Cleavage of caspase-9 was detected approximately 4 h following seizure cessation within ipsilateral hippocampus and was accompanied by increased cleavage of the substrate Leu-Glu-His-Asp-p-nitroanilide (LEHDpNA) and subsequent strong caspase-9 immunoreactivity within neurons exhibiting DNA fragmentation.	Histidine	179-182	caspase 9	Rattus norvegicus	234-243
11753565-4	2001	Cleavage of caspase-9 was detected approximately 4 h following seizure cessation within ipsilateral hippocampus and was accompanied by increased cleavage of the substrate Leu-Glu-His-Asp-p-nitroanilide (LEHDpNA) and subsequent strong caspase-9 immunoreactivity within neurons exhibiting DNA fragmentation.	asp-p-nitroanilide	183-201	caspase 9	Rattus norvegicus	12-21
11753565-4	2001	Cleavage of caspase-9 was detected approximately 4 h following seizure cessation within ipsilateral hippocampus and was accompanied by increased cleavage of the substrate Leu-Glu-His-Asp-p-nitroanilide (LEHDpNA) and subsequent strong caspase-9 immunoreactivity within neurons exhibiting DNA fragmentation.	lehdpna	203-210	caspase 9	Rattus norvegicus	12-21
11493022-5	2001	In vivo intracerebroventricular z-IETD-fluoromethyl ketone administration significantly reduced seizure-induced activities of caspases 8, 9, and 3 as well as reducing Bid and caspase-9 cleavage, cytochrome c release, DNA fragmentation, and neuronal death.	z-ietd-fluoromethyl ketone	32-58	caspase 9	Rattus norvegicus	175-184
11323518-6	2001	The ANT inhibitor bongkrekic acid prevented Bax and ANT interactions and inhibited Bax-triggered caspase-9 release from isolated brain mitochondria in vitro.	Bongkrekic Acid	18-33	caspase 9	Rattus norvegicus	97-106
11323518-7	2001	Bongkrekic acid also offered significant neuroprotection against ischemia-induced caspase-3 and caspase-9 activation and cell death in the brain.	Bongkrekic Acid	0-15	caspase 9	Rattus norvegicus	96-105
11751909-4	2002	The mitochondrial death pathway was suggested to be involved in BITC-induced apoptosis because the treatment of cells with BITC-induced caspase-9-dependent apoptosis and mitochondrial transmembrane potential (Delta Psi m) alteration.	benzyl isothiocyanate	64-68	caspase 9	Rattus norvegicus	136-145
11751909-4	2002	The mitochondrial death pathway was suggested to be involved in BITC-induced apoptosis because the treatment of cells with BITC-induced caspase-9-dependent apoptosis and mitochondrial transmembrane potential (Delta Psi m) alteration.	benzyl isothiocyanate	123-127	caspase 9	Rattus norvegicus	136-145
11850844-5	2002	In MT-450 mammary carcinoma cells hyperforin increased the activity of caspase-9 and caspase-3, and hyperforin-mediated apoptosis was blocked by the broad-range caspase inhibitor zVAD.fmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	179-183	caspase 9	Rattus norvegicus	71-80
11708901-9	2001	These results led to the conclusion that Trp-P-1 mainly drives the caspase-8-mediated pathway that involves Bid, accompanied by a delay in the p53/NF-kappa B-mediated side pathway that involves Bax, Bcl-2, and caspase-9.	Tryptophan	41-44	caspase 9	Rattus norvegicus	210-219
11392460-6	2001	In accordance, cocaine dose-dependently increased activities of caspase-3, caspase-8, and caspase-9 in the fetal heart by 0.5-, 0.6-, and 0.6-fold, respectively, at 30 mg/kg per day, and by 3.3-, 2.9-, and 2.3-fold, respectively, at 60 mg/kg per day.	Cocaine	15-22	caspase 9	Rattus norvegicus	90-99
11323386-0	2001	DNA-damaging carcinogen 3-amino-1,4-dimethyl-5H-pyrido[4,3-b]indole (Trp-P-1) induces apoptosis via caspase-9 in primary cultured rat hepatocytes.	3-amino-1,4-dimethyl-5H-pyrido(4,3-b)indole	24-67	caspase 9	Rattus norvegicus	100-109
11323386-0	2001	DNA-damaging carcinogen 3-amino-1,4-dimethyl-5H-pyrido[4,3-b]indole (Trp-P-1) induces apoptosis via caspase-9 in primary cultured rat hepatocytes.	3-amino-1,4-dimethyl-5H-pyrido(4,3-b)indole	69-76	caspase 9	Rattus norvegicus	100-109
11042672-10	2000	Phenylephrine-mediated protection was abrogated by the phosphatidylinositol 3-kinase (PI 3-kinase) inhibitor wortmannin and was mimicked by the caspase-9 peptidic inhibitor LEHD-fmk.	Phenylephrine	0-13	caspase 9	Rattus norvegicus	144-153
11042672-10	2000	Phenylephrine-mediated protection was abrogated by the phosphatidylinositol 3-kinase (PI 3-kinase) inhibitor wortmannin and was mimicked by the caspase-9 peptidic inhibitor LEHD-fmk.	lehd-fmk	173-181	caspase 9	Rattus norvegicus	144-153
11045015-8	2000	These results suggest that cytochrome c and caspase-9 initiate the activation of executor caspase-3 in H2O2-treated PC12 cells, and that Bcl-2 inhibits H2O2-induced release of cytochrome c from mitochondria and then proteolytic processing of procaspase-9.	Hydrogen Peroxide	103-107	caspase 9	Rattus norvegicus	44-53
10918609-3	2000	Etoposide, cisplatin and tumor necrosis factor-alpha induced apoptosis of C6 rat glioma cells which was associated with ceramide formation due to activation of neutral sphingomyelinase, followed by release of mitochondrial cytochrome c into the cytosol and activation of caspases-9 and -3.	Etoposide	0-9	caspase 9	Rattus norvegicus	271-288
10918609-3	2000	Etoposide, cisplatin and tumor necrosis factor-alpha induced apoptosis of C6 rat glioma cells which was associated with ceramide formation due to activation of neutral sphingomyelinase, followed by release of mitochondrial cytochrome c into the cytosol and activation of caspases-9 and -3.	Cisplatin	11-20	caspase 9	Rattus norvegicus	271-288
10918609-5	2000	Bax overexpression enhanced etoposide-induced apoptosis through acceleration of cytochrome c release and caspases activation.	Etoposide	28-37	caspase 9	Rattus norvegicus	105-113
33793875-12	2021	Moreover, ATV reduced testicular malondialdehyde, nitric oxide, caspase-9 and caspase-3 while elevated reduced glutathione and superoxide dismutase along with catalase activity.	Atorvastatin	10-13	caspase 9	Rattus norvegicus	64-73
10861165-12	2000	This increase in caspase-9 activity was blocked by isoflurane at 1.6 MAC and halothane at 1.2 MAC.	Isoflurane	51-61	caspase 9	Rattus norvegicus	17-26
10861165-12	2000	This increase in caspase-9 activity was blocked by isoflurane at 1.6 MAC and halothane at 1.2 MAC.	Halothane	77-86	caspase 9	Rattus norvegicus	17-26
10769169-8	2000	Caspase activation during hypoxia was blocked bycarbobenzoxy-Val-Ala-Asp-fluoromethyl ketone and overexpression of Bcl-2.	bycarbobenzoxy-val-ala-asp-fluoromethyl ketone	46-92	caspase 9	Rattus norvegicus	0-7
10769169-9	2000	Of particular interest, caspase activation was also suppressed bythe chymotryptic inhibitors N-tosyl-L-phenylalaninechloromethyl ketone (TPCK) and Ala-Pro-Phe chloromethyl ketone (APF),and the general serine protease inhibitor 4-(2-aminoethyl)benzenesulphonyl fluoride.	Tosylphenylalanyl Chloromethyl Ketone	93-135	caspase 9	Rattus norvegicus	24-31
10769169-9	2000	Of particular interest, caspase activation was also suppressed bythe chymotryptic inhibitors N-tosyl-L-phenylalaninechloromethyl ketone (TPCK) and Ala-Pro-Phe chloromethyl ketone (APF),and the general serine protease inhibitor 4-(2-aminoethyl)benzenesulphonyl fluoride.	ala-pro-phe chloromethyl ketone	147-178	caspase 9	Rattus norvegicus	24-31
10769169-9	2000	Of particular interest, caspase activation was also suppressed bythe chymotryptic inhibitors N-tosyl-L-phenylalaninechloromethyl ketone (TPCK) and Ala-Pro-Phe chloromethyl ketone (APF),and the general serine protease inhibitor 4-(2-aminoethyl)benzenesulphonyl fluoride.	apf	180-183	caspase 9	Rattus norvegicus	24-31
10769169-9	2000	Of particular interest, caspase activation was also suppressed bythe chymotryptic inhibitors N-tosyl-L-phenylalaninechloromethyl ketone (TPCK) and Ala-Pro-Phe chloromethyl ketone (APF),and the general serine protease inhibitor 4-(2-aminoethyl)benzenesulphonyl fluoride.	4-(2-aminoethyl)benzenesulphonyl fluoride	227-268	caspase 9	Rattus norvegicus	24-31
10769169-13	2000	c/dATP stimulated caspase-9 processing and downstreamcaspase activation were significantly suppressed in the presence ofTPCK and APF.	Carbon	0-1	caspase 9	Rattus norvegicus	18-27
10769169-13	2000	c/dATP stimulated caspase-9 processing and downstreamcaspase activation were significantly suppressed in the presence ofTPCK and APF.	2'-deoxyadenosine triphosphate	2-6	caspase 9	Rattus norvegicus	18-27
10889445-10	2000	These results show that the differential susceptibility of glial cell types to menadione-induced oxidative stress and apoptosis appears to correlate with increased oxidative mtDNA damage and support the hypothesis that mtDNA damage could participate in the initiation of apoptosis through the enhanced release of cytochrome c and the activation of caspase 9.	Vitamin K 3	79-88	caspase 9	Rattus norvegicus	348-357
10604926-5	2000	Both caspase-9 and caspase-3 inhibitors (Z-LEHD-FMK and Ac-DEVD-CHO, respectively) blocked cocaine-induced apoptosis.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	41-51	caspase 9	Rattus norvegicus	5-14
10604926-5	2000	Both caspase-9 and caspase-3 inhibitors (Z-LEHD-FMK and Ac-DEVD-CHO, respectively) blocked cocaine-induced apoptosis.	acetyl-aspartyl-glutamyl-valyl-aspartal	56-67	caspase 9	Rattus norvegicus	5-14
10604926-5	2000	Both caspase-9 and caspase-3 inhibitors (Z-LEHD-FMK and Ac-DEVD-CHO, respectively) blocked cocaine-induced apoptosis.	Cocaine	91-98	caspase 9	Rattus norvegicus	5-14
10604926-12	2000	Furthermore, the release of cytochrome c from the mitochondria and its subsequent activation of caspase-9 and caspase-3 play a key role in cocaine-induced apoptosis.	Cocaine	139-146	caspase 9	Rattus norvegicus	96-105
10501228-4	1999	In the presence of cytochrome c and ATP, caspase-9 and -3 were activated, which initiated chromatin condensation and DNA cleavage in rat pheochromocytoma (PC12) nuclei.	Adenosine Triphosphate	36-39	caspase 9	Rattus norvegicus	41-57
33763176-8	2021	Decreases in HI-induced caspase-9 and caspase-3 activity were also observed.	hi	13-15	caspase 9	Rattus norvegicus	24-33
19517528-5	2009	Newly synthesized PC by PEMT2 contained more acyl groups of oleic acid (P < 0.01) and was mainly located in mitochondria; pemt2 over-expression increased the mitochondrial membrane fluidity and the release of cytochrome C from the mitochondria into the cytoplasma, which in turn activated caspase-9 and caspase-3, the key molecules in the mitochondrial apoptotic pathway.	Phosphatidylcholines	18-20	caspase 9	Rattus norvegicus	292-301
33762961-12	2021	Post-treatment with BHG decreased the expression of cleaved caspase-9/caspase 9, release of cytochrome C from mitochondria, and mitochondria reactive oxygen species production, increased activities of complex I, II, IV of ovarian tissue.	hexyl glucoside	20-23	caspase 9	Rattus norvegicus	60-69
33762961-12	2021	Post-treatment with BHG decreased the expression of cleaved caspase-9/caspase 9, release of cytochrome C from mitochondria, and mitochondria reactive oxygen species production, increased activities of complex I, II, IV of ovarian tissue.	hexyl glucoside	20-23	caspase 9	Rattus norvegicus	70-79
34558789-3	2022	For the first time, CdCl2 -initiated injury was found to result from the induction of not only apoptosis but also ferroptosis, as evidenced by the increased iron content, ROS production, and mitochondrial membrane potential along with changes in the expressions of iron death-related genes (FTH1, GPX4, ASCL4, PTGS2, and NOX1) and levels of caspase9, Bax, and Bcl-2 proteins.	Cadmium Chloride	20-25	caspase 9	Rattus norvegicus	341-349
34767868-6	2022	Western blot showed that gamma-GC down-regulated the ratio of Bax/Bcl-2 and the protein levels of cytosolic cytopigment c, cleaved-caspase-9, cleaved-caspase-3, and cleaved-PARP.	gamma-glutamylcysteine	25-33	caspase 9	Rattus norvegicus	131-140
34915193-4	2022	Co-administration of IPA significantly enhanced anti-inflammatory cytokine, interleukin-10 but suppressed oxidative and inflammatory stress, caspase-9 and caspase-3 activation with concomitant reduction in 8-hydroxy-2"-deoxyguanosine (8-OHdG) level and histological damage.	ipa	21-24	caspase 9	Rattus norvegicus	141-150
34968465-8	2022	Moreover, RSV alleviated the histopathological changes promoted by FNT and repaired the transcript levels of SIRT1, c-JNK, and caspase-9/3 along with p53 immunoreactivity.	Resveratrol	10-13	caspase 9	Rattus norvegicus	127-138
34987374-6	2021	SA group showed higher levels of Beclin1, Parkin, PINK1, NIX protein, and a lower level of Caspase-9 in brain tissue.	sa	0-2	caspase 9	Rattus norvegicus	91-100
34715137-8	2022	Expression of adenosine 5"-monophosphate-activated protein kinase (AMPK), Bcl-2 associated X protein (Bax), caspase 3 and caspase 9 in kidney tissue was significantly increased, while the antioxidant enzymes, mitochondrial complexes, the ATP levels and B-cell lymphoma protein 2 (Bcl-2) were decreased in kidney in the VCM-treated rats compared to the normal control group.	Vancomycin	319-322	caspase 9	Rattus norvegicus	122-131
34252440-8	2021	Furthermore, dioscin reduced Cyt C released, decreased the expression levels of Caspase-9 and Caspase-3 during apoptosis.	dioscin	13-20	caspase 9	Rattus norvegicus	80-89
34850329-7	2021	It is hypothesized that increased generation of nitric oxide induces the release of cytokines that activates caspase-9.	Nitric Oxide	48-60	caspase 9	Rattus norvegicus	109-118
34627804-2	2021	The maestro 11.1 software was used to predict the binding sites of DHL with LC3, Beclin-1, PI3K, AKT, mTOR, Bax, Bcl-2, Caspase-3, Caspase-9, and Caspase-7.	dehydrocostus lactone	67-70	caspase 9	Rattus norvegicus	131-140
34627804-5	2021	The docking results showed that DHL had binding sites with LC3, Beclin-1, PI3K, AKT, mTOR, Bax, Bcl-2, Caspase-3, Caspase-9, and Caspase-7.	dehydrocostus lactone	32-35	caspase 9	Rattus norvegicus	114-123
34505328-6	2021	However, mifepristone and lithospermum combination regimen promoted the expression level of malondialdehyde (MDA), activated caspase 3, caspase 9 and Bax, meanwhile, reduced the expression of superoxide dismutase (SOD) and Bcl-2.	Mifepristone	9-21	caspase 9	Rattus norvegicus	136-145
34216727-12	2021	H2O2 stimulated the activation of Nrf2 and JNK signaling pathways, but TGD increased the extent of Nrf2 antioxidant activation, decreased the activation of JNK, and eventually reversed the H2O2-induced protein expression of p-MKK7, Keap1, HO-1, Cleaved Caspase3 (CL-Casp3), Cleaved Caspase9 (CL-Casp9), Bax, and Bcl-2.	Hydrogen Peroxide	189-193	caspase 9	Rattus norvegicus	282-290
34216727-12	2021	H2O2 stimulated the activation of Nrf2 and JNK signaling pathways, but TGD increased the extent of Nrf2 antioxidant activation, decreased the activation of JNK, and eventually reversed the H2O2-induced protein expression of p-MKK7, Keap1, HO-1, Cleaved Caspase3 (CL-Casp3), Cleaved Caspase9 (CL-Casp9), Bax, and Bcl-2.	Hydrogen Peroxide	189-193	caspase 9	Rattus norvegicus	295-300
34304702-0	2021	PTB domain and leucine zipper motif 1 (APPL1) inhibits myocardial ischemia/hypoxia-reperfusion injury via inactivation of apoptotic protease activating factor-1 (APAF-1)/Caspase9 signaling pathway.	Leucine	15-22	caspase 9	Rattus norvegicus	170-178
34363182-10	2021	Furthermore, DEX and SB203582 diminished LPS-induced apoptosis, indicated by decreased Bax and Tom20 fluorescent double-stained cells, reduced annexin V-FITC/PI apoptosis rate, and reduced protein expression levels of Bax, cytochrome C, cleaved caspase-9, and cleaved caspase-3.	Dexmedetomidine	13-16	caspase 9	Rattus norvegicus	245-254
34363182-10	2021	Furthermore, DEX and SB203582 diminished LPS-induced apoptosis, indicated by decreased Bax and Tom20 fluorescent double-stained cells, reduced annexin V-FITC/PI apoptosis rate, and reduced protein expression levels of Bax, cytochrome C, cleaved caspase-9, and cleaved caspase-3.	sb203582	21-29	caspase 9	Rattus norvegicus	245-254
34216727-12	2021	H2O2 stimulated the activation of Nrf2 and JNK signaling pathways, but TGD increased the extent of Nrf2 antioxidant activation, decreased the activation of JNK, and eventually reversed the H2O2-induced protein expression of p-MKK7, Keap1, HO-1, Cleaved Caspase3 (CL-Casp3), Cleaved Caspase9 (CL-Casp9), Bax, and Bcl-2.	Hydrogen Peroxide	0-4	caspase 9	Rattus norvegicus	282-290
34216727-12	2021	H2O2 stimulated the activation of Nrf2 and JNK signaling pathways, but TGD increased the extent of Nrf2 antioxidant activation, decreased the activation of JNK, and eventually reversed the H2O2-induced protein expression of p-MKK7, Keap1, HO-1, Cleaved Caspase3 (CL-Casp3), Cleaved Caspase9 (CL-Casp9), Bax, and Bcl-2.	Hydrogen Peroxide	0-4	caspase 9	Rattus norvegicus	295-300
34436844-7	2021	RESULTS: As the intervention time extended, the expression of caspase-3 mRNA and caspase-9 mRNA in different Dexamethasone groups gradually increased in a duration-dependent manner.	Dexamethasone	109-122	caspase 9	Rattus norvegicus	81-90
34504562-10	2021	By contrast, Tofa attenuated cell apoptosis, which was coupled with upregulated Bcl-2 expression, downregulated cleaved-caspase-3 and downregulated cleaved-caspase-9 levels, in OGD/R-induced IEC-6 cells.	tofacitinib	13-17	caspase 9	Rattus norvegicus	156-165
34241806-8	2021	A protective role of NP via downregulation of TRPV1 activity on the STZ-induced increase of apoptosis, mitochondrial fROS, lipid peroxidation, caspase -3 (CASP-3), caspase -9 (CASP-9), TRPV1 current density, glutathione (GSH), cytosolic free Zn2+, and Ca2+ concentrations in the DRGs and HIPPO was also observed.	Streptozocin	68-71	caspase 9	Rattus norvegicus	164-174
34241806-10	2021	The STZ-mediated increase of TRPV1, CASP-3, and CASP-9 expressions was decreased in the DRGs and HIPPO by the treatment of NP.	Streptozocin	4-7	caspase 9	Rattus norvegicus	48-54
34302802-11	2021	These doses of plumbagin also caused enhancement of mATPase activity, elevated generation of mLPO as well as increases in the concentrations of caspases 9 and 3.	plumbagin	15-24	caspase 9	Rattus norvegicus	144-160
34587120-4	2021	RESULTS: DOX increased ROS formation and upregulated proteins expression of AT1R, NOX2, NOX4, caspase-3, caspase-9 and MAPK signaling including p-p38, p-JNK, p-ERK in H9c2 cells.	Doxorubicin	9-12	caspase 9	Rattus norvegicus	105-114
34517917-11	2021	Moreover, nesfatin-1 treatment attenuated CoCl2-induced increase in ROS production and mitochondrial dysfunction, decreased mitochondrial membrane potential, Bax/Bcl-2 imbalance, as well as c-caspase-9 and c-caspase-3 levels.	cobaltous chloride	42-47	caspase 9	Rattus norvegicus	192-201
34152018-5	2021	The results showed that GSPE ameliorated CIS-induced the apoptosis of testicular cells and inhibited the protein levels of Bad, Cyt c, caspase-9, caspase-3, caspase-12, GRP78, CHOP, IRE1alpha, p-IRE1alpha, XBP-1S, PERK, p-PERK, eIF2alpha, and p-eIF2alpha.	gspe	24-28	caspase 9	Rattus norvegicus	135-144
34080663-11	2021	Furthermore, the expression levels of ERS-associated apoptotic proteins, including c-Jun N-terminal kinase, Bax, cytochrome c, caspase-3, caspase-12 and caspase-9 were reduced following treatment with TA.	Tannins	201-203	caspase 9	Rattus norvegicus	153-162
34152018-7	2021	These results indicated that GSPE can improve CIS-induced testicular cells apoptosis via activating PI3K/Akt/mTOR and inhibiting Bad/Cyt c/caspase-9/caspase-3 pathways.	gspe	29-33	caspase 9	Rattus norvegicus	139-148
34152018-14	2021	This toxicity was attenuated by GSPE treatment via activated PI3K/Akt/mTOR pathway, and inhibiting Bad/CytC/caspase-9/caspase-3 as well as PREK/eIF2alpha, IRE1alpha/XBP-1S/caspase-12 pathways.	gspe	32-36	caspase 9	Rattus norvegicus	108-117
34128436-11	2021	Although Cd exposure caused an increase in the messenger RNA (mRNA) levels of Bcl-2, Caspase-3 and Caspase-9 in the testicular tissues (p < 0.05), Bcl-2 expression was unchanged (p > 0.05).	Cadmium	9-11	caspase 9	Rattus norvegicus	99-108
34115930-9	2021	Levosimendan downregulated the expression of the apoptosis-related proteins Bax, cleaved caspase-3 and cleaved caspase-9, as well as upregulated Bcl-2 and p-ERK expression in vivo and in vitro.	Simendan	0-12	caspase 9	Rattus norvegicus	111-120
34138955-10	2021	Only the hypothermia + VPA group showed significantly attenuated cleaved caspase-9 levels than the normothermia group.	Valproic Acid	23-26	caspase 9	Rattus norvegicus	73-82
35421786-9	2022	Besides, the level of Bax, caspase-9 and caspase-3 were elevated, while the Bcl-2 level was reduced following the Cd intoxication.	Cadmium	114-116	caspase 9	Rattus norvegicus	27-36
34135573-9	2021	Results: High concentrations of DEX (>=100 muM) significantly reduced cell viability, induced neuronal apoptosis, upregulated the protein expression of cleaved caspase 3, Bax, cleaved caspase 9, and Cyt-c. DEX also considerably promoted the release of ROS.	Dexmedetomidine	32-35	caspase 9	Rattus norvegicus	184-193
34135573-9	2021	Results: High concentrations of DEX (>=100 muM) significantly reduced cell viability, induced neuronal apoptosis, upregulated the protein expression of cleaved caspase 3, Bax, cleaved caspase 9, and Cyt-c. DEX also considerably promoted the release of ROS.	Dexmedetomidine	206-209	caspase 9	Rattus norvegicus	184-193
34587404-6	2021	Furthermore, western blotting findings displayed an augmented expression of PI3K, AKT, NF-kappaB, PCNA, cyclin D1, Ki-67, and Bcl-2, while reducing expression of p53, Bax, caspase-3, and caspase-9 in DMBA-induced cancer-bearing animals.	6,11-dimethylbenzo(b)naphtho(2,3-d)thiophene	200-204	caspase 9	Rattus norvegicus	187-196
35427818-16	2022	Also, the results of PD showed extremely significant differences in the levels of caspase-9 and IL-1beta at the different time points in MTG (P < 0.01) compared with 0 min.	(Methylthio)acetic acid	137-140	caspase 9	Rattus norvegicus	82-91
35571249-5	2022	DOX enhanced the activities of caspase family members in cardiomyocytes, while NaHS attenuated DOX-enhanced caspase-3, caspase-2, and caspase-9 activities by 223.1%, 73.94%, and 52.29%, respectively.	sodium bisulfide	79-83	caspase 9	Rattus norvegicus	134-143
35427818-17	2022	The levels of caspase-9 and IL-1beta in NTG rats showed little fluctuation and were relatively stable; however, their levels in MTG showed a downward trend with time.	Nitroglycerin	40-43	caspase 9	Rattus norvegicus	14-23
35427818-17	2022	The levels of caspase-9 and IL-1beta in NTG rats showed little fluctuation and were relatively stable; however, their levels in MTG showed a downward trend with time.	(Methylthio)acetic acid	128-131	caspase 9	Rattus norvegicus	14-23
35258777-11	2022	In addition, EA pretreatment notably reduced the AS-induced increased level of cleaved caspase-9, cleaved caspase-3 and expression of Cyt c, Bax/Bcl-2 ratio, as well as neuronal apoptosis rate in aged rats.	Arsenic	49-51	caspase 9	Rattus norvegicus	87-96
35158127-8	2022	On the other hand, rolay jelly caused augmented GSH and CAT activities, as well as upregulated Bax, BDNF, caspase-3, caspase-6, caspase-9 protein expressions in rats injuried by the fluoride exposure.	rolay jelly	19-30	caspase 9	Rattus norvegicus	128-137
35571249-5	2022	DOX enhanced the activities of caspase family members in cardiomyocytes, while NaHS attenuated DOX-enhanced caspase-3, caspase-2, and caspase-9 activities by 223.1%, 73.94%, and 52.29%, respectively.	Doxorubicin	95-98	caspase 9	Rattus norvegicus	134-143
35239232-11	2022	Cell proliferative markers proliferating cell nuclear antigen and Cyclin-D1 protein expressions were downregulated; in contrast, Bcl-2, Bax, caspase-3, and caspase-9 gene expressions were upregulated and then it followed that protein expression of PI3K/AKT was downregulated in PRU-treated groups.	prunetin	278-281	caspase 9	Rattus norvegicus	156-165
35386216-8	2022	Data also show that HSA administration induces an increased susceptibility of expression of proapoptotic proteins such as Apaf-1, caspase-9, IFN-gamma, IFNGR1, and p53, and a reduced expression of antiapoptotic proteins such as E2, ESR1, TNF-alpha, COX-2, and Bcl-xL 1 in their mechanisms of action.	Octadecanoic acid, 12-hydroxy-, (R)-	20-23	caspase 9	Rattus norvegicus	130-139
35064410-10	2022	Serum TNF-alpha, IL1-beta, MMP-1 and MMP-2 activities and tissue casp-3 and casp-9 activities significantly increased but the bcl-2/bax ratio significantly decreased in the MTX group compared those of the control group.	Methotrexate	173-176	caspase 9	Rattus norvegicus	76-82
35182546-10	2022	Increases in Bax, cleaved caspase-3 and cytochrome c levels, caspase-3 and caspase-9 activity, and decrease in Bcl-2 level by I/R injury were attenuated by 5-CS treatment and pretreatment of 5-HD blocked its effects.	5-cs	156-160	caspase 9	Rattus norvegicus	75-84
35173561-0	2022	Helicid Improves Lipopolysaccharide-Induced Apoptosis of C6 Cells by Regulating SH2D5 DNA Methylation via the CytC/Caspase9/Caspase3 Signaling Pathway.	helicide	0-7	caspase 9	Rattus norvegicus	115-123
35084700-8	2022	Furthermore, treatment with Sal B down-regulated HG-induced PARP, cleaved-caspase 3, cleaved-caspase 9, Bax, NLRP3, ASC, and IL-1 beta expression, but mitigated HG-mediated down-regulation of Bcl-2 expression (P<0.05).	salvianolic acid B	28-33	caspase 9	Rattus norvegicus	93-102
35355865-7	2022	The results of the vitro cell culture showed that glutathione pretreatment protected corpus cavernosum smooth muscle cells (CCSMC) from H2O2-induced apoptosis by decreasing Caspase 9 and Caspase 3 expressions.	Glutathione	50-61	caspase 9	Rattus norvegicus	173-182
35173561-13	2022	These results suggest that helicid may affect the CytC/caspase9/caspase3 apoptosis signaling pathway and improve the apoptosis indices by mediating DNA methylation of SH2D5.	helicide	27-34	caspase 9	Rattus norvegicus	55-63
35071601-11	2022	Moreover, protein levels of caspase-3, caspase-9, and BAX were significantly higher in TZM-treated cells but were significantly lower after pretreatment with Rg2.	rg2	158-161	caspase 9	Rattus norvegicus	39-48
35118072-11	2021	ISO stimulated mPTP opening, resulting in an increase in the release of cytc, which further increased the ratio of cleaved caspase9/caspase9 and enhanced the protein activity of caspase9.	iso	0-3	caspase 9	Rattus norvegicus	123-131
35071601-12	2022	Conclusion: Ginsenoside Rg2 inhibited TZM-induced cardiotoxicity, and the mechanism may be related to the downregulation of the expression of proapoptotic proteins caspase-3, caspase-9, and BAX and the inhibition of TZM-induced apoptosis in cardiomyocytes.	ginsenoside Rg2	12-27	caspase 9	Rattus norvegicus	175-184
35118072-11	2021	ISO stimulated mPTP opening, resulting in an increase in the release of cytc, which further increased the ratio of cleaved caspase9/caspase9 and enhanced the protein activity of caspase9.	iso	0-3	caspase 9	Rattus norvegicus	132-140
35118072-11	2021	ISO stimulated mPTP opening, resulting in an increase in the release of cytc, which further increased the ratio of cleaved caspase9/caspase9 and enhanced the protein activity of caspase9.	iso	0-3	caspase 9	Rattus norvegicus	178-186
34023410-20	2021	This study showed that retinoic acid regulates bcl-2 family proteins and caspase proteins in focal cerebral ischemia.	Tretinoin	23-36	caspase 9	Rattus norvegicus	73-80
34979825-7	2022	RESULTS: The results showed that the pretreatment of VSMCs with DMY not only significantly increased cell viability, reduced intracellular ROS release, alleviated the morphological changes of apoptosis, and decreased the apoptosis rate, but also upregulated Bcl-2 expression and downregulated Caspase-3, Caspase-9, Bax expression, and ultimately attenuated the H2O2-stimulated apoptosis.	dihydromyricetin	64-67	caspase 9	Rattus norvegicus	304-313
33998977-7	2021	In addition, this study also showed that apigenin significantly suppressed the toxic effects of EDF by quenching ROS production thereby abrogating the caspase-9/-3 and apoptosis activation in hepatocytes.	Apigenin	41-49	caspase 9	Rattus norvegicus	151-160
33974882-5	2021	In control rats, 5 mg/kg/d trans-resveratrol administration for 30 days increased gene expressions of tumor suppressor protein 53, Bcl2-associated X protein, B-cell lymphoma-2 (Bcl2), Caspase-3 (CASP3), CASP8 and CASP9, p38alphaMAPK, c-Jun N-terminal kinase-1 (JNK1), and extracellular signal-regulated kinase-1 (ERK1).	Resveratrol	27-44	caspase 9	Rattus norvegicus	213-218
33976387-9	2022	In addition, PF treatment reduced the caspase9 activity, rescued the release of cytochrome c from mitochondria, and maintained the integrity of mitochondria membrane.	peoniflorin	13-15	caspase 9	Rattus norvegicus	38-46
33933022-0	2021	The effects of L-carnitine on renal function and gene expression of caspase-9 and Bcl-2 in monosodium glutamate-induced rats.	Sodium Glutamate	91-111	caspase 9	Rattus norvegicus	68-77
33933022-6	2021	RESULTS: MSG significantly increased the serum level of MDA, BUN, creatinine, uric acid and renal Caspase-9, NGAL and KIM-1 expression, but it decreased the serum activity also renal expression of SOD, catalase, GPX, and Bcl-2 expression compared to the control group.	Sodium Glutamate	9-12	caspase 9	Rattus norvegicus	98-107
33840231-9	2021	Alogliptin and/or taxifolin induced significant improvement of liver function tests with significant increase in the survival rate, tissue antioxidant enzymes, Nrf2, caspase 3, caspase 9, Beclin-1 and JNK activities associated with significant decrease in serum AFP and AFU, tissue MDA, TGF-beta1, IL-1alpha and TLR4 expression compared to HCC group.	alogliptin	0-10	caspase 9	Rattus norvegicus	177-186
33959665-4	2021	Meanwhile, Western blot analysis showed that in STZ-induced DM immature rats, BB decreased the expression of apoptosis-related proteins Bax, cleaved caspase-3, and cleaved caspase-9 while enhancing the Bcl-2 expression; BB downregulated the expression of ACC related to fat anabolism, while upregulating the expression of CPT-1 related to fat catabolism.	Streptozocin	48-51	caspase 9	Rattus norvegicus	172-181
33959665-4	2021	Meanwhile, Western blot analysis showed that in STZ-induced DM immature rats, BB decreased the expression of apoptosis-related proteins Bax, cleaved caspase-3, and cleaved caspase-9 while enhancing the Bcl-2 expression; BB downregulated the expression of ACC related to fat anabolism, while upregulating the expression of CPT-1 related to fat catabolism.	bilobalide	78-80	caspase 9	Rattus norvegicus	172-181
33600885-7	2021	In addition, the highly specific autophagy inhibitor SAR405 administration reduced TBI-induced apoptosis-related protein cleaved caspase-3 and cleaved caspase-9 levels in the ipsilateral cortex, as well as brain edema and neurological defects accessed by mNSS.	SAR405	53-59	caspase 9	Rattus norvegicus	151-160
33847039-14	2021	CONCLUSION: Our study has led to research into the association between activation of Fas, Caspase-8, and Caspase-9 pathways and bile acid-induced fetal cardiomyocyte apoptosis, which may be one of the mechanisms on fetal cardiac death in ICP.	Bile Acids and Salts	128-137	caspase 9	Rattus norvegicus	105-114
33847039-0	2021	Fas, Caspase-8, and Caspase-9 pathway-mediated bile acid-induced fetal cardiomyocyte apoptosis in intrahepatic cholestasis pregnant rat models.	Bile Acids and Salts	47-56	caspase 9	Rattus norvegicus	20-29
33847039-11	2021	And we found increased expression levels of Fas, Caspase-8, and Caspase-9 proteins and mRNA in the fetal cardiomyocyte in EE2-treated group but not in control- or EE2 + UDCA-treated groups.	Norinyl	122-125	caspase 9	Rattus norvegicus	64-73
33840231-9	2021	Alogliptin and/or taxifolin induced significant improvement of liver function tests with significant increase in the survival rate, tissue antioxidant enzymes, Nrf2, caspase 3, caspase 9, Beclin-1 and JNK activities associated with significant decrease in serum AFP and AFU, tissue MDA, TGF-beta1, IL-1alpha and TLR4 expression compared to HCC group.	taxifolin	18-27	caspase 9	Rattus norvegicus	177-186
33465395-6	2021	L-817,818 administration downregulated the expression of apoptosis-related proteins caspase-9 and caspase-3 in COH retinas.	l-817	0-5	caspase 9	Rattus norvegicus	84-93
33439051-5	2021	Furthermore, fenitrothion provoked many histopathological changes in the fetal liver and markedly up-regulated the mRNA gene expression of p53, caspase-9 along with elevation in the immunoreactivity of Bax and caspase-3, but it down-regulated the expression level of paraoxonase-1.	Fenitrothion	13-25	caspase 9	Rattus norvegicus	144-153
33162165-6	2021	Caspase-9 increased significantly from 0.12 ppm ozone (p < 0.01) in both gender rats, while caspase-3 was initially activated at 0.5 ppm ozone.	Ozone	48-53	caspase 9	Rattus norvegicus	0-9
33884184-8	2021	TAM decreased (P < 0.05) antioxidant, anti-inflammatory cytokine (IL-10), besides increase in (P < 0.05) lipid peroxidation (LPO), pro-inflammatory cytokines (IL-1beta, TNF-alpha), nitric oxide (NO), xanthine oxidase (XO), myeloperoxidase (MPO), and apoptotic caspases (Casp-3 and -9) levels.	Tamoxifen	0-3	caspase 9	Rattus norvegicus	260-268
33679421-9	2021	Meanwhile, luteolin significantly suppressed METH-induced elevation of p53, caspase9, caspase3, cleaved caspase3, the ratio of Bax/Beclin-2, as well as autophagy-related Beclin-1, Atg5, and LC3-II.	Methamphetamine	45-49	caspase 9	Rattus norvegicus	76-84
33562483-8	2021	Linalool enhanced cardiac antioxidant activities, reduced inflammatory cytokines (tumor necrosis factor-alpha (TNF-alpha), nuclear factor-kappa-B (NF-kappaB), interleukin 1 beta (IL-1beta), interleukin 6 (IL-6)), apoptotic markers (Caspase-3, Caspase-9, and Bax), and elevated Bcl2.	linalool	0-8	caspase 9	Rattus norvegicus	243-252
33190410-5	2021	Dexamethasone (Dex) was used to induce apoptosis in osteoblasts, and this resulted in a significant increase in levels of p-JNK, p-c-Jun, Bax, caspase-3, caspase-9, cytochrome C, Beclin-1, and LC3, and a decrease in levels of P62 and Bcl-2.	Dexamethasone	0-13	caspase 9	Rattus norvegicus	154-163
32613488-6	2021	Compared with the NaF group, pretreatment with selenium enhanced the activity of antioxidant enzymes, mitochondrial membrane potential, and protein expression of Bcl-2, while the levels of NO and MDA, number of apoptotic cells, mRNA expression of Bax, Bad, caspase-3, caspase-8, and caspase-9, and protein expression of Bax were decreased.	Selenium	47-55	caspase 9	Rattus norvegicus	283-292
33376508-9	2021	Curcumin was also revealed to downregulate c-Jun N-terminal kinases (JNK), cytochrome c, caspase-3 and caspase-9 expression upon treatment with 100 and 200 mg/kg curcumin, which may result in inhibition of the mitochondrial apoptotic pathway in renal cells.	Curcumin	0-8	caspase 9	Rattus norvegicus	103-112
33376508-9	2021	Curcumin was also revealed to downregulate c-Jun N-terminal kinases (JNK), cytochrome c, caspase-3 and caspase-9 expression upon treatment with 100 and 200 mg/kg curcumin, which may result in inhibition of the mitochondrial apoptotic pathway in renal cells.	Curcumin	162-170	caspase 9	Rattus norvegicus	103-112
33551799-8	2020	Compared with vehicle treatment, paeonol significantly upregulated Bcl-2 protein expression and significantly downregulated the cleaved forms of caspase-8, caspase-9, caspase-3 and PARP protein expression in the I/R injured myocardium.	paeonol	33-40	caspase 9	Rattus norvegicus	156-165
33285470-16	2021	Moreover, physcion reversed the Hcy-induced apoptosis related parameter changes such as decreased mitochondrial membrane potential (MMP) and Bcl-2/Bax protein ratio, and increased protein expression of caspase-9/3 in HUVECs.	Homocysteine	32-35	caspase 9	Rattus norvegicus	202-213
32981412-0	2021	Combine Colorants of Tartrazine and Erythrosine induce kidney injury: Involvement of TNF-alpha gene, Caspase-9 and KIM-1 gene expression and kidney functions indices.	Erythrosine	36-47	caspase 9	Rattus norvegicus	101-110
33316931-1	2020	The present study evaluates the regulatory effect of Nano-Curcumin (Nano-CUR) against tartrazine (TZ)-induced injuries on apoptosis-related gene expression (i.e., p53, CASP-3 and CASP-9), antioxidant status, and DNA damages in bone marrow in treated rats.	Curcumin	58-66	caspase 9	Rattus norvegicus	179-185
33392217-5	2020	Western blotting analyses showed that Bax, cytochrome C, caspase-3, caspase-9, and apoptosis-inducing factor expression levels were obviously decreased, whereas Bcl-2 expression levels obviously increased after AEE treatment.	aspirin eugenol ester	211-214	caspase 9	Rattus norvegicus	68-77
33316931-1	2020	The present study evaluates the regulatory effect of Nano-Curcumin (Nano-CUR) against tartrazine (TZ)-induced injuries on apoptosis-related gene expression (i.e., p53, CASP-3 and CASP-9), antioxidant status, and DNA damages in bone marrow in treated rats.	Tartrazine	86-96	caspase 9	Rattus norvegicus	179-185
33316931-18	2020	Moreover, the results revealed a remarkable up-regulation in the level of expression for the three examined genes, including p53, CASP-3, and CASP-9 in TZ-ingested rats compared to the control.	Tartrazine	152-154	caspase 9	Rattus norvegicus	142-148
33064729-6	2020	In addition, NaHS declined pro-apoptotic proteins related to mitochondrial pathway apoptosis in CS rat offspring pFRG, such as Bax, Cytochrome C, caspase9 and caspase3.	sodium bisulfide	13-17	caspase 9	Rattus norvegicus	146-154
33010109-6	2020	Enhanced expression of Caspase 3, Caspase 9, and Bax and decreased expression of Bcl-2 induced by fluoride were also reversed by gastrodin.	gastrodin	129-138	caspase 9	Rattus norvegicus	34-43
32172678-5	2020	Hepatic tissues were used for the determination of NFkappaB, Nrf2, TNF-alpha, caspase-3, caspase-8 and caspase-9.Results: Sodium ascorbate significantly attenuated HCC-induced reduction in the expression of NrF2 associated with a reduction in concentrations of hydrogen peroxide and superoxide anion.	Ascorbic Acid	122-138	caspase 9	Rattus norvegicus	103-112
32529603-9	2020	Cryopreservation with DMSO activated apoptosis through the mitochondrial pathway: the Bax/Bcl-2 protein ratio increased, mitochondrial membrane potential decreased, and initiator caspase-9 was activated.	Dimethyl Sulfoxide	22-26	caspase 9	Rattus norvegicus	179-188
32438104-6	2020	Moreover, pretreatment of NAC reduced the number of apoptosis in kidney tissues induced by CLP, decreased the mRNA levels of caspase-3, caspase-9, cytochrome c, and poly ADP-ribose polymerase, and increased mitochondrial membrane activity in renal cortical cells (complex I/II/III/IV).	Acetylcysteine	26-29	caspase 9	Rattus norvegicus	136-145
33155210-17	2020	Moreover, the expressions of Apaf1, Caspase-9 and Survivin were clearly higher, while that of Bcl-2 was prominently lower in tumor tissues in oxaliplatin group than model group (p<0.05).	Oxaliplatin	142-153	caspase 9	Rattus norvegicus	36-45
32781062-8	2020	Wogonin prevented apoptotic damage by enhanced protein distribution of caspase-9, caspase-3, and Bax due to Cd exposure.	wogonin	0-7	caspase 9	Rattus norvegicus	71-80
32676729-9	2020	Moreover, the expression of cleaved initiator caspase-9 and effector caspase-6 was higher in compulsive METH takers in comparison to shock-sensitive rats.	Methamphetamine	104-108	caspase 9	Rattus norvegicus	46-55
32771557-7	2020	However, taurine and CARE interventions significantly decreased apoptosis markers (caspase 3 and caspase 9) and significantly increased Akt in heart of diabetic rats compare to DM groups (p < 0.05).	Taurine	9-16	caspase 9	Rattus norvegicus	97-106
32464304-7	2020	In conclusion, probucol can significantly improve the pathological damage of myocardial tissue in VMC rats, and its mechanism may be related to improving the expression of myocardium-related proteins Caspase-3 and Caspase-9, inhibiting oxidative stress response, and down-regulating Cav-3 and Smad3 gene expression in myocardial tissue of VMC rats.	Probucol	15-23	caspase 9	Rattus norvegicus	214-223
33061292-6	2020	Furthermore, cell experiments showed that pravastatin can alleviate the injury of H9C2 myocardial cells caused by I/R, inhibit the apoptosis of myocardial cells, and lead to a significant reduction in pro-apoptotic genes Bax, caspase-3 and caspase-9 transcription levels, an obvious increase in anti-apoptotic gene Bcl-2, and an increase in cell activity.	Pravastatin	42-53	caspase 9	Rattus norvegicus	240-249
33198873-15	2020	CONCLUSIONS: H2S attenuates intestinal injury in IRI rats by up-regulating PI3K/Akt signal pathway and down-regulating caspase-9 and mTOR.	Deuterium	13-16	caspase 9	Rattus norvegicus	119-128
32663572-5	2020	Mechanistically, nicotine exposure markedly increased cleaved Caspase 3 and cleaved Caspase 9 indicating the involvement of intrinsic apoptotic pathway (mitochondrial cell death pathway).	Nicotine	17-25	caspase 9	Rattus norvegicus	84-93
32901682-7	2020	Both gene and protein expression of Caspase-9 in diabetic and ethanol-diabetic groups suggest the involvement of the apoptosis cascade from this study model.	Ethanol	62-69	caspase 9	Rattus norvegicus	36-45
32464442-9	2020	Furthermore, pretreatment of curcumin with arsenic expressively alleviated arsenic-induced toxicity and cell death by reversing the expressions of proteins; mTOR, Akt, Nrf2, ERK1, Bcl-x, Xiap, ULK, LC3, p53, Bax, cytochrome c, caspase 9 and cleaved caspase 3.	Arsenic	43-50	caspase 9	Rattus norvegicus	227-236
32603889-9	2020	Moreover, pretreated with Rg1 significantly reduced the expression of Cyt-C, Caspase-9 and Caspase-3 to inhibit the cell apoptosis.	ginsenoside Rg1	26-29	caspase 9	Rattus norvegicus	77-86
32603889-12	2020	In addition, western blotting showed that the increase of Cyt-C, Caspase-9 and Caspase-3 was inhibited by H2O2.	Hydrogen Peroxide	106-110	caspase 9	Rattus norvegicus	65-74
32464442-7	2020	Moreover, arsenic (10 muM) treatment significantly down-regulated the inhibition factors of autophagy/apoptosis; mTOR, Akt, Nrf2, ERK1, Bcl-x, Xiap protein expressions, up-regulated the enhanced factors of autophagy/apoptosis; ULK, LC3, p53, Bax, cytochrome c, caspase 9, cleaved caspase 3 proteins and eventually caused autophagic and apoptotic cell death.	Arsenic	10-17	caspase 9	Rattus norvegicus	261-270
32464442-9	2020	Furthermore, pretreatment of curcumin with arsenic expressively alleviated arsenic-induced toxicity and cell death by reversing the expressions of proteins; mTOR, Akt, Nrf2, ERK1, Bcl-x, Xiap, ULK, LC3, p53, Bax, cytochrome c, caspase 9 and cleaved caspase 3.	Arsenic	75-82	caspase 9	Rattus norvegicus	227-236
32464442-9	2020	Furthermore, pretreatment of curcumin with arsenic expressively alleviated arsenic-induced toxicity and cell death by reversing the expressions of proteins; mTOR, Akt, Nrf2, ERK1, Bcl-x, Xiap, ULK, LC3, p53, Bax, cytochrome c, caspase 9 and cleaved caspase 3.	Curcumin	29-37	caspase 9	Rattus norvegicus	227-236
32705166-7	2020	As shown by hypodiploid nuclei and confirmed by western blot analysis, Doxo increased caspase 9 expression and reduced procaspase 3 levels, which induced cell death.	Doxorubicin	71-75	caspase 9	Rattus norvegicus	86-95
32703432-6	2020	In addition, salidroside treatment also restrained the ER stress-mediated apoptotic pathway, as indicated by decreased pro-apoptotic proteins p-JNK, TRAF2, BAX, and cleaved caspase 9 and caspase 12, as well as upregulation of Bcl-2.	rhodioloside	13-24	caspase 9	Rattus norvegicus	173-182
32705179-8	2020	In addition, butorphanol treatment resulted in a significant upregulation of Bax, and downregulation of Bcl-2, activated caspase-3, caspase-9 and poly ADP-ribose polymerase, increased the expression of X-linked inhibitor of apoptosis protein and enhanced ATP activity.	Butorphanol	13-24	caspase 9	Rattus norvegicus	132-141
32706450-12	2020	In addition, Dex repressed Caspase-9 expression and apoptotic cell numbers in spinal cord tissues in CCI rats.	Dexmedetomidine	13-16	caspase 9	Rattus norvegicus	27-36
32139897-5	2020	The protective effect of hypotonic challenge against H2O2-induced apoptosis was mediated through inhibiting mitochondria-dependent apoptotic pathway, evidenced by increased Bcl-2/Bax ratio, stabilizing mitochondrial membrane potential (MMP), decreased cytochrome c release from the mitochondria to the cytoplasm, and inhibition of the activation of caspase-9 and caspase-3.	Hydrogen Peroxide	53-57	caspase 9	Rattus norvegicus	349-358
32869594-8	2020	Compared with the LY294002+EA group, the number of neuronal apoptosis in the left cortex was decreased in the EA group (P<0.01), and the expression of Bax, Caspase-9 and Cyt-C was decreased (P<0.01, P<0.05), and the expression of p-Akt/Akt and Bcl-2 was increased (P<0.01).	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	18-26	caspase 9	Rattus norvegicus	156-165
32903480-6	2020	In vitro, Lut inhibited the upregulation of Dex-induced phospho-STAT1, cleaved caspase9, and cleaved caspase3.	Dexamethasone	44-47	caspase 9	Rattus norvegicus	79-87
32953731-8	2020	Apoptosis was further inhibited with LIG, as shown with Terminal dUTP nick-end labeling (TUNEL) staining and expression of Caspase-3, Caspase-9, Bax, and Bcl-2.	ligustilide	37-40	caspase 9	Rattus norvegicus	134-143
32411568-13	2020	In cisplatin-treated cultured hippocampal neurons, Dex treatment and miR-429-3p overexpression significantly increased mitochondrial DNA gene mt-ND1expression and decreased caspase-9 expression.	Cisplatin	3-12	caspase 9	Rattus norvegicus	173-182
32043372-13	2020	Also, DXP treatment decreased the number of caspase-positive cells significantly compared to group 3.	dexpanthenol	6-9	caspase 9	Rattus norvegicus	44-51
32581829-6	2020	Crocetin significantly alleviated LPS-induced cytotoxicity, cellular apoptosis, and oxidative stress through increased Bcl-2 activity and PI3K-Akt signaling and suppression of caspase 3 and caspase 9 activities.	crocetin	0-8	caspase 9	Rattus norvegicus	190-199
32153200-7	2020	In addition, at the concentration of 1500 muM, SO2 markedly increased the level of caspase-3 and caspase-9.	Sulfur Dioxide	47-50	caspase 9	Rattus norvegicus	97-106
32527252-0	2020	Mechanism of Heshouwuyin inhibiting the Cyt c/Apaf-1/Caspase-9/Caspase-3 pathway in spermatogenic cell apoptosis.	heshouwuyin	13-24	caspase 9	Rattus norvegicus	53-62
32527252-12	2020	CONCLUSION: The inhibition of spermatogenic cell apoptosis by Heshouwuyin was closely related to the Cyt c/Apaf-1/Caspase-9/Caspase-3 pathway.	heshouwuyin	62-73	caspase 9	Rattus norvegicus	114-123
32411568-13	2020	In cisplatin-treated cultured hippocampal neurons, Dex treatment and miR-429-3p overexpression significantly increased mitochondrial DNA gene mt-ND1expression and decreased caspase-9 expression.	Dexmedetomidine	51-54	caspase 9	Rattus norvegicus	173-182
32295448-14	2020	HighlightsTesticular mitochondria are less sensitive to induction of permeability transition than liver mitochondria in rats exposed to D-galactose for 6 weeks, despite the occurrence of alterations in the antioxidant defense system and generation of ROS in sperm cells as in hepatocytes.The occurrence of mitochondrial permeability transition in liver of galactose-exposed rats is consistent with malondialdehyde production, alteration in antioxidant levels, enhanced ATPase activity, caspases-9 and 3 activation, immune dysfunction, and DNA fragmentation.The study of biochemical basis of reduced sensitivity of testis to permeability transition under conditions which the liver is extremely susceptible may become useful in age associated-neurodegenerative diseases where apoptosis is upregulated and has to be properly managed to achieve downregulation.	Galactose	136-147	caspase 9	Rattus norvegicus	486-502
31971015-6	2020	NR1 inhibited the increase in levels of Bax, caspase-9, and caspase-3, which was instigated by ACR.	Acrylamide	95-98	caspase 9	Rattus norvegicus	45-54
32633389-0	2020	MiR-808 inhibits cardiomyocyte apoptosis and expressions of caspase-3 and caspase-9 in rats with myocardial infarction by regulating TGF-beta1 signaling pathway.	mir-808	0-7	caspase 9	Rattus norvegicus	74-83
32633389-12	2020	The expression levels of caspase-3 and caspase-9 in the miR-808 group were lower than those in the model group (p<0.05).	mir-808	56-63	caspase 9	Rattus norvegicus	39-48
32633389-13	2020	CONCLUSIONS: MiR-808 can inhibit cardiomyocyte apoptosis in rats with MI by down-regulating TGF-beta1 expression and inhibiting the expressions of caspase-3 and caspase-9.	mir-808	13-20	caspase 9	Rattus norvegicus	161-170
32201950-9	2020	Celastrol reduced enzyme activity and protein expression of caspase-3, caspase-6 and caspase-9, decreased Bip, Atf6, Chop and Xbp-1 expression both at protein and mRNA levels.	celastrol	0-9	caspase 9	Rattus norvegicus	85-94
32547397-7	2020	Furthermore, Hyp treatment decreased the expressions of apoptotic proteins including caspase-3, caspase-9, and Bax in RVECs of DM rats, while increased the expression of anti-apoptotic protein Bcl-2.	hyperoside	13-16	caspase 9	Rattus norvegicus	96-105
32419697-13	2020	Moreover, DEX notably reduced expressions of caspase-3, caspase-9, cyt-c, and bax and increased expression of bcl-2.	Dexmedetomidine	10-13	caspase 9	Rattus norvegicus	56-65
32414226-9	2022	MiR-379 mimic was found to reduce the expression of caspase3 and caspase9 in H9c2 cells and thereby reduce H2O2-induced cell damage.	Hydrogen Peroxide	107-111	caspase 9	Rattus norvegicus	65-73
32477152-7	2020	Meanwhile, CUMS rats treated with fluoxetine showed reductions in neuronal apoptosis and a downregulation of the apoptotic protein Bax, cleaved caspase 3, and caspase 9 levels.	Fluoxetine	34-44	caspase 9	Rattus norvegicus	159-168
32426037-8	2020	In addition, (Z)-2-acetoxy-3-(3,4-dihydroxyphenyl) acrylic acid-treated tissues displayed decreased expression of Bax, caspase-3, and caspase-9 and increased expression of Bcl-2, which was in part due to the promotion of Akt phosphorylation.	(z)-2-acetoxy-3-(3,4-dihydroxyphenyl) acrylic acid	13-63	caspase 9	Rattus norvegicus	134-143
32323742-10	2020	In addition, curculigoside significantly decreased the expression of cytochrome c, apoptotic protease activating factor-1, cleaved caspase-9 and cleaved caspase-3.	curculigoside	13-26	caspase 9	Rattus norvegicus	131-140
32422500-7	2020	We found that MAPs could attenuate alloxan-induced apoptosis by increasing the expression of Bcl-2 and decreasing the expression of Bax and the activities of caspase-3 and caspase-9.	Alloxan	35-42	caspase 9	Rattus norvegicus	172-181
31808139-8	2020	CCH decreased the levels of NeuN, Cyt-C (mitochondrial), SOD, and CAT, and increased the levels of MDA, phosphorylated ASK1 and phosphorylated p38, cleaved Caspase-9 and -3, and Cyt-C (cytoplasm), which were reversed by WIN treatment.	1-acetyl-2-(coumariniminecarboxamide-3-yl)hydrazine	0-3	caspase 9	Rattus norvegicus	156-172
32302311-6	2020	When EPO was co-administered with NMDA80, attenuated cell death occurred through the downregulation of the apoptotic indicators: mu-calpain was activated first (peak at ~18hrs), followed by Bax and caspase 9 (peak at ~40hrs).	nmda80	34-40	caspase 9	Rattus norvegicus	198-207
31620823-9	2020	Compared with the control group, the mRNA expression levels of Bax and caspase-9 genes increased in the rats" testes receiving Cd, the mRNA expression levels of mitofusin 1 (Mfn1) and mitofusin2 (Mfn2) genes decreased, and those of Bcl-2 remained unchanged.	Cadmium	127-129	caspase 9	Rattus norvegicus	71-80
31955887-10	2020	Besides, delayed administration of PEG-UK attenuated the up regulation of Caspase8 and Caspase9 and the cleavage of Caspase3 and poly (ADP-ribose) polymerase 1 (PARP1) in ischemic lesion sites.	peg-uk	35-41	caspase 9	Rattus norvegicus	87-95
32440327-7	2020	In addition, rutin decreased DNA damage and inhibited apoptotic cell death by decreasing the levels of proapoptotic proteins (Bax, caspase-3, caspase-9) and increasing the level of anti-apoptotic protein Bcl-2.	Rutin	13-18	caspase 9	Rattus norvegicus	142-151
31620823-13	2020	According to the obtained results, Cd exerts its apoptotic effects through the mitochondrial pathway by increasing the ratio of Bax/Bcl-2 and activating caspases in the rats" testes, and vitamin E plays a protective role against Cd-induced apoptosis.	Cadmium	35-37	caspase 9	Rattus norvegicus	153-161
31620823-10	2020	Vitamin E was found to significantly decrease the mRNA expression of Bax and caspase-9 genes and increase the mRNA Mfn1, Mfn2, and Bcl-2 in the rats" testes receiving Cd.	Vitamin E	0-9	caspase 9	Rattus norvegicus	77-86
32095825-11	2020	Moreover, SA pretreatment significantly inhibited apoptosis, blocked mPTP opening, suppressed the release of DeltaPsim, prevented the cytochrome c releasing from mitochondria into cytoplasm, and repressed the cleavage of caspase-9 and caspase-3.	sappanone A	10-12	caspase 9	Rattus norvegicus	221-230
32515177-11	2020	Hcy also increased oxidative stress in the PC12 cells and the proapoptotic proteins Bax, Caspase-3, and Caspase-9.	Homocysteine	0-3	caspase 9	Rattus norvegicus	104-113
32158395-10	2020	DEX decreased the levels of blood urea nitrogen (BUN) and creatinine (Cre), urine kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL), reactive oxygen species (ROS), and apoptosis proteins (such as cleaved caspase-9 and cleaved caspase-3).	Dexmedetomidine	0-3	caspase 9	Rattus norvegicus	238-247
31918279-9	2020	Activation of Wnt signaling pathway by Licl up-regulated beta-catenin, CyclinD1, Axin2, Caspase-3, Caspase-9, MMP-3, MMP-13 and IL-1beta.	Lithium Chloride	39-43	caspase 9	Rattus norvegicus	99-108
31830459-10	2020	In addition, hydralazine also increased p-PI3K, p-AKT, p-eNOS expression and decreased Cleaved Caspase-3, Cleaved Caspase-9 expression in the hearts.	Hydralazine	13-24	caspase 9	Rattus norvegicus	114-123
31704101-7	2020	Furthermore, combined administration of Can and Nan increased oxidative stress (significantly increased malondialdehyde and nitric oxide levels and reduced glutathione content), elevated brain pro-inflammatory cytokines (tumour necrosis factor alpha and interleukin 1 beta), and upregulated caspase-3, caspase-8, and caspase-9 mRNA expression and cytochrome c levels.	nan	48-51	caspase 9	Rattus norvegicus	317-326
31661991-7	2020	Additionally, MEHP induced the collapse of mitochondrial transmembrane potential and release of cytochrome c. Addition of autophagy inhibitor 3-methyladenine relieved MEHP-induced apoptosis as assessed by the expression of cleaved caspase 3, cleaved caspase 9, and terminal deoxynucleotidyl transferase dUTP nick end labeling assay, indicating that MEHP-induced apoptosis was autophagy dependent.	mono-(2-ethylhexyl)phthalate	14-18	caspase 9	Rattus norvegicus	250-259
31661991-7	2020	Additionally, MEHP induced the collapse of mitochondrial transmembrane potential and release of cytochrome c. Addition of autophagy inhibitor 3-methyladenine relieved MEHP-induced apoptosis as assessed by the expression of cleaved caspase 3, cleaved caspase 9, and terminal deoxynucleotidyl transferase dUTP nick end labeling assay, indicating that MEHP-induced apoptosis was autophagy dependent.	3-methyladenine	142-157	caspase 9	Rattus norvegicus	250-259
31661991-7	2020	Additionally, MEHP induced the collapse of mitochondrial transmembrane potential and release of cytochrome c. Addition of autophagy inhibitor 3-methyladenine relieved MEHP-induced apoptosis as assessed by the expression of cleaved caspase 3, cleaved caspase 9, and terminal deoxynucleotidyl transferase dUTP nick end labeling assay, indicating that MEHP-induced apoptosis was autophagy dependent.	mono-(2-ethylhexyl)phthalate	167-171	caspase 9	Rattus norvegicus	250-259
31661991-7	2020	Additionally, MEHP induced the collapse of mitochondrial transmembrane potential and release of cytochrome c. Addition of autophagy inhibitor 3-methyladenine relieved MEHP-induced apoptosis as assessed by the expression of cleaved caspase 3, cleaved caspase 9, and terminal deoxynucleotidyl transferase dUTP nick end labeling assay, indicating that MEHP-induced apoptosis was autophagy dependent.	mono-(2-ethylhexyl)phthalate	167-171	caspase 9	Rattus norvegicus	250-259
31727597-10	2020	Furthermore, gastrodin significantly increased Bcl-2 expression, while reduced level of Bax, active caspase-3 and active caspase-9, also reduced the number of active caspase-3 or TUNEL positive neurons at 72 hours post-ICH.	gastrodin	13-22	caspase 9	Rattus norvegicus	121-130
31885809-12	2019	Moreover, PCr increased Bcl-2, caspase 3, and caspase 9 protein expressions and decreased Bax, cleaved caspase 3, and cleaved caspase 9 expressions as well as the JAK2/STAT3 signaling pathway.	4-cresol	10-13	caspase 9	Rattus norvegicus	46-55
32784309-8	2020	Compared with the sham group, the ratio of eNOS, Bcl-2/Bax was significantly decreased, and p-eNOS, iNOS, caspase-3, caspase-9, and Cyt-c were significantly elevated in the ISO group (p < 0.05).	Isoproterenol	173-176	caspase 9	Rattus norvegicus	117-126
31589841-10	2019	Treatment with 17-AAG inhibited the viability of capsular residual epithelial cells and induced the cells apoptosis, characterized by increases in ROS levels, apoptotic DNA injury, and the activation of caspases 9 and 3.	tanespimycin	15-21	caspase 9	Rattus norvegicus	203-219
30734599-9	2019	SS-31 prevented oxidative stress and mitochondria-dependent apoptosis signalling by HOCl-alb in vivo and in vitro, as evidenced by the release of cytochrome c (cyt c), binding of apoptosis activated factor-1 (Apaf-1) and caspase-9, and activation of caspases.	arginyl-2,'6'-dimethyltyrosyl-lysyl-phenylalaninamide	0-5	caspase 9	Rattus norvegicus	221-230
30734599-9	2019	SS-31 prevented oxidative stress and mitochondria-dependent apoptosis signalling by HOCl-alb in vivo and in vitro, as evidenced by the release of cytochrome c (cyt c), binding of apoptosis activated factor-1 (Apaf-1) and caspase-9, and activation of caspases.	arginyl-2,'6'-dimethyltyrosyl-lysyl-phenylalaninamide	0-5	caspase 9	Rattus norvegicus	250-258
31829167-8	2019	RESULTS: ED alleviated intestinal mucosal damage caused by burn injury, down-regulated the levels of MDA, cytochrome C, cleaved caspase-9 and cleaved caspase-3, but up-regulated the levels of TSH, SOD, CAT and Bcl-2.	edaravone	9-11	caspase 9	Rattus norvegicus	128-137
31885809-12	2019	Moreover, PCr increased Bcl-2, caspase 3, and caspase 9 protein expressions and decreased Bax, cleaved caspase 3, and cleaved caspase 9 expressions as well as the JAK2/STAT3 signaling pathway.	4-cresol	10-13	caspase 9	Rattus norvegicus	126-135
31773713-10	2019	Also, ranolazine downregulated caspase-9 expression and upregulated pAKT and Bcl-2 expression in rat cardiomyocytes.	Ranolazine	6-16	caspase 9	Rattus norvegicus	31-40
31773713-11	2019	Moreover, ranolazine significantly inhibited myocardial apoptosis and caspase-9 expression, promoted AKT phosphorylation, and upregulated pAKT and Bcl-2 expression in vitro, compared to those in the control group (p<0.001).	Ranolazine	10-20	caspase 9	Rattus norvegicus	70-79
31632569-11	2019	Moreover, MR inhibited apoptosis of gastric mucosal cell as presented by TUNEL, coupled with an upregulation in Bcl-2 expression and a downregulation in Bax, cleaved caspase-3 and cleaved caspase-9 expression.	morroniside	10-12	caspase 9	Rattus norvegicus	188-197
31464433-6	2019	In addition, the qRT-PCR and western blotting results indicated that NaF exposure upregulated the mRNA and protein expression of Bax, Calpain, Caspase 12, Caspase 9, Caspase 7, Caspase 3, CAD, PARP, and AIF while downregulated Bcl-2 (P &lt; 0.01) and decreased the bone ultimate load by 27.1%, the ultimate stress by 10.1%, and the ultimate deformity by 23.3% at 120 days.	Sodium Fluoride	69-72	caspase 9	Rattus norvegicus	155-164
31561418-7	2019	In addition, MTX upregulated renal iNOS, COX-2, TNF-alpha, IL-1beta, Bax, caspase-9, and caspase-3, and decreased Bcl-2, Nrf2, and HO-1.	Methotrexate	13-16	caspase 9	Rattus norvegicus	74-83
30981808-5	2019	The results showed that CBL treatment not only normalized the increased MDA levels in the alcoholic rats and enhanced antioxidant defense, but also reduced the Bax/Bcl-2 ratio and cleaved caspase-9 and -3 in the hippocampus.	cerebrolysin	24-27	caspase 9	Rattus norvegicus	188-204
31511220-8	2019	CONCLUSIONS: Dexmedetomidine can effectively alleviate lung injury in rats during CPB possibly by targeting caspase-3 and caspase-9 proteins that are related to PI3K/Akt signaling pathway.	Dexmedetomidine	13-28	caspase 9	Rattus norvegicus	122-131
31212066-8	2019	CARD9 suppressed the activation of caspase-9 by interacting with Apaf-1 via its CARD domain in H9c2 cells exposed to H2O2.	Hydrogen Peroxide	117-121	caspase 9	Rattus norvegicus	35-44
31212066-9	2019	Ablation of caspase-9 activity by z-lehd-fmk effectively prevented the detrimental effect of CARD9 deficiency on cardiomyocytes.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	34-44	caspase 9	Rattus norvegicus	12-21
30990955-12	2019	In chlorpyrifos-treated animals, we have observed a significant decrease in the protein expression level of Bcl-2, but a remarkable increase in the expression levels of Bax, cytochrome c, caspase-8, and caspase-9 in both cerebrum and cerebellum.	Chlorpyrifos	3-15	caspase 9	Rattus norvegicus	203-212
31412679-10	2019	Vindoline restored the structure of the renal parenchyma and was accompanied by significant decrease in the expression of caspase 9 in diabetic rats when compared to the diabetic controls.	vindoline	0-9	caspase 9	Rattus norvegicus	122-131
31173166-7	2019	In conclusion, the present findings indicated that anti-miR-128 may exert neuroprotective effects in epilepsy, through the SIRT1/p53/Bax/Cytochrome c/caspase signaling pathway.	mir-128	56-63	caspase 9	Rattus norvegicus	150-157
30990955-13	2019	Interestingly, when chlorpyrifos-treated animals were supplemented with quercetin, a significant increase in the expression of Bcl-2 and an appreciable decline in the expression levels of Bax, cytochrome c, caspase-8, and caspase-9 was observed.	Chlorpyrifos	20-32	caspase 9	Rattus norvegicus	222-231
30990955-13	2019	Interestingly, when chlorpyrifos-treated animals were supplemented with quercetin, a significant increase in the expression of Bcl-2 and an appreciable decline in the expression levels of Bax, cytochrome c, caspase-8, and caspase-9 was observed.	Quercetin	72-81	caspase 9	Rattus norvegicus	222-231
31308624-10	2019	In addition, DEX dose-dependently reduced apoptotic PC12 cells induced by lidocaine,as reflected by the decreased expression of apoptosis-related Bax, caspase-3 and caspase-9 and increased expression of anti-apoptotic Bcl-2 compared to the cells only treated with lidocaine.	Dexmedetomidine	13-16	caspase 9	Rattus norvegicus	165-174
31371925-12	2019	In addition, opening and the decrease of DeltaPsim were attenuated by LP and the expressions of cytochrome c, APAF-1, cleaved caspase-9 and cleaved caspase-3 were also decreased by LP.	Lycopene	181-183	caspase 9	Rattus norvegicus	126-135
31308624-10	2019	In addition, DEX dose-dependently reduced apoptotic PC12 cells induced by lidocaine,as reflected by the decreased expression of apoptosis-related Bax, caspase-3 and caspase-9 and increased expression of anti-apoptotic Bcl-2 compared to the cells only treated with lidocaine.	Lidocaine	74-83	caspase 9	Rattus norvegicus	165-174
31402807-7	2019	Gene expression analysis revealed that the DEN+PBO+AI-LPI group showed increased transcript levels of Ccne1, Cdkn1b, Rb1, Bax, Bcl2, Casp3, and Casp9 compared with the DEN+PBO group; however, the DEN+PBO+AI-EPI group did not show changes in the transcript levels of any genes examined compared with the DEN+PBO.	Diethylnitrosamine	43-46	caspase 9	Rattus norvegicus	144-149
30684233-8	2019	on DMBA-induced tumor-bearing rats was down-regulated Cyclin D1, Bcl-2 expression, and up-regulated proapoptotic proteins such as Bax, p53, Cytochrome-C, Caspase-9, and Caspase-3 as compared to DIM 10 mg/kg b.wt.	9,10-Dimethyl-1,2-benzanthracene	3-7	caspase 9	Rattus norvegicus	154-163
31143910-6	2019	Moreover, EVSGPGLSPN inhibited apoptosis by suppressing the expression of cytochrome C, caspase-9, caspase-3, and PARP.	evsgpglspn	10-20	caspase 9	Rattus norvegicus	88-97
31143910-8	2019	Thus, EVSGPGLSPN may protect against hydrogen peroxide induced neurotoxicity by enhancing the activity of antioxidant enzymes and blocking the NF-kappaB/caspase pathways.	evsgpglspn	6-16	caspase 9	Rattus norvegicus	153-160
31017253-9	2019	Furthermore, the combination of LP and IPoC inhibited the expression of glucose-regulated protein 78 and C/EBP homologous protein, increased the phosphorylation levels of AKT, ERK1/2 and glycogen synthase kinase-3beta, repressed mitochondrial permeability transition pore opening, and reduced the expression of cytochrome c, cleaved caspase-9 and cleaved caspase-3.	Lycopene	32-34	caspase 9	Rattus norvegicus	333-342
30725434-7	2019	CsA significantly decreased the Bax/Bcl-2 ratio, cl-casp-9/casp-9, and cl-casp-3/casp-3 in a concentration-dependent manner.	Cyclosporine	0-3	caspase 9	Rattus norvegicus	52-58
30725434-7	2019	CsA significantly decreased the Bax/Bcl-2 ratio, cl-casp-9/casp-9, and cl-casp-3/casp-3 in a concentration-dependent manner.	Cyclosporine	0-3	caspase 9	Rattus norvegicus	59-65
30928397-8	2019	COS treatment also results in reduced caspase-3 and caspase-9 expressions, and an increase in the phosphorylation of MAPKs (mitogen-activated protein kinases) in DOX-exposed H9C2 cells.	carbonyl sulfide	0-3	caspase 9	Rattus norvegicus	52-61
31205460-6	2019	Both boiled and roasted curcuminoids could significantly improve cell viability, mitigate intracellular accumulation of reactive oxygen species and reduce malondialdehyde activity, reduce caspase-3 and caspase-9 protein expression, and increase superoxide dismutase activity of PC12 cells compared with the control group.	curcuminoids	24-36	caspase 9	Rattus norvegicus	202-211
31007732-11	2019	The data suggested that PG downregulated the activated caspase-3, caspase-9 and poly-ADP-ribose polymerase expression and reduced the Bax: Bcl2 ratio.	pectolinarigenin	24-26	caspase 9	Rattus norvegicus	66-75
31198493-10	2019	Moreover, BBPs upregulated the expressions of PI3K, Akt, p-Akt, and Bcl-2, whereas they downregulated the expressions of caspase-9, caspase-3, and Bax in H2O2-stimulated PC12 cells.	Hydrogen Peroxide	154-158	caspase 9	Rattus norvegicus	121-130
30874465-5	2019	The mRNA and protein expression of LAMA4, JNK, p38 MAPK, ERK, Bcl-2, Bax, Caspase-9, and p53 was determined in concert with the treatment of H2O2, si-NC, or si-LAMA4 in cultured RGCs.	Silicon	27-29	caspase 9	Rattus norvegicus	74-83
31057171-7	2019	Furthermore, the cytochrome C, Caspase-3, and Caspase-9 levels were restored after GSK-3ss inhibitors Licl treatment.	Lithium Chloride	102-106	caspase 9	Rattus norvegicus	46-55
31057171-8	2019	CONCLUSIONS Our results show that GSK-3ss regulates the production of cytochrome C, Caspase-3, and Caspase-9 in STZ-induced rat brain and may therefore contribute to DM-caused cognitive dysfunction via inhibition of neural cell apoptosis.	Streptozocin	112-115	caspase 9	Rattus norvegicus	99-108
31114478-6	2019	The results showed that levels of DJ-1, p-Akt and p-IkappaB kinase (IKK) increased after ICH and peaked at 24 h. Besides, NaB significantly upregulated DJ-1 in both cytoplasm and mitochondria, and also increased the levels of p-Akt, p-IKK and Bcl-2/Bax ratio, but decreased the levels of caspase-3 and caspase-9.	nab	122-125	caspase 9	Rattus norvegicus	302-311
30849457-5	2019	Increase malondialdehyde (MDA) content and CASPASE 9 protein level were associated both with CoCl2 and CoNPs treatments, consistent with lipid perioxidation and apoptosis.	cobaltous chloride	93-98	caspase 9	Rattus norvegicus	43-52
31178973-7	2019	Moreover, we observed that ICA could significantly protect against mitochondrial depolarization following AGE stimulation and inactivate the mitochondria-dependent caspase-9/3 apoptosis pathway.	icariin	27-30	caspase 9	Rattus norvegicus	164-173
31060191-20	2019	The myocardial expressions of Caspase-3, Caspase-9 and Cyt-C at 4 hours after resuscitation were significantly higher in the CPR group, DMSO group and iCORM-2 group than those in sham group; the myocardial expressions of Caspase-3 and Caspase-9 were significantly higher in CORM-2 group than those in sham group (both P&lt;0.05), while Cyt-C expression was similar between CORM-2 group and sham group.	Dimethyl Sulfoxide	136-140	caspase 9	Rattus norvegicus	41-50
30957795-6	2019	By IHC, the TLR4, MyD88, NF-kappaB, caspase-3 and caspase-9 protein activities of allicin treated groups were significantly suppressed compared with those of LPS group (P&lt;0.05, respectively) in lung tissues.	allicin	82-89	caspase 9	Rattus norvegicus	50-59
30659940-9	2019	Baicalein treatment significantly protected diabetes rats from neuron death; significantly attenuated the overexpression of cPLA2, 12/15-LOX, p38MAPK, phospho-p38MAPK, caspase-3, caspase-9 and Abeta1-42; and upregulated the expression of Bcl-2.	baicalein	0-9	caspase 9	Rattus norvegicus	179-188
30600648-10	2019	The release of cytochrome C from mitochondria to cytoplasm and the activation of caspase-9 and caspase-3 were significantly decreased in the ZEA + Z-IETD-FMK group.	Zearalenone	141-144	caspase 9	Rattus norvegicus	81-90
30600648-10	2019	The release of cytochrome C from mitochondria to cytoplasm and the activation of caspase-9 and caspase-3 were significantly decreased in the ZEA + Z-IETD-FMK group.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	147-157	caspase 9	Rattus norvegicus	81-90
30746596-5	2019	EG pretreatment attenuated H2O2-induced mitochondrial dysfunction as indicated by the decreased caspase-9/-3 activation, PARP cleavage, mitochondrial membrane potential (MMP) depletion, Bax/Bcl-2 ratio, cytochrome c release and ROS overproduction.	Hydrogen Peroxide	27-31	caspase 9	Rattus norvegicus	96-105
30712210-8	2019	SO2 and NaHSO3 decreased the expression of Bcl-2 and the ratio of Bcl-2/Bax, increased the expression of Bax and P53 accumulation and phosphorylation, and activated caspase-9 and caspase-3.	Sulfur Dioxide	0-3	caspase 9	Rattus norvegicus	165-174
30942158-10	2019	Stomach caspase-8 immun+ cell numbers showed a slight increase while caspase-9 immun+ cell numbers reduced in indomethacin given group compared to control animals.	Indomethacin	110-122	caspase 9	Rattus norvegicus	69-78
30676544-6	2019	Our results showed that DHG treatment significantly increased cell viability and decreased PC12 cell apoptosis induced by hydrogen peroxide by increasing the mitochondrial membrane potential, decreasing the cytochrome c release, inhibiting the activities of caspase-3 and caspase-9, and regulating the expression of apoptosis-related proteins.	7,4'-dimethoxy-6-hydroxyaurone-4-O-beta-glucopyranoside	24-27	caspase 9	Rattus norvegicus	272-281
30676544-6	2019	Our results showed that DHG treatment significantly increased cell viability and decreased PC12 cell apoptosis induced by hydrogen peroxide by increasing the mitochondrial membrane potential, decreasing the cytochrome c release, inhibiting the activities of caspase-3 and caspase-9, and regulating the expression of apoptosis-related proteins.	Hydrogen Peroxide	122-139	caspase 9	Rattus norvegicus	272-281
30712210-8	2019	SO2 and NaHSO3 decreased the expression of Bcl-2 and the ratio of Bcl-2/Bax, increased the expression of Bax and P53 accumulation and phosphorylation, and activated caspase-9 and caspase-3.	sodium hydrogen sulfite	8-14	caspase 9	Rattus norvegicus	165-174
30273099-7	2019	Similarly, CIP(100 mg/kgbw) and AC (30 mg/kgbw), significantly enhanced RLM ATPase activity, induced cytochrome C release and increased levels of RLM malondialdehyde generation and triggered the activation of caspases-9 and 3 in liver post-mitochondrial fraction.	Amoxicillin-Potassium Clavulanate Combination	32-34	caspase 9	Rattus norvegicus	209-225
30961682-4	2019	This activation promoted myocardial apoptosis, which was accompanied by modulation of Bax/Bcl-2, caspase-3 and caspase-9 expression following deferoxamine administration.	Deferoxamine	142-154	caspase 9	Rattus norvegicus	111-120
30827825-9	2019	Apoptosis become found through DNA fragmentation assay and quantification of Caspase 3, Caspase 9, Bcl2 and Cytochrome C. Doxorubicin mediated oxidative stress and apoptosis in testicular milieu is through deregulation of Nrf2, PGC-1alpha, AHR, ARNT, PXR, SUMO-1, UCP2, UCP3, ANX A5, Caspase 3, Caspase 9, Bcl2, Cytochrome C, GR, and GPX.	Doxorubicin	122-133	caspase 9	Rattus norvegicus	88-97
30827825-9	2019	Apoptosis become found through DNA fragmentation assay and quantification of Caspase 3, Caspase 9, Bcl2 and Cytochrome C. Doxorubicin mediated oxidative stress and apoptosis in testicular milieu is through deregulation of Nrf2, PGC-1alpha, AHR, ARNT, PXR, SUMO-1, UCP2, UCP3, ANX A5, Caspase 3, Caspase 9, Bcl2, Cytochrome C, GR, and GPX.	Doxorubicin	122-133	caspase 9	Rattus norvegicus	295-304
30809145-14	2019	We found that propofol ameliorated H9c2 cells apoptosis during OGD/R via inhibiting mitochondrial cytochrome c release and caspase-9, caspase-6, caspase-7 and caspase-3 activation.	Propofol	14-22	caspase 9	Rattus norvegicus	123-132
30485494-6	2019	Furthermore, pretreatment with BBM protected the heart tissue from ISO-induced apoptosis as evident from decreased terminal dUTP nickend-labeling positive cells and decreased expression of Bax, cytochrome c, cleaved caspase-9, and caspase-3, and poly (ADP-ribose) polymerase and increased expression of Bcl-2 in ISO-induced rats.	berbamine	31-34	caspase 9	Rattus norvegicus	216-225
30159796-7	2019	Furthermore, ISO triggers calcium overload and ATP depletion in the rat"s heart mitochondria followed by the mitochondrial cytochrome-C release and the activation of intrinsic pathway of apoptosis by upregulating the myocardial pro-apoptotic Bax, P53, APAF-1, active caspase-3, active caspase-9 and down regulating the expressions of anti-apoptotic Bcl-2.	Isoproterenol	13-16	caspase 9	Rattus norvegicus	285-294
29904091-9	2019	In addition, naloxone administration dose-dependently increased Bcl-2 levels, decreased Bax levels, stabilized the mitochondrial transmembrane potential, and inhibited cytochrome c release and caspase 3 and caspase 9 activation.	Naloxone	13-21	caspase 9	Rattus norvegicus	207-216
30535448-6	2019	An increase in cleaved caspase-3, cleaved caspase-8 and cleaved caspase-9 occurred in GdCl3-treated C6 cells as detected by immunoblotting analysis.	gadolinium chloride	86-91	caspase 9	Rattus norvegicus	64-73
30372856-6	2018	The intervention of Baicalin increased the expression of anti-apoptotic protein XIAP and Bcl-2, reduced the expression of apoptotic protein Caspase-9 in rat liver; and similarly, Baicalin increased the expression of Bcl-2, while inhibited Caspase-9 and AT1 in rat kidney.	baicalin	20-28	caspase 9	Rattus norvegicus	140-149
31272354-7	2019	Infusion of amiloride into the lateral ventricle attenuated upregulation of Caspase-3/Caspase-9 and this further improved neurological severity score and brain edema.	Amiloride	12-21	caspase 9	Rattus norvegicus	86-95
30423403-6	2019	DEN-induced rats exhibited increased gene expression of NF-kappaB, COX-2, CYP2E1, VEGF, Bcl-2, PI3K/AKT/mTOR and significantly decreased the gene expression of p53, Bax, caspase-9 and caspase-3.	Diethylnitrosamine	0-3	caspase 9	Rattus norvegicus	170-179
30423403-8	2019	Further, blotting analysis also revealed increased expression of NF-kappaB, COX-2, Bcl-2 and decreased expression of Bax, caspase-9 and caspase-3 proteins in DEN-induced rats.	Diethylnitrosamine	158-161	caspase 9	Rattus norvegicus	122-131
30662323-11	2019	The suppression of apoptosis by baicalein in H2O2-stimulated cells was associated with reduction of increased Bax/Bcl-2 ratio, activation of caspase-9 and -3, and degradation of poly (ADP-ribose) polymerase.	baicalein	32-41	caspase 9	Rattus norvegicus	141-157
30662323-11	2019	The suppression of apoptosis by baicalein in H2O2-stimulated cells was associated with reduction of increased Bax/Bcl-2 ratio, activation of caspase-9 and -3, and degradation of poly (ADP-ribose) polymerase.	Hydrogen Peroxide	45-49	caspase 9	Rattus norvegicus	141-157
30657579-17	2019	The mRNA expressions of HIF-1a, p-Akt, Caspase-3, and Caspase-9 in lung tissue of rats was significantly reduced after dexmedetomidine pretreatment.	Dexmedetomidine	119-134	caspase 9	Rattus norvegicus	54-63
30503840-4	2019	Mechanistic studies indicated that dioscin notably up-regulated the expression level of MAPK13 through decreasing miR-351-5p level, and thereby decreased the expression levels of p-PKD1, NF-kappaB, Apaf-1, cleaved Caspase-3 and cleaved Caspase-9.	dioscin	35-42	caspase 9	Rattus norvegicus	236-245
30372856-6	2018	The intervention of Baicalin increased the expression of anti-apoptotic protein XIAP and Bcl-2, reduced the expression of apoptotic protein Caspase-9 in rat liver; and similarly, Baicalin increased the expression of Bcl-2, while inhibited Caspase-9 and AT1 in rat kidney.	baicalin	20-28	caspase 9	Rattus norvegicus	239-248
29579407-12	2018	Application of Z-VAD-FMK (a pan caspase inhibitor) or Z-LEHD-FMK (caspase-9 inhibitor) with ketamine effectively attenuated the ketamine-induced apoptosis in rat thymocytes.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	54-64	caspase 9	Rattus norvegicus	66-75
30255981-10	2018	Glycyrrhizic acid also significantly ameliorated DMH-induced decreased activities of caspase-9 and caspase-3.	Glycyrrhizic Acid	0-17	caspase 9	Rattus norvegicus	85-94
30255981-10	2018	Glycyrrhizic acid also significantly ameliorated DMH-induced decreased activities of caspase-9 and caspase-3.	1,2-Dimethylhydrazine	49-52	caspase 9	Rattus norvegicus	85-94
30538798-8	2018	Further studies have shown that HCEA inhibits t-BHP-induced apoptosis by increasing B-cell lymphoma-2 (BCL-2) activity and decreasing caspase-3 and caspase-9 activity.	hcea	32-36	caspase 9	Rattus norvegicus	148-157
30538798-8	2018	Further studies have shown that HCEA inhibits t-BHP-induced apoptosis by increasing B-cell lymphoma-2 (BCL-2) activity and decreasing caspase-3 and caspase-9 activity.	tert-Butylhydroperoxide	46-51	caspase 9	Rattus norvegicus	148-157
29579407-12	2018	Application of Z-VAD-FMK (a pan caspase inhibitor) or Z-LEHD-FMK (caspase-9 inhibitor) with ketamine effectively attenuated the ketamine-induced apoptosis in rat thymocytes.	Ketamine	92-100	caspase 9	Rattus norvegicus	66-75
29579407-12	2018	Application of Z-VAD-FMK (a pan caspase inhibitor) or Z-LEHD-FMK (caspase-9 inhibitor) with ketamine effectively attenuated the ketamine-induced apoptosis in rat thymocytes.	Ketamine	128-136	caspase 9	Rattus norvegicus	66-75
29748834-11	2018	f-Dox-NE displayed downregulation of anti-apoptotic (Bcl-2 and MMP-9) proteins and upregulation of pro-apoptotic proteins (caspase-9 and BAX).	f-dox	0-5	caspase 9	Rattus norvegicus	123-132
29761825-9	2018	Rats undergoing ZnCl2 treatment demonstrated a low expression of autophagy parameters (Beclin-1 and LAMP-2), which was correlated with low induction of apoptosis (caspase-9, caspase-3, and p-JNK), and reduction of inflammation (IL-1ss, IL-6, and MCP-1) (p &lt; 0,05).	zinc chloride	16-21	caspase 9	Rattus norvegicus	163-172
30177808-7	2018	Iron increased Caspase 9, Cytochrome c, APAF1, Caspase 3 and cleaved PARP, without affecting cleaved Caspase 8 levels.	Iron	0-4	caspase 9	Rattus norvegicus	15-24
30250633-11	2018	Additionally, DEX downregulated the expression of Bax, cytochrome C, cleaved caspase 9, and cleaved caspase 3 proteins in mitochondria-dependent pathways.	Dexmedetomidine	14-17	caspase 9	Rattus norvegicus	77-86
30040928-9	2018	AMB and SEL also ameliorated 6-OHDA-induced mitochondrial dysfunction in terms of MTT reduction, alpha-synuclein pathology, loss of nigral cells, and intrinsic pathway of apoptosis by modulating cytochrome-C, caspase-9, and caspase-3 expressions.	Oxidopamine	29-35	caspase 9	Rattus norvegicus	209-218
30213108-4	2018	Specifically, stilbenoids significantly promoted Akt phosphorylation; suppressed Bcl-2/Bax expression; and inhibited caspase-9, caspase-3, and PARP cleavage.	stilbenoids	14-25	caspase 9	Rattus norvegicus	117-126
30177808-8	2018	CBD reversed iron-induced effects, recovering apoptotic proteins Caspase 9, APAF1, Caspase 3 and cleaved PARP to the levels found in controls.	Iron	13-17	caspase 9	Rattus norvegicus	65-74
29687464-9	2018	MTX up-regulated BAX expression and caspase 9 immunoreactivity that were ameliorated in HA + MTX group.	Methotrexate	0-3	caspase 9	Rattus norvegicus	36-45
29663489-12	2018	Incubating in high glucose enhanced the expression levels of cleaved caspase-3, cleaved caspase-9, Bax, and cytochrome c but decreased the level of the anti-apoptotic protein Bcl-2.	Glucose	19-26	caspase 9	Rattus norvegicus	88-97
29663489-13	2018	ALA inhibited the expression of cleaved caspase-3, cleaved caspase-9, Bax, and cytochrome c but enhanced the expression of Bcl-2.	Thioctic Acid	0-3	caspase 9	Rattus norvegicus	59-68
29687464-9	2018	MTX up-regulated BAX expression and caspase 9 immunoreactivity that were ameliorated in HA + MTX group.	Methotrexate	93-96	caspase 9	Rattus norvegicus	36-45
29189995-5	2018	Our results point out that arsenic exposure caused oxidative stress in rats" hippocampus, which led to the reactive oxygen species (ROS) generation, mitochondrial swelling, the collapse of the mitochondrial membrane potential, and release of cytochrome c. It also altered Bcl-2/Bax expression ratio and increased caspase-3 and caspase-9 activities.	Arsenic	27-34	caspase 9	Rattus norvegicus	327-336
29521449-5	2018	The mRNA levels of Bax, Caspase-9, and Caspase-3 were decreased, while the Bcl-2 mRNA level was increased in H2 O2 -induced BRL-3A cells treated with DHEA.	Hydrogen Peroxide	109-114	caspase 9	Rattus norvegicus	24-33
29521449-5	2018	The mRNA levels of Bax, Caspase-9, and Caspase-3 were decreased, while the Bcl-2 mRNA level was increased in H2 O2 -induced BRL-3A cells treated with DHEA.	Dehydroepiandrosterone	150-154	caspase 9	Rattus norvegicus	24-33
30072873-4	2018	Furthermore, adapentpronitrile significantly attenuated oxidative stress, downregulated expression of the pro-apoptotic proteins BAX, cytochrome c, caspase-9, and caspase-3, and upregulated expression of the anti-apoptotic protein Bcl-2, although there was no effect on GLP-1R expression.	adapentpronitrile	13-30	caspase 9	Rattus norvegicus	148-157
29864932-7	2018	Furthermore, 2,7""-phloroglucinol-6,6"-bieckol significantly reduced the levels of pro-apoptotic Bax, caspase 9, and caspase 3 proteins, and increased the levels of the anti-apoptotic Bcl-2 protein and poly ADP-ribose polymerase.	2,7''-phloroglucinol-6,6'-bieckol	13-46	caspase 9	Rattus norvegicus	102-111
29626300-11	2018	RT-PCR and western-blot results revealed that taurine down-regulated expression of Bax, Fas, Fas ligand (FasL), caspase 3 and caspase 9 while up-regulating the expression of Bcl-2 in ethanol-cultured hepatocytes.	Taurine	46-53	caspase 9	Rattus norvegicus	126-135
29027106-5	2018	Additionally, AlCl3 treatment activated mitochondrial-mediated signaling pathway, accompanied by mitochondrial membrane potential (DeltaPsim) depolarization, release of cytochrome c from the mitochondria to the cytoplasm, as well as survival signal-related factor caspase-9 and caspase-3 activation.	Aluminum Chloride	14-19	caspase 9	Rattus norvegicus	264-273
29654931-4	2018	Treatment with 50 mg/L Cd also damaged renal cell mitochondria and nuclei, and activated the mitochondrial apoptosis pathway, indicated by increased gene and protein expression/activation of caspase-9, caspase-3, poly ADP-ribose polymerase (PARP) and Bcl-2 adenovirus E1a nineteen kilodalton interacting protein 3 (BNIP3), and translocation of cytochrome c (cyt c), apoptosis-inducing factor (AIF), and endonuclease G (Endo G).	Cadmium	23-25	caspase 9	Rattus norvegicus	191-200
29708300-9	2018	Furthermore, GABA tea, GT, and pure GABA also decreased activated-caspase 9 and activated-caspase 3.	gamma-Aminobutyric Acid	13-17	caspase 9	Rattus norvegicus	66-75
29708300-9	2018	Furthermore, GABA tea, GT, and pure GABA also decreased activated-caspase 9 and activated-caspase 3.	gamma-Aminobutyric Acid	36-40	caspase 9	Rattus norvegicus	66-75
29942246-6	2018	Results: Results showed that in spite of high degradation rates, boiled curcumin mixture still possessed similar protective activities like parent curcumin, and could effectively rescue PC12 cells against H2O2-induced damage, via decreasing production of reactive oxygen species and malondialdehyde, reducing caspase-3 and caspase-9 activities.	Curcumin	72-80	caspase 9	Rattus norvegicus	323-332
29204817-10	2018	MTX (0.5 and 1.0 micromol/L) in combination with OPB (5.0 or 7.5 micromol/L) inhibited the cell proliferation as BrdU incorporation was quite low in DNA synthesis analysis, as well as caspase-9/-3 cascade was activated which led to apoptosis of cancer cells.	Methotrexate	0-3	caspase 9	Rattus norvegicus	184-193
29204817-10	2018	MTX (0.5 and 1.0 micromol/L) in combination with OPB (5.0 or 7.5 micromol/L) inhibited the cell proliferation as BrdU incorporation was quite low in DNA synthesis analysis, as well as caspase-9/-3 cascade was activated which led to apoptosis of cancer cells.	Oxyphenbutazone	49-52	caspase 9	Rattus norvegicus	184-193
29388711-8	2018	Mechanistically, Western blot results revealed that paeoniflorin enhanced protein expression of cleave caspase-9 and -3, and Bax, whereas it suppressed Bcl-2 protein expression in MMQ cells.	peoniflorin	52-64	caspase 9	Rattus norvegicus	103-119
29904397-7	2018	Treatment with thymoquinone decreased inflammatory response [measured by levels of tumor necrosis factor alpha, interleukin (IL)-1beta, IL-6 and IL-18], oxidative stress (measured by levels of superoxide dismutase, catalase, glutathione and malondialdehyde) and cell apoptosis (measured by levels of caspase-3 and caspase-9) in SCI rats.	thymoquinone	15-27	caspase 9	Rattus norvegicus	314-323
29376419-2	2018	Pretreatment with RA significantly suppressed the generation of ROS, protected the morphological changes of cells, decrease the ratio of cell apoptosis, down-regulated the level of caspase-3, caspase-9, Bax/Bcl-2, and up-regulated the level of p-PI3K.	rosmarinic acid	18-20	caspase 9	Rattus norvegicus	192-201
29649568-4	2018	In the current study, we demonstrated that honokiol inhibits the H2O2-induced apoptosis (caspase-9, caspase-3, and bax), levels of oxidative stress mediators (ROS, MDA), expression of inflammatory mediators (Interleukin-6, COX-2, and iNOS), major matrix degrading proteases (MMP-3, MMP-13, ADAMTS5, and ADAMTS4) associated with nucleus pulposus degradation.	honokiol	43-51	caspase 9	Rattus norvegicus	89-98
29331314-7	2018	The hypoxia-induced cytochrome c release, cleaved caspase 3 and cleaved caspase 9 were aggravated by CQ.	Chloroquine	101-103	caspase 9	Rattus norvegicus	72-81
29863267-11	2018	Western blotting showed that the protein expressions of Caspase 3 and Caspase 9 were remarkably elevated in cells after the use of CsA, but were significantly reduced after administration of CST (p < 0.01).	Cyclosporine	131-134	caspase 9	Rattus norvegicus	70-79
29774334-7	2018	Moreover, EPA-PE was more effective than EPA-pPE at inhibiting the protein expressions of Bax and caspase 9.	pe	14-16	caspase 9	Rattus norvegicus	98-107
29774334-7	2018	Moreover, EPA-PE was more effective than EPA-pPE at inhibiting the protein expressions of Bax and caspase 9.	epa-ppe	41-48	caspase 9	Rattus norvegicus	98-107
30310665-9	2018	The WB results showed that the inhibition of FADH/NADPH transport induced a high activity of caspase-9 and caspase-3, and the expressions of cytochrome c (Cyt C), caspase-9 and caspase-3 were high in HG1, which might lead to mitochondrial apoptosis pathway activation.	NADP	50-55	caspase 9	Rattus norvegicus	93-102
30310665-9	2018	The WB results showed that the inhibition of FADH/NADPH transport induced a high activity of caspase-9 and caspase-3, and the expressions of cytochrome c (Cyt C), caspase-9 and caspase-3 were high in HG1, which might lead to mitochondrial apoptosis pathway activation.	NADP	50-55	caspase 9	Rattus norvegicus	163-172
29724983-10	2018	In addition, catalpol pretreatment inhibited cardiomyocyte apoptosis as indicated by a decrease in the TUNEL-positive cell percentage, alterations in the Bax and Bcl-2 expression levels, and a decline in caspase-3 and caspase-9 activities.	catalpol	13-21	caspase 9	Rattus norvegicus	218-227
29577900-6	2018	Moreover, kenpaullone pretreatment significantly reduced ROS fluorescence intensity and significantly down-regulated the level of apoptosis-activating genes (cleaved caspase-3, cleaved caspase-9 and cytochrome C), autophagy markers (LC3A/B), and the Cx43-interacting partner SGSM3.	kenpaullone	10-21	caspase 9	Rattus norvegicus	185-194
28689275-11	2018	EPA/DHA-PS could downregulate the messenger RNA level of Caspase-3, Caspase-9, and Bax, upregulate Bcl-2, inhibit Bax, and increase Bcl-2 at protein level.	Eicosapentaenoic Acid	0-3	caspase 9	Rattus norvegicus	68-77
29512772-5	2018	Furthermore, treatment with CoCl2 increased the cleavage of caspase-9, caspase-3 and apoptosis regulator BAX, and reduced apoptosis regulator Bcl-2 in H9C2 cells, as measured by reverse transcription-quantitative polymerase chain reaction and western blotting, which were significantly reversed by co-treatment with alpha-MG (0.06 and 0.3 mM).	cobaltous chloride	28-33	caspase 9	Rattus norvegicus	60-69
29179590-8	2018	The data indicate that metformin reduces estrogen-induced EH in rats, via activation of the caspase-dependent mitochondrial apoptotic pathway, to the same degree as progesterone.	Metformin	23-32	caspase 9	Rattus norvegicus	92-99
28689275-11	2018	EPA/DHA-PS could downregulate the messenger RNA level of Caspase-3, Caspase-9, and Bax, upregulate Bcl-2, inhibit Bax, and increase Bcl-2 at protein level.	dha-ps	4-10	caspase 9	Rattus norvegicus	68-77
29286130-6	2018	Sal decreased the expression of cleaved caspase-3, cleaved caspase-9, apoptosis regulator BAX and cytochrome C, while it increased the expression of B cell lymphoma-2 and phosphorylated-Akt in Dex-induced osteoblasts.	rhodioloside	0-3	caspase 9	Rattus norvegicus	59-68
29427224-10	2018	Further, DMH treatment revealed alterations in the protein expressions of various genes involved in the p53-mediated apoptotic pathway such as p53, p21, Bcl-2, Bax, caspase-9 and caspase-3, which, however, were shifted towards normal control levels upon simultaneous supplementation with probiotics.	1,2-Dimethylhydrazine	9-12	caspase 9	Rattus norvegicus	165-174
29027056-8	2018	Curcumin supplementation prevented the LPS-induced upregulation in the protein activity of transcription factor NFkappaB, proinflammatory cytokines (TNF-alpha, IL-1beta, and IL-1alpha), inducible nitric oxide synthase (iNOS) as well as the regulating molecules of the intrinsic apoptotic pathway (Bax, Bcl-2, Caspase 3 and Caspase 9) by ELISA.	Curcumin	0-8	caspase 9	Rattus norvegicus	323-332
29360689-10	2018	Western blot analysis showed that the expression of beclin-1, LC3-II, LC3-II/LC3-I, and Bcl-2 was increased in resveratrol-treated rats, whereas the expression of p-Akt, p-mTOR, p62, cleaved caspase-3, caspase-9, and Bcl-2-associated X protein was decreased.	Resveratrol	111-122	caspase 9	Rattus norvegicus	202-211
29511437-6	2018	Remarkably, pretreatment with mdivi-1 not only alleviated isoflurane-induced disturbed mitochondrial translocation of Drp1 and Bax and almost restored morphological changes, but also inhibited cytochrome C release, caspase9 and caspase3 activation in hippocampi.	Isoflurane	58-68	caspase 9	Rattus norvegicus	215-223
29497903-11	2018	The levels of both cleaved caspase-3 and cleaved caspase-9 were decreased in hippocampus exposed to the miR-128 mimic, whereas they were markedly increased in miR-128 inhibitor-treated hippocampus.	mir-128	104-111	caspase 9	Rattus norvegicus	49-58
29257286-10	2018	Furthermore, gigantol upregulated Akt phosphorylation and Bcl-2 expression, downregulated Bax expression, and reduced the expression of caspase-3 and caspase-9 in H2O2-treated rBMSCs, whereas an opposite effect was detected when LY294002, an inhibitor of phosphatidylinositol 3-kinase, was administered in combination with gigantol.	gigantol	13-21	caspase 9	Rattus norvegicus	150-159
29434790-4	2018	The results demonstrated that cyanidin was able to dose-dependently reverse cisplatin-induced cell damage and apoptosis, attenuate the accumulation of reactive oxygen species (ROS), and mitochondrial membrane potential depolarization, downregulate the expression of Bcl-2 homologous antagonist/killer, upregulate the expression of apoptosis regulator Bcl-2, and reduce the activation of caspase 3, caspase 9, but not caspase 8.	cyanidin	30-38	caspase 9	Rattus norvegicus	398-407
29257286-10	2018	Furthermore, gigantol upregulated Akt phosphorylation and Bcl-2 expression, downregulated Bax expression, and reduced the expression of caspase-3 and caspase-9 in H2O2-treated rBMSCs, whereas an opposite effect was detected when LY294002, an inhibitor of phosphatidylinositol 3-kinase, was administered in combination with gigantol.	Hydrogen Peroxide	163-167	caspase 9	Rattus norvegicus	150-159
29257007-6	2018	The presence of radioiodine in the kidneys was shown by the Na+/I-symporter antibody and proliferating cell nuclear antigen, Ki-67, caspase-3, caspase-8, caspase-9, and terminal deoxynucleotidyl transferase mediated deoxyuridine triphosphate nick end labeling assay were used to detect cell proliferation and apoptosis.	Iodine-131	16-27	caspase 9	Rattus norvegicus	154-163
28939271-7	2018	Signal transduction studies showed that PFOS exposure significantly elevated inducible nitric oxide synthase (iNOS), Bax, cytochrome c, cleaved caspase-9 and cleaved caspase-3, indicating the mitochondria-dependent apoptotic pathway was activated.	perfluorooctane sulfonic acid	40-44	caspase 9	Rattus norvegicus	144-153
29308067-9	2018	The concentration of Ca2+and the expression of the GRP78, caspase-9 and caspase-12 proteins significantly increased with increasing calcium ionophore A23187 doses (p &lt; 0.05).	Calcium	132-139	caspase 9	Rattus norvegicus	58-67
29308067-9	2018	The concentration of Ca2+and the expression of the GRP78, caspase-9 and caspase-12 proteins significantly increased with increasing calcium ionophore A23187 doses (p &lt; 0.05).	Calcimycin	150-156	caspase 9	Rattus norvegicus	58-67
29115631-11	2018	The TUNEL assays demonstrated fewer apoptotic cells in the CO + crush group compared with the crush-only group, accompanied by the suppression of caspase-9 and caspase-3 activity.	Carbon Monoxide	59-63	caspase 9	Rattus norvegicus	146-155
29283372-9	2017	Curcumin-Cu(II) or -Zn(II) complexes systems significantly enhanced the superoxide dismutase, catalase, and glutathione peroxidase activities and attenuated the increase of malondialdehyde levels and caspase-3 and caspase-9 activities, in a dose-dependent manner.	curcumin-cu(ii)	0-15	caspase 9	Rattus norvegicus	214-223
29283372-9	2017	Curcumin-Cu(II) or -Zn(II) complexes systems significantly enhanced the superoxide dismutase, catalase, and glutathione peroxidase activities and attenuated the increase of malondialdehyde levels and caspase-3 and caspase-9 activities, in a dose-dependent manner.	Zinc	19-26	caspase 9	Rattus norvegicus	214-223
28990064-8	2017	Compared with the control group, the STZ group and HDX group had a disordered arrangement of myocardial cells with apparent myocardial fibrosis, and echocardiography indicated that the cardiac function was lowered, there was an obvious increase of apoptosis in myocardial tissue, the expression levels of apoptosis-associated protein B-cell lymphoma associated protein X, caspase-3 and caspase-9 were upregulated, and Bcl-2 expression was downregulated.	Streptozocin	37-40	caspase 9	Rattus norvegicus	386-395
27832523-16	2017	17beta-Estradiol (E2), tamoxifen (TMX), and raloxifene (RLX) reduced oxidative stress, apoptosis (including caspase-3 and caspase-9), mitochondrial membrane depolarization, and Ca2+ influx through the inhibition of TRPA1, TRPM2 and TRPV1 activation.	Estradiol	0-16	caspase 9	Rattus norvegicus	122-131
27832523-16	2017	17beta-Estradiol (E2), tamoxifen (TMX), and raloxifene (RLX) reduced oxidative stress, apoptosis (including caspase-3 and caspase-9), mitochondrial membrane depolarization, and Ca2+ influx through the inhibition of TRPA1, TRPM2 and TRPV1 activation.	Estradiol	18-20	caspase 9	Rattus norvegicus	122-131
27832523-16	2017	17beta-Estradiol (E2), tamoxifen (TMX), and raloxifene (RLX) reduced oxidative stress, apoptosis (including caspase-3 and caspase-9), mitochondrial membrane depolarization, and Ca2+ influx through the inhibition of TRPA1, TRPM2 and TRPV1 activation.	Tamoxifen	23-32	caspase 9	Rattus norvegicus	122-131
27832523-16	2017	17beta-Estradiol (E2), tamoxifen (TMX), and raloxifene (RLX) reduced oxidative stress, apoptosis (including caspase-3 and caspase-9), mitochondrial membrane depolarization, and Ca2+ influx through the inhibition of TRPA1, TRPM2 and TRPV1 activation.	Tamoxifen	34-37	caspase 9	Rattus norvegicus	122-131
27832523-16	2017	17beta-Estradiol (E2), tamoxifen (TMX), and raloxifene (RLX) reduced oxidative stress, apoptosis (including caspase-3 and caspase-9), mitochondrial membrane depolarization, and Ca2+ influx through the inhibition of TRPA1, TRPM2 and TRPV1 activation.	Raloxifene Hydrochloride	44-54	caspase 9	Rattus norvegicus	122-131
27832523-16	2017	17beta-Estradiol (E2), tamoxifen (TMX), and raloxifene (RLX) reduced oxidative stress, apoptosis (including caspase-3 and caspase-9), mitochondrial membrane depolarization, and Ca2+ influx through the inhibition of TRPA1, TRPM2 and TRPV1 activation.	Raloxifene Hydrochloride	56-59	caspase 9	Rattus norvegicus	122-131
29468175-11	2018	Rapamycin markedly decreased the number of FJB-positive cells and the expression of cleaved caspase-3 and cleaved caspase-9 proteins as well as increased the activation of autophagy reflected by ULK1, Beclin-1 and LC3.	Sirolimus	0-9	caspase 9	Rattus norvegicus	114-123
29238517-10	2017	Supplementation of NaHS protected against H/R-induced apoptosis, the expression of cleaved caspase-3 and cleaved caspase-9 and the release of cytochrome c. The addition of NaHS also counteracted the reduction of cell viability caused by H/R and decreased the expression of GRP 78, CHOP, cleaved caspase-12, ATF 4, ATF 6 and XBP-1 and the phosphorylation of PERK, eIF 2alpha and IRE 1alpha.	sodium bisulfide	19-23	caspase 9	Rattus norvegicus	113-122
29238517-10	2017	Supplementation of NaHS protected against H/R-induced apoptosis, the expression of cleaved caspase-3 and cleaved caspase-9 and the release of cytochrome c. The addition of NaHS also counteracted the reduction of cell viability caused by H/R and decreased the expression of GRP 78, CHOP, cleaved caspase-12, ATF 4, ATF 6 and XBP-1 and the phosphorylation of PERK, eIF 2alpha and IRE 1alpha.	sodium bisulfide	172-176	caspase 9	Rattus norvegicus	113-122
27832523-8	2017	TRPM2, TRPV1, PARP, and caspase-3 and caspase-9 expressions were also decreased in the neurons by the E2, TMX, and RLX treatments.	Tamoxifen	106-109	caspase 9	Rattus norvegicus	38-47
28494360-5	2017	Compared with the control group, the mRNA levels of caspase-3, caspase-9, and cytochrome c all increased with increasing concentrations of NaF.	Sodium Fluoride	139-142	caspase 9	Rattus norvegicus	63-72
28822073-6	2017	Inhibitions of MPP+-induced both cytochrome c release and caspase-9 activation by IRN were blocked by pre-treatment with DPI or pifithrin-alpha, but not by IRE-1alpha shRNA.	mangion-purified polysaccharide (Candida albicans)	15-19	caspase 9	Rattus norvegicus	58-67
28822073-6	2017	Inhibitions of MPP+-induced both cytochrome c release and caspase-9 activation by IRN were blocked by pre-treatment with DPI or pifithrin-alpha, but not by IRE-1alpha shRNA.	diphenyleneiodonium	121-124	caspase 9	Rattus norvegicus	58-67
28822073-6	2017	Inhibitions of MPP+-induced both cytochrome c release and caspase-9 activation by IRN were blocked by pre-treatment with DPI or pifithrin-alpha, but not by IRE-1alpha shRNA.	pifithrin	128-137	caspase 9	Rattus norvegicus	58-67
28867607-7	2017	The regulatory effect of miR-133 on caspase-9 was measured by luciferase reporter assay.	mir-133	25-32	caspase 9	Rattus norvegicus	36-45
28867607-11	2017	We further identified Caspase-9 as the target of miR-133.	mir-133	49-56	caspase 9	Rattus norvegicus	22-31
28871597-10	2017	Mitochondrial pathway of apoptosis was activated in the small intestines of MTX-treated rats as evidenced by intense immunostaining for cyt c, caspases 9 and 3, and PARP-1 and mitochondrial release of cyt c, activation of caspases, and PARP-1 cleavage by Western blot.	Methotrexate	76-79	caspase 9	Rattus norvegicus	136-159
28871597-10	2017	Mitochondrial pathway of apoptosis was activated in the small intestines of MTX-treated rats as evidenced by intense immunostaining for cyt c, caspases 9 and 3, and PARP-1 and mitochondrial release of cyt c, activation of caspases, and PARP-1 cleavage by Western blot.	Methotrexate	76-79	caspase 9	Rattus norvegicus	143-151
28871597-15	2017	The results of the present study show that the mitochondrial pathway of apoptosis plays a role in MTX-induced small intestinal injury as evidenced by cytochrome c release, activation of caspases 9 and 3, PARP-1 cleavage, and DNA fragmentation.	Methotrexate	98-101	caspase 9	Rattus norvegicus	186-202
28893578-4	2017	However, pretreatment with cinnamaldehyde at 5, 10 and 20muM significantly attenuated cell viability loss, reduced the generation of reactive oxygen species, stabilised mitochondrial membrane potential (MMP), decreased the release of cytochrome c and limited the activities of caspase-9 and -3.	cinnamaldehyde	27-41	caspase 9	Rattus norvegicus	277-293
28800882-5	2017	Preincubation with Sal B led to a significant decrease of caspase-9 and caspase-3 activity and poly ADP-ribose polymerase (PARP) cleavage.	salvianolic acid B	19-24	caspase 9	Rattus norvegicus	58-67
28901511-5	2017	The activation of caspase-9 and -3, and cleavage of procaspase-9 and -3, but not of caspase-8, were involved in NAC-induced apoptosis.	Acetylcysteine	112-115	caspase 9	Rattus norvegicus	18-34
28787644-5	2017	The results indicated that SRM 2786 induced mitochondrial dysfunction by increasing activities of caspase-3 and caspase-9, and structural damages of mitochondria with dissipation of mitochondrial membrane potential.	srm 2786	27-35	caspase 9	Rattus norvegicus	112-121
28432551-5	2017	Anisomycin caused the activation of the main stress kinases, phosphorylation of the p53 protein and the eukaryotic initiation factor eIF2alpha, proteolytic cleavage of protein kinase R, Bid, caspase-9 and -3.	Anisomycin	0-10	caspase 9	Rattus norvegicus	191-207
28540664-3	2017	This study reveals that propofol at clinically relevant concentrations increases the TNF-alpha synthesis and release in neurons, and induces neuronal apoptosis; etanercept significantly reduces neuronal apoptosis, the elevation of cleaved caspase-8 and cleaved caspase-9, or the Akt phosphorylation induced by propofol, while the selective PI3K antagonist blocks the neuroprotection of etanercept.	Propofol	24-32	caspase 9	Rattus norvegicus	261-270
28713991-14	2017	CCl4 increased the activity of caspase-9 and -3 by 6.86- and 7.42-fold, respectively; however, silymarin and PZH-GB ameliorated this effect.	pzh-gb	109-115	caspase 9	Rattus norvegicus	31-47
28532211-5	2017	Rotenone also decreased the mitochondrial membrane potential and increased voltage-dependent anion channel (VDAC), caspase-3, and caspase-9 protein levels, indicating an association of apoptosis with renal damage.	Rotenone	0-8	caspase 9	Rattus norvegicus	130-139
28447724-4	2017	The increase of apoptosis and the activation of caspase-3 and caspase-9, but not caspase-8, were detected following cell exposure with docetaxel, demonstrating that the mitochondrial-mediated apoptosis pathway is largely responsible for docetaxel hepatotoxicity.	Docetaxel	237-246	caspase 9	Rattus norvegicus	62-71
28601953-5	2017	Treatment with Dex caused a remarkable decrease in the expression of Bcl-2; an increase in cytochrome c release; activation of BAX, caspase-9, and caspase-3; and an obvious enhancement in STAT1 phosphorylation.	Dexamethasone	15-18	caspase 9	Rattus norvegicus	132-141
28582851-0	2017	Fenofibrate protects against acute myocardial I/R injury in rat by suppressing mitochondrial apoptosis as decreasing cleaved caspase-9 activation.	Fenofibrate	0-11	caspase 9	Rattus norvegicus	125-134
28130746-15	2017	Furthermore, only combination of ATV and Q10 decreased the 6-OHDA induced expression of cytochrome-C, caspase-9 and caspase-3.	Atorvastatin	33-36	caspase 9	Rattus norvegicus	102-111
28130746-15	2017	Furthermore, only combination of ATV and Q10 decreased the 6-OHDA induced expression of cytochrome-C, caspase-9 and caspase-3.	q10	41-44	caspase 9	Rattus norvegicus	102-111
28130746-15	2017	Furthermore, only combination of ATV and Q10 decreased the 6-OHDA induced expression of cytochrome-C, caspase-9 and caspase-3.	Oxidopamine	59-65	caspase 9	Rattus norvegicus	102-111
28731097-9	2017	Meanwhile, DBA treatment caused differential modulation of apoptosis-associated proteins and mRNAs for phosphorylated apoptosis signal regulating kinase 1 (p-ASK-1), phosphorylated c-jun N-terminal kinase (p-JNK), cyt-c, Bax, Bcl-2, caspase-9 and cleaved caspase-3 accompanied by DNA damage.	dibromoacetic acid	11-14	caspase 9	Rattus norvegicus	233-242
28860760-5	2017	Cu NP exposure activated caspase 3, caspase 8, caspase 9, and tBid, decreased the protein levels of Bcl-2, increased the expression levels of the proteins Bax and cytochrome c, and promoted malondialdehyde (MDA) accumulation and superoxide dismutase (SOD) reduction.	Copper	0-2	caspase 9	Rattus norvegicus	47-56
27443158-7	2017	TRPM2 and TRPV1 channel current densities, [Ca2+] concentration, apoptosis, caspase 3, caspase 9, mitochondrial depolarization, and intracellular ROS production values in the neurons were lower in the DULOX group than in controls.	Duloxetine Hydrochloride	201-206	caspase 9	Rattus norvegicus	87-96
28541776-6	2017	Moreover, the results showed that (-)-PFF exposure caused a significant loss in mitochondrial transmembrane potential (MMP), an upregulation of Ca2+ and Bax protein expression, a downregulation of Bcl-2 protein expression, and the activation of caspase-3 and caspase-9 in a dose-dependent manner; (+)-PFF and rac-PFF exhibited these effects to a lesser degree.	profenofos	34-41	caspase 9	Rattus norvegicus	259-268
28296042-6	2017	Nickel sulfate-triggered Leydig cells apoptosis via mitochondria and ERS pathways was characterized by the upregulated mRNA and proteins expression of Bak, cytochrome c, caspase 9, caspase 3, GRP78, GADD153, and caspase 12, which were inhibited by NAC and TEMPO respectively.	nickel sulfate	0-14	caspase 9	Rattus norvegicus	170-179
28742197-14	2017	RESULTS: MiR-24 mimic and/or si-BIM transfection significantly declined the BIM expression, inhibited caspase-9 and caspase-3 activities, and reduced cell apoptosis in H9C2 cells.	mir-24	9-15	caspase 9	Rattus norvegicus	102-111
28742197-14	2017	RESULTS: MiR-24 mimic and/or si-BIM transfection significantly declined the BIM expression, inhibited caspase-9 and caspase-3 activities, and reduced cell apoptosis in H9C2 cells.	Silicon	29-31	caspase 9	Rattus norvegicus	102-111
28390674-10	2017	In addition, expression of caspase 9 was lower in Cd2+ (5 mumol/L)-treated PC12 cells when co-treated with Zn2+ (2 and 5 mumol/L).	Zinc	107-111	caspase 9	Rattus norvegicus	27-36
28447724-4	2017	The increase of apoptosis and the activation of caspase-3 and caspase-9, but not caspase-8, were detected following cell exposure with docetaxel, demonstrating that the mitochondrial-mediated apoptosis pathway is largely responsible for docetaxel hepatotoxicity.	Docetaxel	135-144	caspase 9	Rattus norvegicus	62-71
28238848-11	2017	Expression of SIRT1, p-AMPK, Beclin-1, LC3-B, and Bcl-2 was elevated in resveratrol-treated animals, whereas expression of p62, Cleaved Caspase-3, Caspase-9, and Bcl-2 associated X protein (Bax) was inhibited.	Resveratrol	72-83	caspase 9	Rattus norvegicus	147-156
28128384-6	2017	MPE significantly inhibited Al-induced increase of myocardial p-JNK, cytoplasmic NF-kappaB, cytochrome C, and caspase-9 protein expressions.	Aluminum	28-30	caspase 9	Rattus norvegicus	110-119
27052339-6	2017	One to 2 h after exposure to DCB230, there were significant reductions in mitochondrial membrane potential and significant increases in cleaved caspase-9, but no significant increases in DNA damage or cell death.	dcb230	29-35	caspase 9	Rattus norvegicus	144-153
28406733-6	2017	The neuroprotective effect of sea cucumber cerebrosides (SCC) was also verified in vitro: the cerebrosides increased the survival rate of PC12 cells, recovered the cellular morphology, downregulated the protein levels of Caspase-9, cleaved Caspase-3, total Caspase-3, and Bax, and upregulated the protein level of Bcl-2, revealing that cerebrosides could inhibit Abeta-induced cell apoptosis.	Cerebrosides	43-55	caspase 9	Rattus norvegicus	221-230
28406733-6	2017	The neuroprotective effect of sea cucumber cerebrosides (SCC) was also verified in vitro: the cerebrosides increased the survival rate of PC12 cells, recovered the cellular morphology, downregulated the protein levels of Caspase-9, cleaved Caspase-3, total Caspase-3, and Bax, and upregulated the protein level of Bcl-2, revealing that cerebrosides could inhibit Abeta-induced cell apoptosis.	Cerebrosides	94-106	caspase 9	Rattus norvegicus	221-230
28406733-6	2017	The neuroprotective effect of sea cucumber cerebrosides (SCC) was also verified in vitro: the cerebrosides increased the survival rate of PC12 cells, recovered the cellular morphology, downregulated the protein levels of Caspase-9, cleaved Caspase-3, total Caspase-3, and Bax, and upregulated the protein level of Bcl-2, revealing that cerebrosides could inhibit Abeta-induced cell apoptosis.	Cerebrosides	94-106	caspase 9	Rattus norvegicus	221-230
28406733-6	2017	The neuroprotective effect of sea cucumber cerebrosides (SCC) was also verified in vitro: the cerebrosides increased the survival rate of PC12 cells, recovered the cellular morphology, downregulated the protein levels of Caspase-9, cleaved Caspase-3, total Caspase-3, and Bax, and upregulated the protein level of Bcl-2, revealing that cerebrosides could inhibit Abeta-induced cell apoptosis.	UNII-042A8N37WH	363-368	caspase 9	Rattus norvegicus	221-230
28337145-7	2017	In mechanism study, dioscin not only significantly regulated the protein levels of Ntcp, OAT1, OCT1, Bsep and Mrp2 to accelerate bile acids excretion, but also regulated the expression levels of Bak, Bcl-xl, Bcl-2, Bax, Caspase 3 and Caspase 9 in vivo and in vitro to improve apoptosis.	dioscin	20-27	caspase 9	Rattus norvegicus	234-243
27421045-8	2017	A tendency toward less necrosis in histopathology, and a slight trend toward lower PDE5, NOS2, and caspase-9 and higher Bcl-2 IHC scores were evident in experimental retinas of sildenafil-treated animals.	Sildenafil Citrate	177-187	caspase 9	Rattus norvegicus	99-108
27135630-6	2017	Baicalin, in a dose-dependent manner, decreased the torsion/detorsion-induced elevations of testicular malondialdehyde, nitric oxide, tumour necrosis factor-alpha, BCL2-associated X protein (Bax), cytosolic cytochrome c and caspase-3 and caspase-9 activities.	baicalin	0-8	caspase 9	Rattus norvegicus	238-247
27864105-8	2017	In animals treated with EGCG, tissue Bcl-2 expression exceeded the values observed after ISO treatment and down-regulated the expression of pro-apoptotic signaling proteins, including Bax, caspase-9 and 3.	epigallocatechin gallate	24-28	caspase 9	Rattus norvegicus	189-204
28017962-10	2017	In contrast, pretreatment with the p38 inhibitor SB203580 (200 mug/kg, ip) significantly attenuated post-TBI-induced expression of both cleaved caspase-9 and cleaved caspase-3 and mitochondrial damage, whereas it had no effects on SIRT1 expression.	SB 203580	49-57	caspase 9	Rattus norvegicus	144-153
28367221-6	2017	Administration of RUT and SB203580, both individually as well as in combination, suppressed the elevation of intracellular ROS, inhibited cell apoptosis, and reversed the THP-induced upregulation of TGF-beta1, p-p38 MAPK, cleaved Caspase-9, Caspase-7, and Caspase-3.	pirarubicin	171-174	caspase 9	Rattus norvegicus	230-239
28119812-10	2017	Relevant mechanisms are thought to include oridonin-induced mitochondrial dysfunction accompanied by low mitochondrial membrane potentials, downregulation of BCL-2 expressions, upregulation of expressions of BAX, caspase-3 and caspase-9.	oridonin	43-51	caspase 9	Rattus norvegicus	227-236
29049998-7	2017	Increased expression of C/EBP homologous protein (CHOP) and cleaved caspase-9 suggested a close relationship between severe ER stress and mitochondria-dependent apoptosis in the cochlear cells of cisplatin-treated rats.	Cisplatin	196-205	caspase 9	Rattus norvegicus	68-77
27234250-5	2017	The results illustrated a considerable decrease in oxidative stress markers such as reactive oxygen species (ROS) and lipid peroxidation (LPO) levels of pancreatic islets which were treated by MgO NPs for 24 h. Also, in that time of exposure, cell apoptosis investigation by flow cytometry and insulin test showed that MgO NPs, in a concentration of 100 mug/ml, decreased the rate of apoptotic cells via inhibiting caspase-9 activity and made a significant increase in the level of insulin secretion.	Magnesium Oxide	193-196	caspase 9	Rattus norvegicus	415-424
28214865-7	2017	RESULTS: In vivo experiment, adriamycin significantly upregulated the protein expression of TGF-beta1, TRPC6, desmin and caspase-9, and decreased nephrin.	Doxorubicin	29-39	caspase 9	Rattus norvegicus	121-130
28367221-6	2017	Administration of RUT and SB203580, both individually as well as in combination, suppressed the elevation of intracellular ROS, inhibited cell apoptosis, and reversed the THP-induced upregulation of TGF-beta1, p-p38 MAPK, cleaved Caspase-9, Caspase-7, and Caspase-3.	SB 203580	26-34	caspase 9	Rattus norvegicus	230-239
28992627-9	2017	RESULTS: The protein expression of cleaved caspase-8, caspase-9 and caspase-3 as well as fibrosis markers increased at 4 and 8 weeks in the STZ-induced diabetic hearts compared with the levels in the control group.	Streptozocin	140-143	caspase 9	Rattus norvegicus	54-63
27109833-0	2017	Protective effect of 2-deoxy-D-glucose on the brain tissue in rat cerebral ischemia-reperfusion models by inhibiting Caspase-apoptotic pathway.	Deoxyglucose	21-38	caspase 9	Rattus norvegicus	117-124
28744317-8	2017	It was found that podophyllotoxin significantly inhibited epididymal epithelial cell proliferation, promoted cell apoptosis, and increased the mRNA and protein levels of TNF-alpha and the expression levels of cytochrome c, caspase-8, caspase-9, and caspase-3.	Podophyllotoxin	18-33	caspase 9	Rattus norvegicus	234-243
27908784-9	2017	Cisplatin-treated cultured hippocampal neurons and NSCs were examined for changes in mitochondrial function, oxidative stress production, caspase-9 activation, and neuronal dendritic spine density.	Cisplatin	0-9	caspase 9	Rattus norvegicus	138-147
27908784-12	2017	Cisplatin induced mitochondrial DNA damage, impaired respiratory activity, increased oxidative stress, and activated caspase-9 in cultured hippocampal neurons and NSCs.	Cisplatin	0-9	caspase 9	Rattus norvegicus	117-126
27109833-12	2017	The mechanism may be that 2-DG starts ERS followed by up-regulation of mRNA and protein of GRP78 and down-regulation of mRNA and protein of cleaved-caspase-9 and cleaved-caspase-3, which blocks the apoptotic pathway.	Deoxyglucose	26-30	caspase 9	Rattus norvegicus	148-157
27804049-7	2017	Levels of downstream apoptotic mediators, caspase-3 and caspase-9, were significantly (p &lt; 0.05) upregulated following H2O2 treatment but were abrogated following FGF-8 application.	Hydrogen Peroxide	122-126	caspase 9	Rattus norvegicus	56-65
27665619-7	2017	Caspase-9 and Apaf-1 were strongly expressed in proximal tubules (PTs) but only weakly expressed in DTs.	dibenzyl trisulfide	100-103	caspase 9	Rattus norvegicus	0-9
27718461-13	2016	Furthermore, Ipt significantly activated the caspase cascades evidenced by increased expression of caspase-9 and caspase-3 in hypoxia PASMCs.	N-(1-methylethyl)-1,1,2-trimethylpropylamine	13-16	caspase 9	Rattus norvegicus	45-52
28096675-8	2017	ZPP group compared to ICH: HO-1 positive rate and mRNA expression were decreased, neurological deficit score and cell apoptosis rate were decreased, Caspase 3, Caspase 8, Caspase 9 activity were decreased, level of TNF-alpha, IL-1beta, IL-6 and IL-8 were decreased, Bcl-2 expression was upregulated, Bax, p-NF-kappaB p65 and p-IkappaBalpha expression were downregulated, and the differences were statistically significant (P&lt;0.01).	zinc protoporphyrin	0-3	caspase 9	Rattus norvegicus	171-180
27688248-5	2016	PF and beta-Ecd cooperate to attenuate the rotenone-induced apoptosis by decrease in Bax expression, caspase-9 activity, and caspase-3 activity.	Rotenone	43-51	caspase 9	Rattus norvegicus	101-110
27718461-13	2016	Furthermore, Ipt significantly activated the caspase cascades evidenced by increased expression of caspase-9 and caspase-3 in hypoxia PASMCs.	N-(1-methylethyl)-1,1,2-trimethylpropylamine	13-16	caspase 9	Rattus norvegicus	99-108
27718461-13	2016	Furthermore, Ipt significantly activated the caspase cascades evidenced by increased expression of caspase-9 and caspase-3 in hypoxia PASMCs.	pasmcs	134-140	caspase 9	Rattus norvegicus	45-52
27718461-13	2016	Furthermore, Ipt significantly activated the caspase cascades evidenced by increased expression of caspase-9 and caspase-3 in hypoxia PASMCs.	pasmcs	134-140	caspase 9	Rattus norvegicus	99-108
27718461-14	2016	CONCLUSIONS: Ipt could inhibit cell proliferation and induce apoptosis associated with cell cycle arrest, decreased ET-1, HIF-1, cyclin D, CDK4, PDGF-BB and Deltapsim, increased Bax/Bcl-2 ratio, enhanced Cyt c release, and activation of caspases in PASMCs under hypoxia status.	N-(1-methylethyl)-1,1,2-trimethylpropylamine	13-16	caspase 9	Rattus norvegicus	237-245
28105094-10	2016	Furthermore, the inflammatory response, oxidative stress, and the caspase-9 and -3 activities were significantly suppressed upon treatment with geraniol.	geraniol	144-152	caspase 9	Rattus norvegicus	66-82
27572285-5	2016	Quercetin (10-40 muM) effects on the expression of Bcl-2, caspase-9, caspase-3, PARP-1, PERK, IRE1, ATF6, calnexin and CHOP for 24 h were analyzed by Western blot.	Quercetin	0-9	caspase 9	Rattus norvegicus	58-67
27572285-10	2016	The cleaved forms of caspase-9, caspase-3 and PARP-1 were also increased by quercetin.	Quercetin	76-85	caspase 9	Rattus norvegicus	21-30
27872485-9	2016	The DEX and ISC+DEX treatments also decreased the expression levels of caspase 3, caspase 9, and poly (ADP-ribose) polymerase in the hippocampus and DRG.	Dexmedetomidine	4-7	caspase 9	Rattus norvegicus	82-91
27872485-9	2016	The DEX and ISC+DEX treatments also decreased the expression levels of caspase 3, caspase 9, and poly (ADP-ribose) polymerase in the hippocampus and DRG.	Dexmedetomidine	16-19	caspase 9	Rattus norvegicus	82-91
27091758-11	2016	The Immunohistochemical expression of Bax, Bcl-2, caspase-3, caspase-9 and PCNA were aberrant in BBN + DMA treated tumor group.	Butylhydroxybutylnitrosamine	97-100	caspase 9	Rattus norvegicus	61-70
27861627-1	2016	We designed this study to investigate whether cadmium induces caspase-independent apoptosis and to investigate the relationship between the caspase-dependent and caspase-independent apoptotic pathways.	Cadmium	46-53	caspase 9	Rattus norvegicus	62-69
27861627-3	2016	Cyclosporin A (CsA) prevented mitochondrial permeability transition pore opening and apoptosis; there was mitochondrial ultrastructural disruption, mitochondrial cytochrome c (cyt c) translocation to the cytoplasm, and subsequent caspase-9 and caspase-3 activation.	Cyclosporine	0-13	caspase 9	Rattus norvegicus	230-239
27861627-3	2016	Cyclosporin A (CsA) prevented mitochondrial permeability transition pore opening and apoptosis; there was mitochondrial ultrastructural disruption, mitochondrial cytochrome c (cyt c) translocation to the cytoplasm, and subsequent caspase-9 and caspase-3 activation.	Cyclosporine	15-18	caspase 9	Rattus norvegicus	230-239
27861627-7	2016	These results suggest that BNIP-3 is involved in the caspase-independent apoptotic pathway and is located upstream of AIF/Endo G; both the caspase-dependent and caspase-independent pathways are involved in cadmium-induced rPT cell apoptosis and act synergistically.	Cadmium	206-213	caspase 9	Rattus norvegicus	139-146
27861627-7	2016	These results suggest that BNIP-3 is involved in the caspase-independent apoptotic pathway and is located upstream of AIF/Endo G; both the caspase-dependent and caspase-independent pathways are involved in cadmium-induced rPT cell apoptosis and act synergistically.	Cadmium	206-213	caspase 9	Rattus norvegicus	139-146
27397544-11	2016	TP (40-160 nmol/L) concentration-dependently increased G2/M arrest, apoptosis and caspase-3/caspase-9 activity in HK-2 cells, whereas the same concentrations of TPG did not show those features when compared with the control group.	triptolide	0-2	caspase 9	Rattus norvegicus	92-101
27600825-14	2016	25-OHC also enhanced endothelial cell apoptosis by decreasing Bcl-2 expression and increasing cleaved caspase-9 and cleaved caspase-3 expressions as well as caspase-3 activity.	25-hydroxycholesterol	0-6	caspase 9	Rattus norvegicus	102-111
26433378-9	2016	In addition, the induction of caspase-3, caspase-8, and caspase-9 activities and the increased numbers of TUNEL-positive cells of the CA1 region were significantly reduced by MB application.	Methylene Blue	175-177	caspase 9	Rattus norvegicus	56-65
27593219-10	2016	Moreover, exposure to H2O2 significantly increased the levels of Bax, p53, cleaved caspase-8, and cleaved caspase-9, and decreased the level of Bcl-2, resulting in cell apoptosis.	Hydrogen Peroxide	22-26	caspase 9	Rattus norvegicus	106-115
27593219-12	2016	Pretreatment with compound 6 (12.5 and 25 mumol/L) dose-dependently inhibited the H2O2-induced increase in the level of cleaved caspase-9 but not of cleaved caspase-8.	Hydrogen Peroxide	82-86	caspase 9	Rattus norvegicus	128-137
27116952-3	2016	The results showed that Pb-mediated mitochondrial permeability transition pore (MPTP) opening together with mitochondrial cytochrome c release, activations of caspase-9 and caspase-3, and subsequent poly-ADP-ribose polymerase (PARP) cleavage can be effectively blocked by the addition of PU.	Lead	24-26	caspase 9	Rattus norvegicus	159-168
27474647-7	2016	Furthermore, CS also inhibited the DBT-inducted activation of caspase-9, and -3 at mRNA and protein expression levels.	Chitosan	13-15	caspase 9	Rattus norvegicus	62-79
27474647-7	2016	Furthermore, CS also inhibited the DBT-inducted activation of caspase-9, and -3 at mRNA and protein expression levels.	di-n-butyltin	35-38	caspase 9	Rattus norvegicus	62-79
27189477-7	2016	Opposite, Bcl-2 and caspase-9, markers of intrinsic pathway activation, were shown to be more influenced by propofol treatment in the cortex.	Propofol	108-116	caspase 9	Rattus norvegicus	20-29
27091758-11	2016	The Immunohistochemical expression of Bax, Bcl-2, caspase-3, caspase-9 and PCNA were aberrant in BBN + DMA treated tumor group.	Cacodylic Acid	103-106	caspase 9	Rattus norvegicus	61-70
27657024-5	2016	Asiatic acid at 10 muM effectively inhibited apoptotic cell death, suppressed the activities of caspase-3 and caspase-9, and reversed Bax/Bcl-2 ratio in hypoxic H9c2 cells.	asiatic acid	0-12	caspase 9	Rattus norvegicus	110-119
27208869-9	2016	Western-blot analysis demonstrated the expression levels of procaspase-9, -7, -3 and cleaved caspase-9, -7, -3 were upregulated, and PARP were downregulated both 24h and 7 days after MNU injection.	Methylnitrosourea	183-186	caspase 9	Rattus norvegicus	63-72
26958745-11	2016	Further studies showed that 4-phenylbutyric acid inhibited endoplasmic reticulum stress-mediated cytokine release, apoptosis, and oxidative stress via inhibition of nuclear factor-kappaB, caspase-3 and caspase-9, and increasing glutathione peroxidase and superoxide dismutase expression, respectively.	4-phenylbutyric acid	28-48	caspase 9	Rattus norvegicus	202-211
27208496-9	2016	Meanwhile, methane treatment significantly increased the anti-apoptotic gene (Bcl-2) expression and decreased the pro-apoptotic gene (Bax) expression, accompanied by the suppression of caspase-3 and caspase-9 activity.	Methane	11-18	caspase 9	Rattus norvegicus	199-208
27357441-4	2016	In addition, CsA treatment blocked the CoCl2-induced increases in ROS production and mitochondrial dysfunction, including a decrease in membrane potential, cytochrome c (cyto-c) release, Bax/Bcl-2 imbalance, as well as the ratios of cl-casp-9/casp-9 and cl-casp-3/casp-3 ratios, via the inhibition of p38 and ERK MAPK signaling pathways.	Cyclosporine	13-16	caspase 9	Rattus norvegicus	236-242
27357441-4	2016	In addition, CsA treatment blocked the CoCl2-induced increases in ROS production and mitochondrial dysfunction, including a decrease in membrane potential, cytochrome c (cyto-c) release, Bax/Bcl-2 imbalance, as well as the ratios of cl-casp-9/casp-9 and cl-casp-3/casp-3 ratios, via the inhibition of p38 and ERK MAPK signaling pathways.	Cyclosporine	13-16	caspase 9	Rattus norvegicus	243-249
27357441-4	2016	In addition, CsA treatment blocked the CoCl2-induced increases in ROS production and mitochondrial dysfunction, including a decrease in membrane potential, cytochrome c (cyto-c) release, Bax/Bcl-2 imbalance, as well as the ratios of cl-casp-9/casp-9 and cl-casp-3/casp-3 ratios, via the inhibition of p38 and ERK MAPK signaling pathways.	cobaltous chloride	39-44	caspase 9	Rattus norvegicus	236-242
27357441-4	2016	In addition, CsA treatment blocked the CoCl2-induced increases in ROS production and mitochondrial dysfunction, including a decrease in membrane potential, cytochrome c (cyto-c) release, Bax/Bcl-2 imbalance, as well as the ratios of cl-casp-9/casp-9 and cl-casp-3/casp-3 ratios, via the inhibition of p38 and ERK MAPK signaling pathways.	cobaltous chloride	39-44	caspase 9	Rattus norvegicus	243-249
27554124-7	2016	Finally, the lead-induced cell apoptosis was evaluated by flow cytometry in the present of caspase inhibitors Z-VAD-FMK and Ac-LEHD-FMK, respectively.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	110-119	caspase 9	Rattus norvegicus	91-98
26318906-10	2016	Treatment with the antioxidant and protein kinase C (PKC-beta) inhibitor hispidin decreased DOX-induced activation of caspase 9 and p66Shc alterations.	hispidin	73-81	caspase 9	Rattus norvegicus	118-127
26318906-10	2016	Treatment with the antioxidant and protein kinase C (PKC-beta) inhibitor hispidin decreased DOX-induced activation of caspase 9 and p66Shc alterations.	Doxorubicin	92-95	caspase 9	Rattus norvegicus	118-127
26178456-6	2016	Furthermore, baicalein triggered a cascade of mitochondrion-associated apoptosis by upregulating cleaved-caspase-3, Bcl2-associated X protein (Bax), and cleaved-caspase-9 while downregulating the protein expression of B-cell lymphoma 2 (Bcl-2).	baicalein	13-22	caspase 9	Rattus norvegicus	161-170
27155462-0	2016	Simvastatin pretreatment reduces caspase-9 and RIPK1 protein activity in rat cardiac allograft ischemia-reperfusion.	Simvastatin	0-11	caspase 9	Rattus norvegicus	33-42
27441301-8	2016	Besides, VPA promoted hepatocellular apoptosis, as attested by enhanced expression of cleaved caspase-9 and increased number of TUNEL-positive hepatocytes.	Valproic Acid	9-12	caspase 9	Rattus norvegicus	94-103
27139338-9	2016	Sal B inhibited the expression of Bax, cleaved caspase-9 and cleaved PARP, while promoted the expression of Bcl-2, LC3-II, Beclin1 and VEGF.	salvianolic acid B	0-5	caspase 9	Rattus norvegicus	47-56
27353299-9	2016	Results showed DZN-induced apoptosis by activation of caspase 9 and caspase 3 and by increasing the Bax/Bcl2 ratio (both protein and messenger RNA levels).	Diazinon	15-18	caspase 9	Rattus norvegicus	54-63
27601854-11	2016	In addition, the expressions of total and cleaved caspase-3, total and cleaved caspase-9 protein, Fas, and FasL in vitro were downregulated by the treatment with baicalin.	baicalin	162-170	caspase 9	Rattus norvegicus	79-88
27155462-8	2016	Simvastatin pretreatment decreased mRNA expression of caspase-3 and -9, and RIPK1 and -3 and protein activity of caspase-9 and RIPK1 in the allografts.	Simvastatin	0-11	caspase 9	Rattus norvegicus	113-122
27134043-9	2016	THP, NPS2390 (inhibitor of CaSR), U73122 (inhibitor of PLC-gamma1) and 2-APB (inhibitor of IP3) further decreased cell apoptosis, along with down-regulation of cytochrome c, caspase-3 and caspase-9 activation, disruption of Deltapsim and the production of inflammatory cytokines.	2-quinoxaline-carboxamide-N-adamantan-1-yl	5-12	caspase 9	Rattus norvegicus	188-197
26979714-7	2016	BBR-induced anti-apoptotic function was demonstrated by decreasing apoptotic proteins (cytochrome c, Bax, caspase3 and caspase9).	Berberine	0-3	caspase 9	Rattus norvegicus	119-127
27134043-9	2016	THP, NPS2390 (inhibitor of CaSR), U73122 (inhibitor of PLC-gamma1) and 2-APB (inhibitor of IP3) further decreased cell apoptosis, along with down-regulation of cytochrome c, caspase-3 and caspase-9 activation, disruption of Deltapsim and the production of inflammatory cytokines.	1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione	34-40	caspase 9	Rattus norvegicus	188-197
27134043-9	2016	THP, NPS2390 (inhibitor of CaSR), U73122 (inhibitor of PLC-gamma1) and 2-APB (inhibitor of IP3) further decreased cell apoptosis, along with down-regulation of cytochrome c, caspase-3 and caspase-9 activation, disruption of Deltapsim and the production of inflammatory cytokines.	tetrahydropalmatine	0-3	caspase 9	Rattus norvegicus	188-197
26991847-4	2016	Compared with the NaF group, the mRNA levels of Cytc and Caspase-9, as well as the protein levels of Cytc in NaF+Se group, significantly decreased.	Sodium Fluoride	18-21	caspase 9	Rattus norvegicus	57-66
27187346-7	2016	Furthermore, 1,3-BPMU enhanced the apoptosis via upregulation of caspase-3 and caspase-9 and the downregulation of Bcl-2 and Bcl-XL mRNA expression as compared to DEN-induced rats.	1,3-bpmu	13-21	caspase 9	Rattus norvegicus	79-88
26992405-12	2016	Importantly, LY294002 mitigated the inhibitory effects of Srx-1 on Deltapsim loss, cytochrome c release, caspase-9/3 activity, and the expression of Bcl-2 family.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	13-21	caspase 9	Rattus norvegicus	105-114
27105999-10	2016	Moreover, flow cytometry indicated that treatment with caerulein induced a significant decrease of apoptotic index and increase of necrosis index in TRAM1-siRNA cells, compared with control groups, as indicated by downregulated expression of cleaved caspase-3, caspase-8, and caspase-9 mRNA expression activity in TRAM1-siRNA cells.	Ceruletide	55-64	caspase 9	Rattus norvegicus	276-285
26769958-8	2016	The superoxide anion scavenger decreased hypoxia-induced Fas ligand, Fas death receptors, Fas-associated death domain (FADD), activated caspase-8, and activated caspase-3 (Fas-dependent apoptotic pathway) as well as Bad, activated caspase-9 and activated caspase-3 (mitochondria-dependent apoptotic pathway), endonuclease G (EndoG), apoptosis-inducing factor (AIF), and TUNEL-positive apoptosis.	Superoxides	4-20	caspase 9	Rattus norvegicus	231-240
27074962-12	2016	Further assays showed depressed up-regulation of caspase-3 and caspase-9 after puerarin pretreatment.	puerarin	79-87	caspase 9	Rattus norvegicus	63-72
27074962-13	2016	CONCLUSIONS Puerarin pretreatment can decrease activity of caspase-3 and caspase-9 activity in PC12 cells, thus protecting cells from oxidative injury.	puerarin	12-20	caspase 9	Rattus norvegicus	73-82
27017380-4	2016	DON treatment inhibited proliferation of PC12 cells, induced significant morphological changes and apoptosis, promoted the release of Cyt C and AIF from the mitochondria, and increased the activities of cleaved-Caspase9 and cleaved-Caspase3.	deoxynivalenol	0-3	caspase 9	Rattus norvegicus	211-219
26854628-4	2016	METHODS AND RESULTS: By using small interference RNA (siRNA) and EndoII overexpression strategy, we found that EndoII siRNA knockdown reduced cell viability and promoted H2O2-induced cell apoptosis, evidenced by loss of mitochondrial membrane potential, release of cytochrome c, and activation of caspase-9, 3 and poly (ADP-ribose) polymerase (PARP).	Hydrogen Peroxide	170-174	caspase 9	Rattus norvegicus	297-306
26795685-16	2016	Moreover, the expression of both NMDAR1 (P&lt;0.001) and Caspase9 (P=0.013) in PEG-UK-treated rats was reduced.	peg-uk	79-85	caspase 9	Rattus norvegicus	57-65
27073423-9	2016	Exposure of neuronal cells to H2O2 significantly increased the levels of reactive oxygen species (ROS), B-cell lymphoma 2-associated X protein, poly (ADP-ribose), cleaved poly (ADP-ribose) polymerase, cytochrome c, apoptosis-inducing factor, cleaved caspase-9 and cleaved caspase-3, in all cases.	Hydrogen Peroxide	30-34	caspase 9	Rattus norvegicus	250-259
27461625-6	2016	RESULTS: The treatment of DMBA-exposed rats with ZOL and RT, both alone and in combination, successfully upregulates the transcriptional levels of Bax, caspase-3, caspase-9, p21, and BRCA 1 in mammary tissues, which may account for the elevated apoptotic activities observed and the eventual inhibition of tumor growth.	6,11-dimethylbenzo(b)naphtho(2,3-d)thiophene	26-30	caspase 9	Rattus norvegicus	163-172
27239852-6	2016	Mitochondrion membrane potential was reduced, cytochrome released into the cytoplasm and caspase-9 and caspase-3 were significantly increased (P &lt; 0.01) after treatment with H(2)O(2).	Water	177-182	caspase 9	Rattus norvegicus	89-98
26819084-12	2016	The activities of caspase-3 and caspase-9 in pancreas were decreased evidently by DJC treatment.	djc	82-85	caspase 9	Rattus norvegicus	32-41
26721368-6	2016	BE and PHE increased caspase-9 level in the cortex and PHE also in the hippocampus.	Beryllium	0-2	caspase 9	Rattus norvegicus	21-30
26721368-6	2016	BE and PHE increased caspase-9 level in the cortex and PHE also in the hippocampus.	phenoxyethanol	7-10	caspase 9	Rattus norvegicus	21-30
27158406-9	2016	Furthermore, BP stimulated autophagy and inhibited apoptosis via modulated the autophagy-associated proteins LC 3, Beclin-1 and p62, and apoptosis-modulating proteins caspase 3, caspase 8, caspase 9, PARP and BCL-2/Bax.	Benzo(a)pyrene	13-15	caspase 9	Rattus norvegicus	189-198
26831257-5	2016	On the other hand, due to its free radical scavenging properties, vitamin C treatment significantly reduced the production of reactive oxygen species, suppressed both activated microglia and astrocytes and reversed other changes including elevated level of Bax/Bcl-2 ratio, cytochrome c and different caspases such as caspase-9 and caspase-3 induced by ethanol in developing rat brain.	Ascorbic Acid	66-75	caspase 9	Rattus norvegicus	301-309
27069541-9	2016	Compared with the model group, rats given Dex had (1) shorter escape latencies, (2) more platform crossings, (3) fewer relaxin-3 and c-fos positive neurons in the hippocampal CA1 area, (4) upregulation of Bcl-2, (5) downregulation of Fas, caspase-8, and caspase-9 proteins, and (6) decreased neuroapoptosis in the hippocampus.	Dexmedetomidine	42-45	caspase 9	Rattus norvegicus	254-263
26691328-4	2016	Cisplatin-induced apoptosis was also increased in A549-Dp71AS cell line via enhancing the Caspase 3, Caspase 8, and Caspase 9 activities.	Cisplatin	0-9	caspase 9	Rattus norvegicus	116-125
26831257-5	2016	On the other hand, due to its free radical scavenging properties, vitamin C treatment significantly reduced the production of reactive oxygen species, suppressed both activated microglia and astrocytes and reversed other changes including elevated level of Bax/Bcl-2 ratio, cytochrome c and different caspases such as caspase-9 and caspase-3 induced by ethanol in developing rat brain.	Ascorbic Acid	66-75	caspase 9	Rattus norvegicus	318-327
26435418-7	2016	SAL also inhibited H9c2 cell apoptosis by inhibiting the activation of pro-apoptotic molecules caspase 3 and caspase 9 as well as activation of the anti-apoptotic molecular Bcl-2.	rhodioloside	0-3	caspase 9	Rattus norvegicus	109-118
26253898-5	2015	RESULTS: Administration of cisplatin caused significant increases in malondialdehyde levels, Bax and caspase 9 genes expression levels concomitant with significant decreases in anti-oxidant enzyme activities, p53 and cytochrome c gene expression levels, along with some histopathological lesions in testicular tissue.	Cisplatin	27-36	caspase 9	Rattus norvegicus	101-110
26551080-9	2015	Hesperidin was found to induce caspase-3, caspase-9, bax expression and downregulate bcl-2, NFkappaB, iNOS, TNF-alpha, PCNA expression.	Hesperidin	0-10	caspase 9	Rattus norvegicus	42-51
26385354-5	2015	Moreover, terminal deoxynucleotidyl transferase dUTP nickend labeling (TUNEL) assay demonstrated that Sal suppressed myocardial apoptosis, which may be related to up-regulation of Bcl-2/Bax ratio and inhibition of caspase-3, caspase-9 activation.	rhodioloside	102-105	caspase 9	Rattus norvegicus	225-234
26274958-10	2015	In addition, kansenone could up-regulate the apoptotic proteins Bax, AIF, Apaf-1, cytochrome c, caspase-3, caspase-9, caspase-8, FasR, FasL, NF-kappaB, and TNFR1 mRNA expression levels, and down-regulate the anti-apoptotic Bcl-2 family proteins, revealing that kansenone induces apoptosis through both the death receptor and mitochondrial pathways.	kansenone	13-22	caspase 9	Rattus norvegicus	107-116
26209154-10	2015	Furthermore we also analyzed that caffeine reduced cytochrome C, Bax/Bcl2 ratio, caspase-9, caspase-3 and PARP-1 level.	Caffeine	34-42	caspase 9	Rattus norvegicus	81-90
26152514-5	2015	Furthermore, phloroglucinol treatment markedly reduced the protein expression of Bax, cytochrome c, and caspase 9, while increasing anti-apoptotic Bcl-2 protein expression.	Phloroglucinol	13-27	caspase 9	Rattus norvegicus	104-113
26469068-8	2015	BMSC-EVs also suppressed the apoptosis via reducing the cleavage of caspase-3, caspase-8 and caspase-9 in colitis rats.	bmsc-evs	0-8	caspase 9	Rattus norvegicus	93-102
24616003-8	2015	The mRNA and protein expression levels of p53, bax, cytochrome c, caspase-9, and caspase-3 in the offspring"s heart were enhanced in various PFOS-treated groups, meanwhile, the bcl-2 expression levels were decreased.	perfluorooctane sulfonic acid	141-145	caspase 9	Rattus norvegicus	66-75
26203862-6	2015	CA also counteracted the HFD- or palmitic acid (PA)-induced increases in caspase-3 and caspase-9 activity.	Palmitic Acid	33-46	caspase 9	Rattus norvegicus	87-96
25693680-5	2015	The immunohistochemical and qRT-PCR results indicated that caspase-3, caspase-9 protein positive expression and mRNA relative expression enhanced with increasing NaF concentration.	Sodium Fluoride	162-165	caspase 9	Rattus norvegicus	70-79
25715966-9	2015	Genistein exerted anti-apoptotic effects by reversing the apoptotic factors Bcl-2 and Bax ratio, along with the suppression of caspase-9 and caspase-3 activities.	Genistein	0-9	caspase 9	Rattus norvegicus	127-136
26164708-5	2015	Compared with cadmium-treated cells, L-theanine could also decrease the ratio of Bax/Bcl-2, as well as the level of cleaved caspase-9, caspase-3 and poly(ADP-ribose) polymerase.	theanine	37-47	caspase 9	Rattus norvegicus	124-133
26203862-6	2015	CA also counteracted the HFD- or palmitic acid (PA)-induced increases in caspase-3 and caspase-9 activity.	Palmitic Acid	48-50	caspase 9	Rattus norvegicus	87-96
26045616-6	2015	The metformin-treated groups exhibited less severe mitochondrial damage (markers: cytochrome c release, citrate synthase activity, mtDNA copy number, mitochondrial respiration) and apoptosis (caspase 9 and caspase 3 activation).	Metformin	4-13	caspase 9	Rattus norvegicus	192-201
26112249-6	2015	Furthermore, the inhibition of caspase 8 impaired TCBQ-induced the activation of caspase 3, as well as the release of Cyt c and the cleavage of Bid, suggesting caspase 8 acting as the upstream molecule of Bid, and TCBQ-induced apoptosis is initiated via caspase 8, leads to the activation of caspase 9/3 through Bid-mediated amplification loop.	tetrachlorobenzoquinone	50-54	caspase 9	Rattus norvegicus	292-301
26396915-13	2015	p38-MAPK inhibitor, SB203580, prevented caspase-9 activation, which further suppoted the involvement of p38-MAPK in C6-glioma apoptosis.	SB 203580	20-28	caspase 9	Rattus norvegicus	40-49
25596671-7	2015	Moreover, baicalin effectively prevented Abeta-induced mitochondrial membrane potential decrease, Bax/Bcl-2 ratio increase, cytochrome c release, and caspase-9/-3 activation.	baicalin	10-18	caspase 9	Rattus norvegicus	150-159
25596671-7	2015	Moreover, baicalin effectively prevented Abeta-induced mitochondrial membrane potential decrease, Bax/Bcl-2 ratio increase, cytochrome c release, and caspase-9/-3 activation.	UNII-042A8N37WH	41-46	caspase 9	Rattus norvegicus	150-159
25955519-5	2015	Furthermore, we found that following exposure to OGD or H2O2, the knockdown of Srxn1 resulted in a decrease in mitochondrial transmembrane potential (Deltapsim) as indicated by JC-1 staining, an increase in the cytoplasmic expression of cytochrome c (Cyt.C), caspase-3, caspase-9, poly(ADP-ribose) polymerase (PARP) and Bax protein at the protein level, but a decrease in the expression of the anti-apoptotic Bcl-2 protein; these effects were tightly associated with the mitochondrial apoptotic pathway.	Hydrogen Peroxide	56-60	caspase 9	Rattus norvegicus	270-279
26112249-6	2015	Furthermore, the inhibition of caspase 8 impaired TCBQ-induced the activation of caspase 3, as well as the release of Cyt c and the cleavage of Bid, suggesting caspase 8 acting as the upstream molecule of Bid, and TCBQ-induced apoptosis is initiated via caspase 8, leads to the activation of caspase 9/3 through Bid-mediated amplification loop.	tetrachlorobenzoquinone	214-218	caspase 9	Rattus norvegicus	292-301
25747863-12	2015	CONCLUSION: Treatment with nanocurcumin exerts its neuroprotective effect through the upward regulation of NF-kappaB (p65) and also reduced mitochondrion related caspase-9a expression.	nanocurcumin	27-39	caspase 9	Rattus norvegicus	162-171
24829152-10	2015	Following Tet preconditioning, the expression of Caspase-3 was significantly reduced compared with the overload training group (P&lt;0.05), while Caspase-9 expression showed a slight decline (P&gt;0.05).	tet	10-13	caspase 9	Rattus norvegicus	146-155
25846801-10	2015	Various regimens of morphine reduced TWI, cortisol levels, Bax activity, caspase-3, caspase-9, TNF-alpha, and IL-1beta and lipid peroxidation.	Morphine	20-28	caspase 9	Rattus norvegicus	84-93
26014124-6	2015	Elevated protein expression levels of Fas, FADD and the apoptotic initiator activated caspase-8, a molecule in the death-receptor-dependent pathway, coupled with increased t-Bid and apoptotic initiator activated caspase-9 were found.	ammonium ferrous sulfate	38-41	caspase 9	Rattus norvegicus	212-221
25750029-10	2015	Risperidone ameliorated increase in the activity of mitochondrial respiratory complex (I, II, IV, and V), decreases in the levels of mitochondrial membrane potential, cytochrome-C and caspase-9 in the hippocampus, hypothalamus, pre-frontal cortex, and amygdala.	Risperidone	0-11	caspase 9	Rattus norvegicus	184-193
25712644-7	2015	RESULTS: The results showed that morphine significantly increased lipid peroxidation, mitochondrial GSH level, concentration of Bax; caspase-3 and caspase-9 activities while decreasing Bcl-2 concentration.	Morphine	33-41	caspase 9	Rattus norvegicus	147-156
25636514-6	2015	Moreover, the uranium-induced apoptosis was found to be associated with the activation of caspase-3, caspase-8 and caspase-9, indicating both a mitochondria-dependent signaling pathway and a death receptor pathway by a crosstalk.	Uranium	14-21	caspase 9	Rattus norvegicus	115-124
26182357-0	2015	Photoactivation of hypericin decreases the viability of RINm5F insulinoma cells through reduction in JNK/ERK phosphorylation and elevation of caspase-9/caspase-3 cleavage and Bax-to-Bcl-2 ratio.	hypericin	19-28	caspase 9	Rattus norvegicus	142-151
26182357-9	2015	Photoactivated hypericin triggered apoptosis through activation of caspase-3 and caspase-9 and elevation of the Bax-to B-cell lymphoma 2 (Bcl-2) ratio.	hypericin	15-24	caspase 9	Rattus norvegicus	81-90
25966233-10	2015	The expression levels of Drp1, ROCK1, and caspase-9 increased in the diabetes group but decreased in the ZLHXTY group from the 4th week after modeling.	zlhxty	105-111	caspase 9	Rattus norvegicus	42-51
25966233-12	2015	Furthermore, ZLHXTY treatment inhibited the activation of ROCK1 and expression of Drp1 and caspase-9, but did not affect the expression of mfn2.	zlhxty	13-19	caspase 9	Rattus norvegicus	91-100
25769956-6	2015	Annexin-V/propidium iodide staining analysis showed that zerumbone impaired the apoptotic response of high glucose-treated INS-1 cells, which was coupled with a significant decline in cleaved caspase-3 and caspase-9.	zerumbone	57-66	caspase 9	Rattus norvegicus	206-215
25769956-6	2015	Annexin-V/propidium iodide staining analysis showed that zerumbone impaired the apoptotic response of high glucose-treated INS-1 cells, which was coupled with a significant decline in cleaved caspase-3 and caspase-9.	Glucose	107-114	caspase 9	Rattus norvegicus	206-215
25871290-10	2015	The data above suggested that ATX protects against early AKI following severe burns in rats, which was attributed to its ability to ameliorate oxidative stress and inhibit apoptosis by modulating the mitochondrial-apoptotic pathway, regarded as the Akt/Bad/Caspases signalling cascade.	astaxanthine	30-33	caspase 9	Rattus norvegicus	257-265
25712644-9	2015	Various dosage of Curcumin attenuated these effects by significantly lowering lipid peroxidation, GSSG level, Bax concentration, caspase-3 and caspase-9 activities, while increasing superoxide dismutase and glutathione peroxidase activity, GSH level and Bcl-2 concentration.	Curcumin	18-26	caspase 9	Rattus norvegicus	143-152
25287674-11	2015	The expressions of caspase-3 and caspase-9 induced by high glucose exposure were also ameliorated in the RGCs treated with EPO.	Glucose	59-66	caspase 9	Rattus norvegicus	33-42
25381639-8	2015	Further, gene expressions of caspase 3 and caspase 9 were also found to be elevated after Al treatment, which however were reduced following Zn co-treatment.	Aluminum	90-92	caspase 9	Rattus norvegicus	43-52
26038701-8	2015	We demonstrate that (1) Metformin inhibits menadione-induced caspase-9,-6,-3 activation and PARP-cleavage in a concentration-dependent manner.	Metformin	24-33	caspase 9	Rattus norvegicus	61-70
26038701-8	2015	We demonstrate that (1) Metformin inhibits menadione-induced caspase-9,-6,-3 activation and PARP-cleavage in a concentration-dependent manner.	Vitamin K 3	43-52	caspase 9	Rattus norvegicus	61-70
25381639-6	2015	Al treatment resulted in a significant increase in the protein expressions of cytochrome c, Bax, Apaf-1, caspase 9, caspase 3 (p17), caspase 8, caspase 6, caspase 7 but decreased the Bcl-2 in both the cerebrum and cerebellum.	Aluminum	0-2	caspase 9	Rattus norvegicus	105-114
25381639-7	2015	However, Zn supplementation to Al treated rats resulted in a reduction in the protein expressions of cytochrome c, Bax, Apaf-1, caspase 9, caspase 3 (p17), caspase 8, caspase 6 and caspase 7 whereas it elevated the Bcl-2 in both the regions.	Zinc	9-11	caspase 9	Rattus norvegicus	128-137
25932128-5	2015	The activities of acetylcholinesterase (AChE), choline acetylase (ChAT), caspase-9 and caspase-3 in STZ-induced diabetic rats" hippocampus were detected via responsive commercial kits.	Streptozocin	100-103	caspase 9	Rattus norvegicus	73-82
25381639-7	2015	However, Zn supplementation to Al treated rats resulted in a reduction in the protein expressions of cytochrome c, Bax, Apaf-1, caspase 9, caspase 3 (p17), caspase 8, caspase 6 and caspase 7 whereas it elevated the Bcl-2 in both the regions.	Aluminum	31-33	caspase 9	Rattus norvegicus	128-137
25381639-8	2015	Further, gene expressions of caspase 3 and caspase 9 were also found to be elevated after Al treatment, which however were reduced following Zn co-treatment.	Zinc	141-143	caspase 9	Rattus norvegicus	43-52
25370745-5	2015	The mRNA and protein expression levels of HIF-1alpha, iNOS, COX-2 and caspase-9 in EVC-treated rats were increased significantly compared with normal rats.	CHEMBL4645817	83-86	caspase 9	Rattus norvegicus	70-79
25541342-8	2015	In addition, lithium-pilocarpine administration was associated with medium-term hippocampal and cortical damage, since it induced neurodegeneration, glial activation and augmented caspase-9 expression.	Lithium	13-20	caspase 9	Rattus norvegicus	180-189
25541342-8	2015	In addition, lithium-pilocarpine administration was associated with medium-term hippocampal and cortical damage, since it induced neurodegeneration, glial activation and augmented caspase-9 expression.	Pilocarpine	21-32	caspase 9	Rattus norvegicus	180-189
25370745-3	2015	ERG-b and mRNA and protein expression levels of HIF-1alpha, iNOS, COX-2 and caspase-9 in normal, EVC-treated and EVC combined with EPO (EVC+EPO)-treated rats were measured by electroretinography, RT-PCR and western blotting, respectively.	CHEMBL4645817	113-116	caspase 9	Rattus norvegicus	76-85
25370745-7	2015	Compared with EVC-treated rats, EPO administration weakened the mRNA and protein expression levels of HIF-1alpha, iNOS, COX-2 and caspase-9.	CHEMBL4645817	14-17	caspase 9	Rattus norvegicus	130-139
25370745-3	2015	ERG-b and mRNA and protein expression levels of HIF-1alpha, iNOS, COX-2 and caspase-9 in normal, EVC-treated and EVC combined with EPO (EVC+EPO)-treated rats were measured by electroretinography, RT-PCR and western blotting, respectively.	CHEMBL4645817	113-116	caspase 9	Rattus norvegicus	76-85
25714970-5	2015	Our results showed that ethanol administration increased the expression of gamma -aminobutyric acid B1 receptor (GABAB1R) and induced neuronal apoptosis via alterations to the Bax/Bcl-2 ratio, release of cytochrome C and activation of caspase-3 and caspase-9.	Ethanol	24-31	caspase 9	Rattus norvegicus	249-258
25788936-4	2015	Biochemical and immunohistochemical tests showed that superoxide dismutase and nuclear respiratory factor 1 expression levels in the brain tissue decreased after ischemia and they increased obviously after daidzein administration; malondialdehyde level and apoptosis-related cysteine peptidase caspase-3 and caspase-9 immunoreactivity in the brain tissue increased after ischemia and they decreased obviously after daidzein administration.	daidzein	206-214	caspase 9	Rattus norvegicus	308-317
25344274-5	2015	Increased Bax/Bcl-2 ratio, mitochondrial membrane potential decrease, cytochrome c release, caspase-9/-3 activation, AIF/Endo G translocation were observed in H2O2-treated cells.	Hydrogen Peroxide	159-163	caspase 9	Rattus norvegicus	92-101
26425111-3	2015	We observed decreased mitochondrial transmembrane potentials, ultrastructure collapse, enhanced caspase-3 activity, and increased concentrations of cleaved PARP, cleaved caspase-9 and cleaved caspase-3 following Cd treatment.	Cadmium	212-214	caspase 9	Rattus norvegicus	170-179
25451757-8	2015	In accordance, anthocyanins reversed Abeta-induced effect on protein expression of mitochondrial apoptotic pathway (Bax, cytochrome C, caspase-9 and caspase-3) and major Alzheimer"s markers i.e. Abeta, APP, P-tau and BACE-1.	Anthocyanins	15-27	caspase 9	Rattus norvegicus	135-144
25790559-7	2015	Caspase-3 and caspase-9 values increased after ischemia and decreased after treatment; this reduction was more pronounced at 24 h. CONCLUSION: Our study revealed that syringic acid treatment in cerebral ischemia reduced oxidative stress and neuronal degeneration.	syringic acid	167-180	caspase 9	Rattus norvegicus	14-23
26056850-10	2015	Also, the level of death proteases (caspase 3 and caspase 9) was found higher in hydroquinone exposed islets.	hydroquinone	81-93	caspase 9	Rattus norvegicus	50-59
25181333-7	2014	In addition, caspase-6, caspase-8 and caspase-9 labeling was present in SGN treated with 30 muM paclitaxel for 48 h. These results suggest that caspase-dependent apoptotic pathways are involved in paclitaxel-induced damage of SGN, but not hair cells in cochlea.	Paclitaxel	96-106	caspase 9	Rattus norvegicus	38-47
25229402-13	2014	In conclusion, our findings demonstrated that Smad3-Nox4 axis-mediated mitochondrial dysfunction is involved in PA-induced podocyte damage likely via increasing ROS generation and activating the cytochrome c-caspase9-caspase3 apoptotic signaling pathway.	Puromycin Aminonucleoside	112-114	caspase 9	Rattus norvegicus	208-216
25461564-6	2014	Our data revealed that BPA exposure increased the protein and mRNA levels of cytochrome C, apoptosis-inducing factor, caspase-3/9, and Bax; caspase-3 and caspase-9 activities; and the apoptosis indices of spermatogenic cells.	bisphenol A	23-26	caspase 9	Rattus norvegicus	154-163
25859307-6	2014	Western blot analysis and quantitative real time RT-PCR showed that NSO treatment inhibited apoptosis stimulated by ethanol through decreasing the Bax/Bcl-2 ratio (both protein and mRNA levels), cleaved caspase-3, cleaved caspase-8 and cleaved caspase-9 level in liver and kidney.	nso	68-71	caspase 9	Rattus norvegicus	244-253
25859307-6	2014	Western blot analysis and quantitative real time RT-PCR showed that NSO treatment inhibited apoptosis stimulated by ethanol through decreasing the Bax/Bcl-2 ratio (both protein and mRNA levels), cleaved caspase-3, cleaved caspase-8 and cleaved caspase-9 level in liver and kidney.	Ethanol	116-123	caspase 9	Rattus norvegicus	244-253
24840537-11	2014	CONCLUSIONS: Stachydrine interfered with the endoplasmic reticulum stress mediated apoptosis pathway by decreasing caspase-12 expression and inhibiting caspase-9 activation.	stachydrine	13-24	caspase 9	Rattus norvegicus	152-161
25181333-7	2014	In addition, caspase-6, caspase-8 and caspase-9 labeling was present in SGN treated with 30 muM paclitaxel for 48 h. These results suggest that caspase-dependent apoptotic pathways are involved in paclitaxel-induced damage of SGN, but not hair cells in cochlea.	Paclitaxel	197-207	caspase 9	Rattus norvegicus	38-47
25066695-6	2014	Overexpression of miR-133, a recognized anti-apoptotic miRNA, produced similar effects to carvedilol: reduction of reactive oxygen species (ROS) and malondialdehyde (MDA) content and increment of superoxide dismutase (SOD) activity and glutathione peroxidase (GPx) level, so as to protect cardiomyocytes from apoptosis by downregulating caspase-9 and caspase-3 expression in the presence of H2O2.	mir-133	18-25	caspase 9	Rattus norvegicus	337-346
25066695-9	2014	In conclusion, our data indicated that carvedilol protected cardiomyocytes by increasing miR-133 expression and suppressing caspase-9 and subsequent apoptotic pathways.	Carvedilol	39-49	caspase 9	Rattus norvegicus	124-133
25331812-3	2014	The aim of this study was to investigate whether endoplasmic reticulum-related pathway is involved in single-prolonged stress (SPS) induced apoptosis in the mPFC of PTSD rats by examining the expression levels of ATF6 alpha (ATF6alpha), two important downstream molecular chaperones of ATF6alpha in the ER stress: Glucose-regulated protein (GRP) 78 and ERP57, and apoptotic factors caspase 12, caspase 9, and caspase 3.	Sodium phenolsulfonate	127-130	caspase 9	Rattus norvegicus	394-403
25331812-7	2014	Moreover, RT-PCR assays demonstrated that there were up-regulations in the transcripts levels of caspase 12, caspase 9, and caspase 3 in response to SPS, which were according with the proteins changes of these apoptotic factors and indicated that ER stress and the activation of caspases contributed to SPS.	Sodium phenolsulfonate	149-152	caspase 9	Rattus norvegicus	109-118
25331812-7	2014	Moreover, RT-PCR assays demonstrated that there were up-regulations in the transcripts levels of caspase 12, caspase 9, and caspase 3 in response to SPS, which were according with the proteins changes of these apoptotic factors and indicated that ER stress and the activation of caspases contributed to SPS.	Sodium phenolsulfonate	149-152	caspase 9	Rattus norvegicus	279-287
25331812-7	2014	Moreover, RT-PCR assays demonstrated that there were up-regulations in the transcripts levels of caspase 12, caspase 9, and caspase 3 in response to SPS, which were according with the proteins changes of these apoptotic factors and indicated that ER stress and the activation of caspases contributed to SPS.	Sodium phenolsulfonate	303-306	caspase 9	Rattus norvegicus	109-118
25066695-6	2014	Overexpression of miR-133, a recognized anti-apoptotic miRNA, produced similar effects to carvedilol: reduction of reactive oxygen species (ROS) and malondialdehyde (MDA) content and increment of superoxide dismutase (SOD) activity and glutathione peroxidase (GPx) level, so as to protect cardiomyocytes from apoptosis by downregulating caspase-9 and caspase-3 expression in the presence of H2O2.	Carvedilol	90-100	caspase 9	Rattus norvegicus	337-346
25172659-5	2014	Flow cytometric analysis showed that inhibition of the intrinsic pathway by a caspase-9 inhibitor (z-LEHD-fmk) significantly suppressed serum deprivation-induced apoptosis.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	99-109	caspase 9	Rattus norvegicus	78-87
25111692-6	2014	GM-induced apoptosis of NRK-52E cells, which was associated with an increased expression of mitochondrial Bax, cytosolic cytochrome c, and cleaved caspase-9 and -3, along with a decrease in bcl-2 expression, was also blocked by RGE.	Gentamicins	0-2	caspase 9	Rattus norvegicus	147-163
25014874-5	2014	DCF induced endoplasmic-reticulum (ER) stress, mitochondrial injury and oxidative stress were reflected by up-regulated HSP-70 (heat shock protein 70) and BiP (binding immunoglobulin protein) gene expression, caspase 9 activation, GSH (glutathione) depletion and HO-1 (heme oxygenase 1) gene up-regulation respectively.	Diclofenac	0-3	caspase 9	Rattus norvegicus	209-218
25087465-7	2014	There were fewer TUNEL-positive cells and caspase-3 and caspase-9 expressions were weaker in the inner and outer hairy cells of the organ of Corti in the gentamicin plus thymoquinone group compared with the group receiving gentamicin alone.	Gentamicins	154-164	caspase 9	Rattus norvegicus	56-65
25190658-6	2014	Caspase-9 activity was assessed by immunohistochemistry, Western blotting, and bVAD-fmk active caspase capture.	Biotin-VAD-FMK	79-87	caspase 9	Rattus norvegicus	0-9
25190658-9	2014	Photoreceptor death after commotio retinae was reduced by caspase-9 inhibition by using Pen-1-XBIR3, and electroretinographic measurements of photoreceptor function was preserved, providing structural and functional neuroprotection.	pen-1-xbir3	88-99	caspase 9	Rattus norvegicus	58-67
25087465-7	2014	There were fewer TUNEL-positive cells and caspase-3 and caspase-9 expressions were weaker in the inner and outer hairy cells of the organ of Corti in the gentamicin plus thymoquinone group compared with the group receiving gentamicin alone.	thymoquinone	170-182	caspase 9	Rattus norvegicus	56-65
25158646-3	2014	The objective of the present study was to determine the effects of NaF treatment on renal cell apoptosis, DNA damage, and the protein expression levels of cytosolic cytochrome C (Cyt C) and cleaved caspases 9, 8, and 3 in vivo.	Sodium Fluoride	67-70	caspase 9	Rattus norvegicus	198-218
25128772-7	2014	Immunohistochemical examinations showed that naringenin significantly reduced the gentamicin-induced expression of kidney injury molecule-1, vascular endothelial growth factor, inducible nitric oxide synthase, and caspase-9, and increased survivin expression in the kidney tissue.	naringenin	45-55	caspase 9	Rattus norvegicus	214-223
25128772-7	2014	Immunohistochemical examinations showed that naringenin significantly reduced the gentamicin-induced expression of kidney injury molecule-1, vascular endothelial growth factor, inducible nitric oxide synthase, and caspase-9, and increased survivin expression in the kidney tissue.	Gentamicins	82-92	caspase 9	Rattus norvegicus	214-223
25158646-9	2014	In addition, NaF treatment increased the protein expression levels of cytosolic Cyt C and cleaved caspases 9, 8, and 3.	Sodium Fluoride	13-16	caspase 9	Rattus norvegicus	98-118
25064822-7	2014	KEY FINDINGS: Sodium nitrite resulted in increased TNF-alpha (1.6-fold), IL-1beta (3.7-fold) and CRP (2.4-fold) levels accompanied by 52%, 59% and 40% reductions in IL-10, IL-4 and cytochrome-C-oxidase, respectively, as well as enhanced JNK, caspase-3, caspase-8 and caspase-9 activities.	Sodium Nitrite	14-28	caspase 9	Rattus norvegicus	267-276
25511266-0	2014	[Roles of cytochrome c, caspase-9, and caspase-3 in pentavalent vanadium-induced neuronal apoptosis].	Vanadium	64-72	caspase 9	Rattus norvegicus	24-33
24755084-5	2014	Caspase-mediated apoptosis pathway contributed importantly to PQ toxicity, as revealed by the activation of caspase-9/-3, cleavage of PARP, and regulation of Bcl-2 and Bax, which were also effectively blocked by beta-HB.	Paraquat	62-64	caspase 9	Rattus norvegicus	108-117
24795108-4	2014	Ethanol-induced apoptotic neurodegeneration was measured via the suppression of Bcl-2, the induction of Bax, the release of cytochrome C and the activation of caspase-9 and caspase-3.	Ethanol	0-7	caspase 9	Rattus norvegicus	159-168
24795108-6	2014	Our results demonstrated the neuroprotective effect of apomorphine by reversing the ethanol-induced apoptotic trend as observed by the increased expression of Bcl-2, down regulation of Bax, inhibition of mitochondrial cytochrome C release and inhibition of activated caspase-9 and caspase-3.	Apomorphine	55-66	caspase 9	Rattus norvegicus	267-276
24795108-6	2014	Our results demonstrated the neuroprotective effect of apomorphine by reversing the ethanol-induced apoptotic trend as observed by the increased expression of Bcl-2, down regulation of Bax, inhibition of mitochondrial cytochrome C release and inhibition of activated caspase-9 and caspase-3.	Ethanol	84-91	caspase 9	Rattus norvegicus	267-276
28962222-8	2014	EGCG also effectively attenuated fluoride-induced renal apoptosis by the up-regulation of anti-apoptotic proteins such as Bcl-2 and down-regulation of Bax, caspase-3, caspase-9 and cytochrome c. Histology and immunohistochemical observations of Kim-1 provided further evidence that EGCG effectively protects the kidney from fluoride-mediated oxidative damage.	epigallocatechin gallate	0-4	caspase 9	Rattus norvegicus	167-176
24604207-9	2014	The data revealed that HES attenuated the activation of capase-3 and caspase-9.	hesperetin	23-26	caspase 9	Rattus norvegicus	69-78
24591003-4	2014	The authors discovered that Zn supplementation inhibited high glucose (HG)-induced NRK-52E cell apoptosis by attenuating reactive oxygen species production, inhibiting HG-induced caspase-3 and caspase-9 activation, and inhibiting the release of cytochrome c from mitochondria to the cytosol.	Zinc	28-30	caspase 9	Rattus norvegicus	193-202
24591003-4	2014	The authors discovered that Zn supplementation inhibited high glucose (HG)-induced NRK-52E cell apoptosis by attenuating reactive oxygen species production, inhibiting HG-induced caspase-3 and caspase-9 activation, and inhibiting the release of cytochrome c from mitochondria to the cytosol.	Glucose	62-69	caspase 9	Rattus norvegicus	193-202
24682240-6	2014	Then PC-12 cells were incubated with agomelatine and duloxetine for 24 h. Treatment of cultured PC-12 cells with agomelatine, duloxetine, and their combination results in a protection on apoptosis, caspase-3, caspase-9, mitochondrial membrane depolarization, cytosolic ROS production, glutathione peroxidase, reduced glutathione, and lipid peroxidation, values.	agomelatine	37-48	caspase 9	Rattus norvegicus	209-218
24682240-6	2014	Then PC-12 cells were incubated with agomelatine and duloxetine for 24 h. Treatment of cultured PC-12 cells with agomelatine, duloxetine, and their combination results in a protection on apoptosis, caspase-3, caspase-9, mitochondrial membrane depolarization, cytosolic ROS production, glutathione peroxidase, reduced glutathione, and lipid peroxidation, values.	Duloxetine Hydrochloride	126-136	caspase 9	Rattus norvegicus	209-218
25151729-8	2014	Simultaneously, Vam3 could upregulate the expression of SIRT1, deacetylate p53, and inhibit the cleavage of caspase 9 and caspase 3 (P &lt; 0.01) of rat articular chondrocytes exposed to SNP.	vam3	16-20	caspase 9	Rattus norvegicus	108-117
28962222-8	2014	EGCG also effectively attenuated fluoride-induced renal apoptosis by the up-regulation of anti-apoptotic proteins such as Bcl-2 and down-regulation of Bax, caspase-3, caspase-9 and cytochrome c. Histology and immunohistochemical observations of Kim-1 provided further evidence that EGCG effectively protects the kidney from fluoride-mediated oxidative damage.	Fluorides	33-41	caspase 9	Rattus norvegicus	167-176
24519986-8	2014	Although caspase-9 mRNA was increased in the SeT of Tg-RGN treated with Thap, no differences were observed at protein level, and no differences were also found on protein levels of apoptosis-inducing factor.	Thapsigargin	72-76	caspase 9	Rattus norvegicus	9-18
24646838-6	2014	Western blot assay showed that in vivo Atg7siRNA transfection not only reduced Atg7 levels in the MPP+-infused SN but attenuated MPP+-induced elevation in LC3-II levels, activation of caspase 9 and reduction in tyrosine hydroxylase levels, indicating that autophagy is pro-death.	mangion-purified polysaccharide (Candida albicans)	129-133	caspase 9	Rattus norvegicus	184-193
24294888-8	2014	VPA also inhibited cytochrome c release and caspase-9 activation, which was significantly inhibited by SP600125, a JNK inhibitor.	pyrazolanthrone	103-111	caspase 9	Rattus norvegicus	44-53
24276417-11	2014	The protein expressions of Bcl-2, Bax, Caspase-8, Caspase-9 and Caspase-3 were significantly increased in response to Bosentan treatment after IR.	Bosentan	118-126	caspase 9	Rattus norvegicus	50-59
24170279-3	2014	Ginsenoside Rg1 also reversed the increased caspase-9 and -3 mRNA levels caused by colistin in PC12 cells.	Ginsenosides	0-11	caspase 9	Rattus norvegicus	44-60
23839155-6	2014	Further analysis showed that B[a]P-induced apoptosis was accompanied by loss of mitochondrial membrane potential, release of cytochrome c from mitochondria to the cytosol, downregulation of antiapoptotic protein B-cell lymphoma-2 (Bcl-2) levels with concurrent upregulation in proapoptotic Bcl-2-associated X protein (Bax) levels, and increase in the levels and activities of caspases-9 and -3.	Benzo(a)pyrene	29-34	caspase 9	Rattus norvegicus	376-393
24534601-5	2014	The results showed that obestatin had no effect on GPR39 expression, while promotes the optical density (OD) value of cells, enhanced protein expression of PPARgamma and C/EBPa, decreased mRNA expression and activity of Caspase-3, and inhibited protein expression of Caspase-7 and Caspase-9 in a dose-dependent manner.	Ghrelin	24-33	caspase 9	Rattus norvegicus	281-290
24586539-6	2014	High glucose stress increased Bax/Bcl2 ratio followed by mitochondrial depolarization and activation of caspase-9/-3 confirming involvement of mitochondrial pathway of apoptosis in the exposed cells.	Glucose	5-12	caspase 9	Rattus norvegicus	104-113
24534601-6	2014	These results suggested that obestatin enhances proliferation and differentiation of preadipocytes promoting PPARgamma and C/EBPa expression, and inhibiting preadipocyte apoptosis by decreasing expression of Caspase-3, Caspase-7 and Caspase-9.	Ghrelin	29-38	caspase 9	Rattus norvegicus	233-242
24396410-7	2014	The caspase inhibitor z-VAD-fmk reduced the expression and activation of caspase-3, caspase-8 and caspase-9 in the irradiated rats, indicating that caspase may be a potential therapeutic target in the treatment of brain radiation injury.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	22-31	caspase 9	Rattus norvegicus	98-107
24231470-6	2014	The down-regulated Bcl-2 mRNA level and up-regulated Bax, Caspase-9, and Caspase-3 mRNA expression induced by H2O2 or t-BHP could be restored by EPA-enriched PL pretreatment.	Hydrogen Peroxide	110-114	caspase 9	Rattus norvegicus	58-67
24317498-9	2014	Downregulation of the Bcl-2 protein and upregulation of Bax, cleaved caspase-9, -12 and -3 proteins suggested that NaF was capable of inducing apoptosis through the mitochondrial and endoplasmic reticulum pathways.	Sodium Fluoride	115-118	caspase 9	Rattus norvegicus	69-90
24225258-4	2014	Moreover, the activities of caspase-9, caspase-8 and caspase-3 all were increased in H2O2-induced PC12 cells.	Hydrogen Peroxide	85-89	caspase 9	Rattus norvegicus	28-37
25028668-7	2014	Ceftriaxone attenuated the increased levels of Bax and cleaved forms of caspases 3 and 9, while it increased Bcl2 levels.	Ceftriaxone	0-11	caspase 9	Rattus norvegicus	72-88
25301366-8	2014	In addition, PQS protected the mitochondrial structure, markedly inhibited mPTP opening and DeltaPsim depolarization, led to upregulation of Bcl-2 and downregulation of Bax in the mitochondria compared to the cytosol, and suppressed the expression of cleaved caspase-9 and cleaved caspase-3, as well as I/R induced translocation of cytochrome c to the cytoplasm.	Panax quinquefolium saponin	13-16	caspase 9	Rattus norvegicus	259-268
23848144-0	2014	Arsanilic acid causes apoptosis and oxidative stress in rat kidney epithelial cells (NRK-52e cells) by the activation of the caspase-9 and -3 signaling pathway.	Arsanilic Acid	0-14	caspase 9	Rattus norvegicus	125-141
23848144-9	2014	Collectively, these results suggest that arsanilic acid causes apoptosis and oxidative stress in rat kidney epithelial cells through activation of the caspase-9 and -3 signaling pathway.	Arsanilic Acid	41-55	caspase 9	Rattus norvegicus	151-167
25535124-7	2014	Flow cytometry revealed a loss of DeltaPsim and Western Blot displayed Caspase-9/3 activation as well as Cyt c release from mitochondria to the the cytosol after the treatment of roxithromycin.	Roxithromycin	179-192	caspase 9	Rattus norvegicus	71-80
24672637-6	2014	We demonstrate that MG can uphold viability of neonatal rat cardiomyocytes exposed to H2O2 by diminishing intracellular ROS, maintaining mitochondrial membrane potential, augmenting endogenous glutathione, and reducing apoptosis as evidenced by impaired Annexin V/PI staining, prevention of DNA fragmentation, and cleaved caspase-9 accumulation.	methyl gallate	20-22	caspase 9	Rattus norvegicus	322-331
24231470-6	2014	The down-regulated Bcl-2 mRNA level and up-regulated Bax, Caspase-9, and Caspase-3 mRNA expression induced by H2O2 or t-BHP could be restored by EPA-enriched PL pretreatment.	tert-Butylhydroperoxide	118-123	caspase 9	Rattus norvegicus	58-67
24349525-13	2013	The resveratrol-associated improvement in type II fiber size and muscle mass recovery after disuse may have been due to decreases in the abundance of pro-apoptotic proteins Bax, cleaved caspase 3 and cleaved caspase 9 in reloaded muscles.	Resveratrol	4-15	caspase 9	Rattus norvegicus	208-217
24564120-7	2014	The average optical density value of Caspase-3, Caspase-8, Caspase-9 and Cyt C were higher in the fluoride exposed middle dose group and high dose group than those in the control group (P &lt; 0.05).	Fluorides	98-106	caspase 9	Rattus norvegicus	59-68
24190484-7	2013	The expression levels of Cyt-c, caspase-3, caspase-9 and pJNK proteins in brain of CIR + Remifentanil group rats were found to significantly decreased compared to CIR group rats.	Citrulline	83-86	caspase 9	Rattus norvegicus	43-52
24190484-7	2013	The expression levels of Cyt-c, caspase-3, caspase-9 and pJNK proteins in brain of CIR + Remifentanil group rats were found to significantly decreased compared to CIR group rats.	Remifentanil	89-101	caspase 9	Rattus norvegicus	43-52
23906897-7	2013	Exposure to metal mixture resulted in a significant decrease in the activity levels of antioxidant enzymes such as manganese-superoxide dismutase (Mn-SOD), Cu/Zn superoxide dismutase (Cu/Zn-SOD), catalase (CAT) and glutathione peroxidase (GPx) while the malondialdehyde (MDA) levels and mRNA expression levels of caspase-3 and caspase-9 were significantly increased in all the three brain regions.	Metals	12-17	caspase 9	Rattus norvegicus	327-336
24061869-10	2013	They also inhibited H2O2-induced mitochondrial membrane depolarization and caspase-9 activation by 27% (P &lt; 0.034) and 50% (P &lt; 0.05), respectively.	Hydrogen Peroxide	20-24	caspase 9	Rattus norvegicus	75-84
24061869-11	2013	This study suggests that the major CHAs found in coffee are likely to be potent antioxidant compounds able to quench radical species as well as inhibit H2O2-induced apoptosis via suppressing mitochondrial membrane depolarization and caspase-9 activation in the cells.	Hydrogen Peroxide	152-156	caspase 9	Rattus norvegicus	233-242
23927876-5	2013	The mechanistic study revealed that the extent of apoptosis was greater for DBT than that for DPT, followed by DMT, as evidenced by acridine orange/ethidium bromide (AO/EB) fluorescent staining method and annexin V-FITC/PI staining flow cytometry analysis, as well as generation of intracellular reactive oxygen species (ROS), mitochondrial membrane potential (MMP) disruption, release of cytochrome c (Cyt c), and consequent activation of caspase-9, and -3.	di-n-butyltin	76-79	caspase 9	Rattus norvegicus	440-457
24483119-11	2013	Besides, the average gray scale of Caspase-9 was significantly higher in the low and middle FSN groups than in the TPT group (P &lt; 0.05, P &lt; 0.01).	1oyt	92-95	caspase 9	Rattus norvegicus	35-44
24483119-11	2013	Besides, the average gray scale of Caspase-9 was significantly higher in the low and middle FSN groups than in the TPT group (P &lt; 0.05, P &lt; 0.01).	tpt	115-118	caspase 9	Rattus norvegicus	35-44
23993482-7	2013	Immunohistochemical analysis revealed that cannabidiol significantly decreased the cadmium-induced expression of tumor necrosis factor-alpha, cyclooxygenase-2, nuclear factor-kappaB, caspase-3, and caspase-9, and increased the expression of endothelial nitric oxide synthase in liver tissue.	Cannabidiol	43-54	caspase 9	Rattus norvegicus	198-207
23993482-7	2013	Immunohistochemical analysis revealed that cannabidiol significantly decreased the cadmium-induced expression of tumor necrosis factor-alpha, cyclooxygenase-2, nuclear factor-kappaB, caspase-3, and caspase-9, and increased the expression of endothelial nitric oxide synthase in liver tissue.	Cadmium	83-90	caspase 9	Rattus norvegicus	198-207
23692127-5	2013	The results showed that 1 and 10 microM/mL ascorbic acid significantly increased the cell viability and the levels of SOD and GSH (both p&lt;0.05), while 0.1, 1 and 10 microM/mL ascorbic acid significantly decreased the generation of ROS, the release of cytochrome-c, formation of DNA fragmentation and the expressions of caspase-9 and -3 mRNA in colistin-treated PC12 cells, compared with the colistin model group.	Ascorbic Acid	43-56	caspase 9	Rattus norvegicus	322-338
23792322-3	2013	The results showed that GSNO pre-treatment not only facilitated the survival of hippocampal CA1 pyramidal neurons, but also abolished the activation of pro-apoptotic Caspase-8, Bid, Caspase-9 and Caspase-3.	S-Nitrosoglutathione	24-28	caspase 9	Rattus norvegicus	182-191
24166606-12	2013	Taken together, the results obtained in this study seem to confirm the neuroprotective effect of memantine on increasing levels of cells with active caspase-3 and active caspase-9.	Memantine	97-106	caspase 9	Rattus norvegicus	170-179
23729662-5	2013	Oxysterols treatment led to the activation of the mitochondrial pathway of apoptosis (cytochrome c release and caspase-9 cleavage) and mitochondrial ROS formation, which were suppressed by the pharmacological inhibition or knockdown of sAC.	Oxysterols	0-10	caspase 9	Rattus norvegicus	111-120
23605682-6	2013	Western blots demonstrated activation of caspase-3 and caspase-9, and their increased expression levels in rotenone-treated cells; betaine decreased caspase-3 and caspase-9 expression levels and suppressed their activation.	Rotenone	107-115	caspase 9	Rattus norvegicus	55-64
23861072-8	2013	In addition, MDHB could increase the level of Bcl-2, decrease the level of Bax, and inhibit the activation of caspase-9 and caspase-3 in Abeta25-35 -treated primary cortical neurons.	methyl 3,4-dihydroxybenzoate	13-17	caspase 9	Rattus norvegicus	110-119
21793157-5	2013	(2) A 24 h treatment of LaCl3 concentration-dependently decreased mitochondrial membrane potential, increased cytochrome c release from mitochondria into cytosol, elevated caspase 9 and 3 expression, and promoted astrocyte apoptosis.	lanthanum chloride	24-29	caspase 9	Rattus norvegicus	172-187
23946597-8	2013	However, pretreatment with pentoxifylline or infliximab dramatically suppressed I/R-induced mucosal injury and cell apoptosis and significantly inhibited the activation of caspase-9/3 and JNK signaling.	Pentoxifylline	27-41	caspase 9	Rattus norvegicus	172-181
23402272-0	2013	Diosmin protects against trichloroethylene-induced renal injury in Wistar rats: plausible role of p53, Bax and caspases.	Diosmin	0-7	caspase 9	Rattus norvegicus	111-119
24010200-4	2013	RESULTS: Compared with the DMSO control group, the low-, medium- and high-dose DEHP groups showed significantly upregulated expressions of Caspase-3 mRNA (1.69 +/- 0.38 vs 3.82 +/- 0.39, 6.91 +/- 0.40 and 15.47 +/- 0.40, P &lt; 0.05), Caspase-3 protein (0.18 +/- 0.0.09 vs 0.32 +/- 0.10, 0.61 +/- 0.08 and 0.89 +/- 0.09, P &lt; 0.05), Caspase-9 mRNA (2.24 +/- 0.41 vs 5.16 +/- 0.43, 9.61 +/- 0.45 and 19.22 +/- 0.43, P &lt; 0.05) and Caspase-9 protein (0.26 +/- 0.07 vs 0.40 +/- 0.08, 0.68 +/- 0.09 and 0.96 +/- 0.08, P &lt; 0.05), as well as increased apoptosis rate of Leydig cells (4.36 +/- 1.11 vs 7.52 +/- 1.09, 12.72 +/- 1.10 and 24.59 +/- 1.11, P &lt; 0.05), all in a dose-dependent manner.	Diethylhexyl Phthalate	79-83	caspase 9	Rattus norvegicus	335-344
24010200-4	2013	RESULTS: Compared with the DMSO control group, the low-, medium- and high-dose DEHP groups showed significantly upregulated expressions of Caspase-3 mRNA (1.69 +/- 0.38 vs 3.82 +/- 0.39, 6.91 +/- 0.40 and 15.47 +/- 0.40, P &lt; 0.05), Caspase-3 protein (0.18 +/- 0.0.09 vs 0.32 +/- 0.10, 0.61 +/- 0.08 and 0.89 +/- 0.09, P &lt; 0.05), Caspase-9 mRNA (2.24 +/- 0.41 vs 5.16 +/- 0.43, 9.61 +/- 0.45 and 19.22 +/- 0.43, P &lt; 0.05) and Caspase-9 protein (0.26 +/- 0.07 vs 0.40 +/- 0.08, 0.68 +/- 0.09 and 0.96 +/- 0.08, P &lt; 0.05), as well as increased apoptosis rate of Leydig cells (4.36 +/- 1.11 vs 7.52 +/- 1.09, 12.72 +/- 1.10 and 24.59 +/- 1.11, P &lt; 0.05), all in a dose-dependent manner.	Diethylhexyl Phthalate	79-83	caspase 9	Rattus norvegicus	434-443
23605682-6	2013	Western blots demonstrated activation of caspase-3 and caspase-9, and their increased expression levels in rotenone-treated cells; betaine decreased caspase-3 and caspase-9 expression levels and suppressed their activation.	Rotenone	107-115	caspase 9	Rattus norvegicus	163-172
23605682-6	2013	Western blots demonstrated activation of caspase-3 and caspase-9, and their increased expression levels in rotenone-treated cells; betaine decreased caspase-3 and caspase-9 expression levels and suppressed their activation.	Betaine	131-138	caspase 9	Rattus norvegicus	163-172
23608114-5	2013	The increased level of H2O2 was associated with the increased caspase-9 and caspase-3 activities.	Hydrogen Peroxide	23-27	caspase 9	Rattus norvegicus	62-71
23884672-0	2013	Effects of combined and individual use of N-methyl-D aspartate receptor antagonist magnesium sulphate and caspase-9 inhibitor z-LEDH-fmk in experimental spinal cord injury.	Z-LEDH-fmk	126-136	caspase 9	Rattus norvegicus	106-115
23503638-9	2013	Compared with those of 10 % FBS, caspase-9 and -3 activities and cleavage of Bid and cytochrome-c were significantly increased in each three high glucose concentrations, accompanied by increased expression of MMP-1, -2, -3, -7, -9, and -13 and TIMP-1 and -2.	Glucose	146-153	caspase 9	Rattus norvegicus	33-49
24570931-6	2013	However, lipid peroxidation and CYP2E1, caspase-9, and -3 expressions were significantly lower and Bcl-xL expression was higher in the ELB group.	4-(4-azanyl-2-oxidanylidene-3~{H}-benzimidazol-1-yl)-~{N}-(4-iodophenyl)piperidine-1-carboxamide	135-138	caspase 9	Rattus norvegicus	40-57
24421747-5	2013	RESULTS: Lead acetate significantly increased the levels of caspase 8, caspase 9 and Bax in liver, kidney and brain of experimental animals especially those with high doses.	Acetates	14-21	caspase 9	Rattus norvegicus	71-80
24010200-1	2013	OBJECTIVE: To investigate the effects of di-(2-ethylhexyl) phthalate (DEHP) on the expressions of Caspase-3 and Caspase-9 genes in rat Leydig cells and the apoptosis of the cells in vitro.	Diethylhexyl Phthalate	41-68	caspase 9	Rattus norvegicus	112-121
24010200-1	2013	OBJECTIVE: To investigate the effects of di-(2-ethylhexyl) phthalate (DEHP) on the expressions of Caspase-3 and Caspase-9 genes in rat Leydig cells and the apoptosis of the cells in vitro.	Diethylhexyl Phthalate	70-74	caspase 9	Rattus norvegicus	112-121
23611999-9	2013	In vascular endothelial cells, artesunate increased the Bax/Bcl-2 ratio, reduced mitochondrial membrane potential, stimulated release of cytochrome C, and cleavage of caspase 9 and 3, suggesting that the mitochondrial apoptotic pathway was involved.	Artesunate	31-41	caspase 9	Rattus norvegicus	167-182
23545180-7	2013	In an in vivo study, in which rat retinal damage was induced by intravitreal injection of N-methyl-d-aspartate (NMDA), bakuchiol markedly reduced translocation of AIF and release of cytochrome c, and inhibited up-regulation of cleaved caspase-3, cleaved caspase-9, and cleaved PARP.	N-Methylaspartate	112-116	caspase 9	Rattus norvegicus	254-263
23545180-7	2013	In an in vivo study, in which rat retinal damage was induced by intravitreal injection of N-methyl-d-aspartate (NMDA), bakuchiol markedly reduced translocation of AIF and release of cytochrome c, and inhibited up-regulation of cleaved caspase-3, cleaved caspase-9, and cleaved PARP.	bakuchiol	119-128	caspase 9	Rattus norvegicus	254-263
23545180-9	2013	Moreover, bakuchiol attenuated ONC-induced up-regulation of apoptotic proteins, including cleaved PARP, cleaved caspase-3, and cleaved caspase-9.	bakuchiol	10-19	caspase 9	Rattus norvegicus	135-144
23683031-10	2013	CsA increased the protein expression of bax, cleaved caspase-9, caspase-3 and the activity of caspase-3; however, the anti-apoptotic bcl-2 protein was reduced.	Cyclosporine	0-3	caspase 9	Rattus norvegicus	53-62
23862406-0	2013	Zinc oxide nanoparticles induce rat retinal ganglion cell damage through bcl-2, caspase-9 and caspase-12 pathways.	Zinc Oxide	0-10	caspase 9	Rattus norvegicus	80-89
23862406-6	2013	Moreover, our results also demonstrated that the overproduction of reactive oxygen species (ROS) and elevated level of caspase-12 as well as decreased levels of bcl-2 and caspase-9 occurred after treatment with different concentrations of ZnO nanoparticles when compared to those in untreated cells.	Zinc Oxide	239-242	caspase 9	Rattus norvegicus	171-180
23862406-7	2013	In summary, our findings suggest that ZnO nanoparticles could lead to the over generations of ROS and caspase-12 as well as decreased levels of bcl-2 and caspase-9.	Zinc Oxide	38-41	caspase 9	Rattus norvegicus	154-163
23167626-9	2013	Our results suggest that damage to regions of the proximal tubules is dose-related, and caspase-9-dependent, mitochondria-related apoptotic cell death could play an important role in permethrin-induced nephrotoxicity.	Permethrin	183-193	caspase 9	Rattus norvegicus	88-97
23443133-9	2013	Furthermore, western blot analysis showed that propofol treatment significantly elevated levels of active forms of caspase-3, caspase-8, caspase-9 and cytochrome C in the embryonic neural stem cells.	Propofol	47-55	caspase 9	Rattus norvegicus	137-146
23443133-10	2013	Propofol induced rat embryonic neural stem cell apoptosis and activated caspase-3, caspase-8, caspase-9 and cytochrome C, suggesting that propofol-induced stem cell apoptosis may be regulated through both the extrinsic and intrinsic apoptotic pathways.	Propofol	0-8	caspase 9	Rattus norvegicus	94-103
23443133-10	2013	Propofol induced rat embryonic neural stem cell apoptosis and activated caspase-3, caspase-8, caspase-9 and cytochrome C, suggesting that propofol-induced stem cell apoptosis may be regulated through both the extrinsic and intrinsic apoptotic pathways.	Propofol	138-146	caspase 9	Rattus norvegicus	94-103
23475456-7	2013	Furthermore, hesperidin inhibited mitochondria-dependent downstream caspase-mediated apoptotic pathway, such as that involving caspase-9 and caspase-3.	Hesperidin	13-23	caspase 9	Rattus norvegicus	127-136
25206391-5	2013	These findings indicate that extracts from rabbit skin inflamed by the vaccinia virus can attenuate neurotoxicity induced by intrathecal injection of bupivacaine in pregnant rats, possibly by inhibiting caspase-9 protein expression and suppressing nerve cell apoptosis.	Bupivacaine	150-161	caspase 9	Rattus norvegicus	203-212
23266522-8	2013	Furthermore, the activities of SOD and GSH in rat hippocampal tissue were found to have increased with a concomitant reduction in MDA levels, Bax expression, cytochrome c release, and the activity of caspase-9/3.	Glutathione	39-42	caspase 9	Rattus norvegicus	200-211
22819561-4	2013	Furthermore, Piperine treatment diminished cytochrome-c release from mitochondria and reduced caspase-3 and caspase-9 activation induced by 6-OHDA.	piperine	13-21	caspase 9	Rattus norvegicus	108-117
22819561-4	2013	Furthermore, Piperine treatment diminished cytochrome-c release from mitochondria and reduced caspase-3 and caspase-9 activation induced by 6-OHDA.	Oxidopamine	140-146	caspase 9	Rattus norvegicus	108-117
23530988-15	2013	Intrinsic caspase 9 activity was inhibited by estradiol, and by xenoestrogen combinations (at 10-14 and 10-8 M).	Estradiol	46-55	caspase 9	Rattus norvegicus	10-19
23458715-11	2013	Earlier activation of caspase 8 versus caspase 9 demonstrated that BPS initiates apoptosis via the extrinsic pathway, consistent with activation via a membrane receptor.	bis(4-hydroxyphenyl)sulfone	67-70	caspase 9	Rattus norvegicus	39-48
23069749-10	2013	Treatment with brimonidine protected SGNs against glutamate- or H(2)O(2)-induced cell damage, enhanced SGNs survival, decreased the elevation of Bax, Caspase-9, Caspase-3, p-ERK1/2, and artemin triggered by glutamate or H(2)O(2), and altered the expressions of Bcl-2 and iNOS.	Brimonidine Tartrate	15-26	caspase 9	Rattus norvegicus	150-159
23470917-7	2013	Significant differences in the expressions of caspase-3, and caspase-9 was also noted between training group and HP group, but there was no marked difference in the expressions of ICAM-1, VCAM-1 and PECAM-1 between these two groups.	Hematoporphyrins	113-115	caspase 9	Rattus norvegicus	61-70
23041257-5	2013	PC12 cell apoptosis induced by DBDCT was confirmed by annexin V/propidium iodide staining, and characterized by cleavage of caspase-9 and caspase-3 proteins.	dbdct	31-36	caspase 9	Rattus norvegicus	124-133
23041257-9	2013	In rats exposed to DBDCT, apoptosis was also observed in brain, as shown by the detection of cleaved caspase-9 and caspase-3 proteins and increased TUNEL positive staining.	dbdct	19-24	caspase 9	Rattus norvegicus	101-110
23611046-8	2013	In the fasting+histamine group, caspase-3 and caspase-9 immunostaining was significantly positive in both renal tubules and glomeruli (p&lt;0.05).	Histamine	15-24	caspase 9	Rattus norvegicus	46-55
24117073-5	2013	Treatment of genistein could suppress the expression of mitochondrial pro-apoptotic proteins including Bad, caspase-8, caspase-9, and caspase-3 in H9c2 treated with ISO.	Genistein	13-22	caspase 9	Rattus norvegicus	119-128
23192364-5	2013	Enhanced translocation of Cyt-c from mitochondria to cytosol and AIF/Endo-G from mitochondria to nucleus, activation of caspase-9/3, DNA damage, and chromatin condensation were observed in glucose-stressed hepatocytes, indicating the involvement of mitochondrial pathway in high glucose-induced apoptosis.	Glucose	189-196	caspase 9	Rattus norvegicus	120-129
22189415-6	2012	When cochlear organotypic cultures prepared from P5 rats were treated with kanamycin, TAT-FNK significantly reduced the extent of caspase-9 activation and HC death.	Kanamycin	75-84	caspase 9	Rattus norvegicus	130-139
23573126-3	2013	The cardioprotective effects of quercetin are achieved by reducing the activity of Src kinase, signal transducer and activator of transcription 3 (STAT3), caspase 9, Bax, intracellular reactive oxygen species production, and inflammatory factor and inducible MnSOD expression.	Quercetin	32-41	caspase 9	Rattus norvegicus	155-164
23092809-5	2013	Studies on the mechanism of apoptosis showed that ALX accelerated the markers of mitochondrial dependent apoptotic pathway (enhanced cytochrome C release in cytosol from mitochondria, altered the expression of Bax, Bcl-2, Apaf-1, caspase-9, caspase-3).	Alloxan	50-53	caspase 9	Rattus norvegicus	230-239
24008351-8	2013	On the other hand, GGA prevented the methamphetamine-induced increases in the enzymatic activity of caspase-9 and caspase-3.	Methamphetamine	37-52	caspase 9	Rattus norvegicus	100-109
23281070-5	2012	Whereas simultaneous treatment with quercetin normalized all the biochemical parameters, consequently it inhibited apoptosis mediated by Aroclor-1254 by downregulating aryl hydrocarbon receptor, p53 and apoptotic protein (Bax, caspase-9, caspase-3) and upregulating the antiapoptotic protein (Bcl-2) expression patterns; thereby, quercetin reduces alteration in hepatocellular morphology.	Quercetin	36-45	caspase 9	Rattus norvegicus	227-236
22978712-0	2012	Lycopene counteracts the hepatic response to 7,12-dimethylbenz[a]anthracene by altering the expression of Bax, Bcl-2, caspases, and oxidative stress biomarkers.	Lycopene	0-8	caspase 9	Rattus norvegicus	118-126
22978712-0	2012	Lycopene counteracts the hepatic response to 7,12-dimethylbenz[a]anthracene by altering the expression of Bax, Bcl-2, caspases, and oxidative stress biomarkers.	9,10-Dimethyl-1,2-benzanthracene	45-75	caspase 9	Rattus norvegicus	118-126
22978712-4	2012	OBJECTIVE: In this study, we report the effect of lycopene on 7,12-dimethylbenz[a]-anthracene (DMBA)-induced expression of Bax, Bcl-2, caspases, and oxidative stres biomarkers in the liver.	Lycopene	50-58	caspase 9	Rattus norvegicus	135-143
22978712-4	2012	OBJECTIVE: In this study, we report the effect of lycopene on 7,12-dimethylbenz[a]-anthracene (DMBA)-induced expression of Bax, Bcl-2, caspases, and oxidative stres biomarkers in the liver.	7,12-dimethylbenz[a]-	62-83	caspase 9	Rattus norvegicus	135-143
22978712-4	2012	OBJECTIVE: In this study, we report the effect of lycopene on 7,12-dimethylbenz[a]-anthracene (DMBA)-induced expression of Bax, Bcl-2, caspases, and oxidative stres biomarkers in the liver.	anthracene	83-93	caspase 9	Rattus norvegicus	135-143
22978712-4	2012	OBJECTIVE: In this study, we report the effect of lycopene on 7,12-dimethylbenz[a]-anthracene (DMBA)-induced expression of Bax, Bcl-2, caspases, and oxidative stres biomarkers in the liver.	9,10-Dimethyl-1,2-benzanthracene	95-99	caspase 9	Rattus norvegicus	135-143
22978712-8	2012	RESULTS: We observed that the levels of Bax, caspase-3, and caspase-9 decreased to 44, 67, and 43%, respectively, and Bcl-2 increased by 80% in DMBA-treated rats.	9,10-Dimethyl-1,2-benzanthracene	144-148	caspase 9	Rattus norvegicus	60-69
22978712-10	2012	Lycopene increased the expression of caspase-3 (82.09%) and caspase-9 (58.96%), and attenuated the level of hepatic malondialdehyde (41%) and 8-isoprostane (40%) when compared to the respective controls.	Lycopene	0-8	caspase 9	Rattus norvegicus	60-69
22978712-13	2012	CONCLUSION: The study reports that lycopene counteracts the hepatic response to DMBA by altering the expression of Bax, Bcl-2, caspases, and oxidative stress biomarkers in animal model.	Lycopene	35-43	caspase 9	Rattus norvegicus	127-135
22978712-13	2012	CONCLUSION: The study reports that lycopene counteracts the hepatic response to DMBA by altering the expression of Bax, Bcl-2, caspases, and oxidative stress biomarkers in animal model.	9,10-Dimethyl-1,2-benzanthracene	80-84	caspase 9	Rattus norvegicus	127-135
22847887-6	2012	In NASH rats with IR liver injury, hepatic inflammation, necrosis, apoptosis, leukocyte infiltration, and microcirculatory dysfunction were significantly attenuated by the acute administration of sorafenib through the inhibition of the hepatic release of macrophage inflammatory protein 2, keratinocyte chemoattractant, granulocyte-monocyte colony-stimulating factor, and hepatic caspase-3 and caspase-9 as well as DNA fragmentation.	Sorafenib	196-205	caspase 9	Rattus norvegicus	394-403
23457494-8	2013	RESULTS: GA supplementation suppressed the development of precancerous lesions and it also reduced the infiltration of mast cells, suppressed the immunostaining of Ki-67, NF-kB-p65, COX-2, iNOS and VEGF while enhanced the immunostaining of p53, connexin-43, caspase-9 and cleaved caspase-3.	Glycyrrhizic Acid	9-11	caspase 9	Rattus norvegicus	258-267
22982719-9	2012	Decreased HIF-1alpha, caspase 9, caspase 3 and increased Bcl-2/Bax ratio were responsible for the anti-apoptosis of berberine pretreatment.	Berberine	116-125	caspase 9	Rattus norvegicus	22-31
23118555-5	2012	In addition, resveratrol dose-dependently and significantly downregulated the expression of anti-apoptotic protein includes Bcl-2, Bcl-xL and Mcl-1 and also activates cleavage caspase-9 and-3 via the downregulation of procaspase-9 and -3 in a dose-dependent manner which indicates that involvement of intrinsic mitochondria-mediated apoptotic pathway.	Resveratrol	13-24	caspase 9	Rattus norvegicus	176-191
23118555-6	2012	In conclusion, resveratrol increases cellular cytotoxicity and inhibits the proliferation of B103 neuroblastoma cells by inducing mitochondria-mediated intrinsic caspase dependent pathway which suggests this natural compound could be used as therapeutic purposes for neuroblastoma malignancies.	Resveratrol	15-26	caspase 9	Rattus norvegicus	162-169
22564900-4	2012	Western blotting results showed that CTN induced formation of processed p53, caspase-9, and caspase-3 proteins in a dose-dependent manner; CTN also induced a dose-dependent increase in caspase-3 catalytic activity.	Citrinin	37-40	caspase 9	Rattus norvegicus	77-86
22564900-6	2012	Taken together, these results suggested that CTN reduced testosterone secretion by inducing apoptosis in rat Leydig cells, a mechanism that might account for CTN stimulation of p53 expression followed by activation of multiple caspases.	Citrinin	45-48	caspase 9	Rattus norvegicus	227-235
22714038-2	2012	In this study we found that chlorpyrifos (CPF) induced apoptosis in dopaminergic neuronal components of PC12 cells as demonstrated by the activation of caspases and nuclear condensation.	Chlorpyrifos	28-40	caspase 9	Rattus norvegicus	152-160
22714038-2	2012	In this study we found that chlorpyrifos (CPF) induced apoptosis in dopaminergic neuronal components of PC12 cells as demonstrated by the activation of caspases and nuclear condensation.	Chlorpyrifos	42-45	caspase 9	Rattus norvegicus	152-160
22714038-5	2012	Importantly, N-acetyl cysteine (NAC) treatment effectively blocked apoptosis via the caspase-9 and caspase-3 pathways while NAC attenuated the inhibition of mitochondrial complex I activity as well as the oxidative metabolism of dopamine (DA).	Acetylcysteine	13-30	caspase 9	Rattus norvegicus	85-94
22714038-5	2012	Importantly, N-acetyl cysteine (NAC) treatment effectively blocked apoptosis via the caspase-9 and caspase-3 pathways while NAC attenuated the inhibition of mitochondrial complex I activity as well as the oxidative metabolism of dopamine (DA).	Acetylcysteine	32-35	caspase 9	Rattus norvegicus	85-94
22592642-5	2012	Danthron decreased the level of mitochondrial membrane potential (DeltaPsi( m )), stimulated the release of cytochrome c from mitochondria to cytosol and promoted the levels of caspase-9 and caspase-3, or induced the release of AIF and Endo G from mitochondria.	danthron	0-8	caspase 9	Rattus norvegicus	177-186
22710069-0	2012	Rotenone-induced parkinsonism elicits behavioral impairments and differential expression of parkin, heat shock proteins and caspases in the rat.	Rotenone	0-8	caspase 9	Rattus norvegicus	124-132
22710069-11	2012	Collectively, our studies indicated the following findings in the striatum and substantia nigra following chronic rotenone exposure in an experimental PD model: (i) behavioral deficit that correlated with histopathological changes and down regulation of TH signaling, (ii) decreased levels of the cytoprotective proteins parkin, DJ1 and Hsp70 and robust expression of mitochondrial chaperone Hsp60 according to Western blot, (iii) increased immunoreactivity for caspase 9, caspase 3 and ubiquitin and decreased parkin immunoreactivity.	Rotenone	114-122	caspase 9	Rattus norvegicus	462-471
22402252-11	2012	Key findings include elucidation of cell signaling mechanism of high-glucose induced calcium-dependent cysteine protease calpain-1 activation, which triggers non-conventional caspases as alternate mode of cell death.	Glucose	69-76	caspase 9	Rattus norvegicus	175-183
22369161-6	2012	Results illustrated that piroxicam and c-phycocyanin treatments stimulate cytochrome c release by downregulating the Bcl-2 (an antiapoptotic protein) expression significantly, while promoting the level of Bax (a proapoptotic protein), thereby activating caspases (caspases-9 and -3) and Apaf-1.	Piroxicam	25-34	caspase 9	Rattus norvegicus	254-262
22997880-8	2012	The liberation of cytochrome c from mitochondria to cytosol, the cleavages of the initiator caspase 9 and the effector caspase 3 have been observed after pretreatment with acrolein followed by H/ R in H9c2 cells.	Acrolein	172-180	caspase 9	Rattus norvegicus	92-101
22997880-9	2012	CONCLUSION: Acrolein could aggravate H/R injury and that this effect may be related, in part, to the modification of proteins involved the release of cytochrome c from mitochondria to cytosol and activation of caspases cascade reaction.	Acrolein	12-20	caspase 9	Rattus norvegicus	210-218
22167661-11	2012	Melatonin and estrogen treatment prevented the oxidative damage and the activation of caspases.	Melatonin	0-9	caspase 9	Rattus norvegicus	86-94
21476075-8	2012	Western blot analysis showed that doxorubicin administration markedly increased the levels of caspase-9, 3, -8, -12, Fas, Bid and disturbed the Bcl-2 family protein balance.	Doxorubicin	34-45	caspase 9	Rattus norvegicus	94-103
22311472-6	2012	The increased H(2)O(2) concentration was associated with increased cytochrome c concentration, caspase-9 and caspase-3 activities that resulted in the induction of morphological features characteristic of egg apoptosis.	Hydrogen Peroxide	14-22	caspase 9	Rattus norvegicus	95-104
22281060-7	2012	Intensities of caspase-3 and caspase-9 labeling were also significantly increased by administration of VPA.	Valproic Acid	103-106	caspase 9	Rattus norvegicus	29-38
22803376-1	2012	OBJECTIVE: To observe the protective effect of alcohol extract of Potentilla anserina against myocardial apoptosis induced by acute myocardial ischemia/reperfusion by arteria coronaria ligation and the effect on the expressions of Caspase-3 and Caspase-9 in myocardial apoptosis signal pathway.	Alcohols	47-54	caspase 9	Rattus norvegicus	245-254
22803376-15	2012	Immunohistochemistry showed that administration of all dosages of alcohol extract of P. anserina could significantly reduce Caspase-3 and Caspase-9 protein expressions after I/R injury (P &lt; 0.05).	Alcohols	66-73	caspase 9	Rattus norvegicus	138-147
22803376-16	2012	CONCLUSION: The administration with alcohol extract of P. anserina can protect the myocardial tissue from apoptosis after acute myocardial ischemia and reperfusion injury in rats and inhibit the expressions of Caspase-9 and Caspase-3 mRNA and proteins.	Alcohols	36-43	caspase 9	Rattus norvegicus	210-219
22369161-6	2012	Results illustrated that piroxicam and c-phycocyanin treatments stimulate cytochrome c release by downregulating the Bcl-2 (an antiapoptotic protein) expression significantly, while promoting the level of Bax (a proapoptotic protein), thereby activating caspases (caspases-9 and -3) and Apaf-1.	Piroxicam	25-34	caspase 9	Rattus norvegicus	264-281
22166790-5	2012	Pre-treatment with antioxidant vitamin E or N-acetylcysteine (NAC) completely abolished the I6-induced generation of ROS, loss of MMP, release of cytochrome c, activation of caspase-9 and caspase-3, and cleavage of PARP.	Vitamin E	31-40	caspase 9	Rattus norvegicus	174-183
22166790-4	2012	In addition, I6-induced reactive oxygen species (ROS) caused the disruption of mitochondria membrane potential (MMP), the release of cytochrome c, the activation of caspase-9 and caspase-3, and cleavage of poly(ADP-ribose) polymerase (PARP), resulting in activation of mitochondrial-mediated intrinsic death pathway.	Reactive Oxygen Species	24-47	caspase 9	Rattus norvegicus	165-174
22166790-4	2012	In addition, I6-induced reactive oxygen species (ROS) caused the disruption of mitochondria membrane potential (MMP), the release of cytochrome c, the activation of caspase-9 and caspase-3, and cleavage of poly(ADP-ribose) polymerase (PARP), resulting in activation of mitochondrial-mediated intrinsic death pathway.	Reactive Oxygen Species	49-52	caspase 9	Rattus norvegicus	165-174
21497497-8	2012	Curcumin treatment prevented the enhanced proteasome chymotrypsin-like activity and the trend toward increased caspase-9-associated apoptosome activity at I8 in immobilized muscles.	Curcumin	0-8	caspase 9	Rattus norvegicus	111-120
22244881-11	2012	Apocynin and/or NAC also mitigated Zn- and PQ-induced alterations in oxidative stress, NADPH oxidase activation and cytochrome c release, caspases-9 and -3 activation and CD11b expression.	acetovanillone	0-8	caspase 9	Rattus norvegicus	138-155
22244881-11	2012	Apocynin and/or NAC also mitigated Zn- and PQ-induced alterations in oxidative stress, NADPH oxidase activation and cytochrome c release, caspases-9 and -3 activation and CD11b expression.	Acetylcysteine	16-19	caspase 9	Rattus norvegicus	138-155
22166790-5	2012	Pre-treatment with antioxidant vitamin E or N-acetylcysteine (NAC) completely abolished the I6-induced generation of ROS, loss of MMP, release of cytochrome c, activation of caspase-9 and caspase-3, and cleavage of PARP.	Acetylcysteine	44-60	caspase 9	Rattus norvegicus	174-183
22166790-5	2012	Pre-treatment with antioxidant vitamin E or N-acetylcysteine (NAC) completely abolished the I6-induced generation of ROS, loss of MMP, release of cytochrome c, activation of caspase-9 and caspase-3, and cleavage of PARP.	Acetylcysteine	62-65	caspase 9	Rattus norvegicus	174-183
22093918-4	2012	Moreover, APAP induced renal damage by inducing apoptotic death and inflammation in renal tubular cells, manifested by an increase in the expression of caspase-3, caspase-9, NFkB, iNOS, Kim-1 and decrease in Bcl-2 expression.	Acetaminophen	10-14	caspase 9	Rattus norvegicus	163-172
22048644-13	2012	Consequently, cypermethrin induced a mitochondria-mediated apoptosis, characterized by rise in Bax/Bcl-2 ratio and cleavage of caspase-9, -3, and -7, and the effect was prevented by HB-EGF.	cypermethrin	14-26	caspase 9	Rattus norvegicus	127-136
22138235-10	2012	Results also suggest that taurine could protect cardiac tissue from ALX induced apoptosis via the regulation of Bcl2 family and caspase 9/3 proteins.	Taurine	26-33	caspase 9	Rattus norvegicus	128-137
22138235-10	2012	Results also suggest that taurine could protect cardiac tissue from ALX induced apoptosis via the regulation of Bcl2 family and caspase 9/3 proteins.	Alloxan	68-71	caspase 9	Rattus norvegicus	128-137
23109892-7	2012	In addition, sRAGE treatment significantly inhibited H/R-induced mitochondrial depolarization and mPTP opening, reduced mitochondrial cytochrome c leakage, caspase-3 and caspase-9 activity, and decreased the ratio of Bax to Bcl-2.	r	14-15	caspase 9	Rattus norvegicus	170-179
22301162-5	2012	We examined the decrease of mitochondrial membrane potential (MMP), the increase of reactive oxygen species (ROS) production, the increase of lipid peroxidation and decrease of superoxide dismutase (SOD) activity in Sertoli cells after treatment with MC-LR in vitro, and higher expression of caspase-9 and caspase-3, the increase of apoptosis rate.	cyanoginosin LR	251-256	caspase 9	Rattus norvegicus	292-301
22685683-11	2012	Preconditioning of newborn rats with LPS increased TLR4, Caspase-9 and -3 levels, but failed to affect basal expression of HSP60, Bax, and Bcl-2.	lps	37-40	caspase 9	Rattus norvegicus	57-73
22685683-12	2012	Subsequent caerulein stimulation increased TLR4, Bcl-2, and caspases, but diminished HSP60 and Bax proteins in pancreatic acinar cells.	Ceruletide	11-20	caspase 9	Rattus norvegicus	60-68
22814015-9	2012	The apoptotic proteins, apaf-1, caspase-9 and caspase-3 were highly diminished in DMBA group but restored to normal level in NSAIDs groups.	9,10-Dimethyl-1,2-benzanthracene	82-86	caspase 9	Rattus norvegicus	32-41
21978835-6	2011	Furthermore, hyperoside inhibited mitochondria-dependent downstream caspase-mediated apoptotic pathway, such as that involving caspase-9, caspase-3, and poly ADP-ribose polymerase (PARP).	hyperoside	13-23	caspase 9	Rattus norvegicus	127-136
21710242-7	2011	RESULTS: The pups in the NEC + CAPE group had better histopathologic and apoptosis evaluations (TUNEL and caspase-9) and the severity of bowel damage was significantly lower in the NEC + CAPE group compared to the NEC group (P &lt; 0.01).	caffeic acid phenethyl ester	31-35	caspase 9	Rattus norvegicus	106-115
21784110-8	2011	Taken together, the results strongly indicate that mitochondrial caspase-9 is not a downstream substrate of ER-specific caspase-12 and that pro-inflammatory cytokines cause apoptotic beta cell death through activation of caspase-9 primarily by hydroxyl radical-mediated mitochondrial damage.	Hydroxyl Radical	244-260	caspase 9	Rattus norvegicus	221-230
22312704-11	2011	GdCl3, a specific activator of CaSR, further enhanced CaSR expression and cardiomyocyte apoptosis and led to the upregulation of cytochrome c, cleaved caspase-9, cleaved caspase-3, and Bax, as well as the downregulation of Bcl-2.	gadolinium chloride	0-5	caspase 9	Rattus norvegicus	151-160
21741406-4	2011	MeHg induced a 38% increase in Bax protein and an increase in cytosolic cytochrome c at 4h, followed by later increases in caspase-9 (40% at 12h; 33% at 24h) and caspase-8 (33% at 24h), compared to controls.	mehg	0-4	caspase 9	Rattus norvegicus	123-132