PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
30031269-9	2018	Nrf2 activation was mediated by miR-200a, and a miR-200a antagomir offset the effects of melatonin-conditioned medium on Nrf2 expression.	Melatonin	89-98	microRNA 200a	Mus musculus	32-40
30031269-9	2018	Nrf2 activation was mediated by miR-200a, and a miR-200a antagomir offset the effects of melatonin-conditioned medium on Nrf2 expression.	Melatonin	89-98	microRNA 200a	Mus musculus	48-56
30423573-13	2018	CONCLUSION: The overexpression of miR-200a may downregulate FOXC1, thereby inhibiting the activation of the PI3K/AKT signaling pathway and ultimately suppressing ASMC proliferation and airway remodeling in asthmatic mice.	asmc	162-166	microRNA 200a	Mus musculus	34-42
29495181-1	2018	Objective: To observe the effect of overexpression of miRNA200a (miR-200a) recombinant lentivirus on the expression of Wnt/beta-catenin signaling pathway in mouse lung epithelial cell line MLE-12 induced by silica (SiO(2)) .	Silicon Dioxide	207-213	microRNA 200a	Mus musculus	65-73
29495181-6	2018	Conclusion: Overexpression of miR-200a can inhibit the expression of related genes of Wnt/beta-catenin signaling pathway in silica-induced mouse lung epithelial cells.	Silicon Dioxide	124-130	microRNA 200a	Mus musculus	30-38
24433831-8	2014	Our findings revealed the progesterone signaling/miR-200a/zeb2 axis regulating the progesterone signaling to insure the balance of self-renewal and differentiation of ES cells.	Progesterone	26-38	microRNA 200a	Mus musculus	49-57
29285219-0	2017	MicroRNA-200a activates Nrf2 signaling to protect osteoblasts from dexamethasone.	Dexamethasone	67-80	microRNA 200a	Mus musculus	0-13
29285219-6	2017	miR-200a expression activated Nrf2 signaling, which inhibited dexamethasone-induced reactive oxygen species production and OB-6 cell death/apoptosis.	Dexamethasone	62-75	microRNA 200a	Mus musculus	0-8
29285219-6	2017	miR-200a expression activated Nrf2 signaling, which inhibited dexamethasone-induced reactive oxygen species production and OB-6 cell death/apoptosis.	Reactive Oxygen Species	84-107	microRNA 200a	Mus musculus	0-8
33197602-9	2021	Furthermore, overexpression of Keap1 and beta-cateninin in H2O2-treated NMVCs with recovered miR-200a elevated inflammation and apoptosis, respectively.	Hydrogen Peroxide	59-63	microRNA 200a	Mus musculus	93-101
20417623-5	2010	Of these 10 miRNA targets, subsequent functional investigations involving knockdown of mir-200a, mir-130a and mir-410 levels suggested that they may decrease the capability of MIN6 cells to secrete insulin in response to stimulatory levels of glucose.	Glucose	243-250	microRNA 200a	Mus musculus	87-95
33197602-4	2021	METHODS: We observed down-regulation of miR-200a levels and up-regulation of Keap1 and beta-catenin levels in H2O2-treated newborn murine ventricular cardiomyocytes (NMVCs) and the infarcted heart tissues of MI mouse models, compared to the non-treated NMVCs and normal heart tissues of healthy mice.	Hydrogen Peroxide	110-114	microRNA 200a	Mus musculus	40-48
33197602-6	2021	Flow cytometry with Annexin and PI staining indicated the inhibition of H2O2-triggered cell apoptosis through ectopically expressed miR-200a.	Hydrogen Peroxide	72-76	microRNA 200a	Mus musculus	132-140
33197602-7	2021	Western blotting and ELISA analyses that detected pro-inflammatory cell factors [interleukin (IL)-1beta, IL-6, and tumor necrosis factor (TNF)-alpha] confirmed that miR-200a prevented H2O2-induced NMVC inflammation.	Hydrogen Peroxide	184-188	microRNA 200a	Mus musculus	165-173
33197602-8	2021	Moreover, miR-200a inhibited up-regulation of Keap1 and beta-catenin expression in H2O2-treated NMVCs by directly binding with the 3"-UTR regions of both Keap1 and beta-catenin.	Hydrogen Peroxide	83-87	microRNA 200a	Mus musculus	10-18
33197602-8	2021	Moreover, miR-200a inhibited up-regulation of Keap1 and beta-catenin expression in H2O2-treated NMVCs by directly binding with the 3"-UTR regions of both Keap1 and beta-catenin.	nmvcs	96-101	microRNA 200a	Mus musculus	10-18
33204070-0	2020	Downregulation of miR-200a Protects Mouse Leydig Cells Against Triptolide by Triggering Autophagy.	triptolide	63-73	microRNA 200a	Mus musculus	18-26
33204070-7	2020	Results: TP dose-dependently upregulated the expression of miR-200a in MLTC-1 cells.	triptolide	9-11	microRNA 200a	Mus musculus	59-67
33204070-8	2020	In addition, TP inhibited the proliferation of MLTC-1 cells via inducing apoptosis and oxidative stress; however, these phenomena were notably reversed by miR-200a antagomir.	triptolide	13-15	microRNA 200a	Mus musculus	155-163
33204070-12	2020	Meanwhile, the cell protective effects of miR-200a against TP were reversed by autophagy inhibitor 3MA, indicating that autophagy plays an important role.	triptolide	59-61	microRNA 200a	Mus musculus	42-50
33204070-12	2020	Meanwhile, the cell protective effects of miR-200a against TP were reversed by autophagy inhibitor 3MA, indicating that autophagy plays an important role.	3-methyladenine	99-102	microRNA 200a	Mus musculus	42-50
33197602-10	2021	CONCLUSION: The results showed that miR-200a expression was inhibited in murine cardiomyocytes due to H2O2 stress in MI cardiac tissues and overexpressed miR-200a could protect the cells from death by regulating the Keap1/Nrf2 and beta-catenin signal transduction pathways.	Hydrogen Peroxide	102-106	microRNA 200a	Mus musculus	36-44
32886103-0	2020	Piceatannol inhibits pyroptosis and suppresses oxLDL-induced lipid storage in macrophages by regulating miR-200a/Nrf2/GSDMD axis.	3,3',4,5'-tetrahydroxystilbene	0-11	microRNA 200a	Mus musculus	104-112
32886103-3	2020	Our study identified miR-200a/Nrf2/GSDMD signaling pathway as critical mediators in the effect of piceatannol on macrophages.	3,3',4,5'-tetrahydroxystilbene	98-109	microRNA 200a	Mus musculus	21-29
32886103-7	2020	Moreover, we investigated the role of miR-200a/Nrf2 signaling pathway in the effect of piceatannol.	3,3',4,5'-tetrahydroxystilbene	87-98	microRNA 200a	Mus musculus	38-46
32886103-8	2020	The results declared that after transfection of si-miR-200a or si-Nrf2 plasmids, the effects of piceatannol on macrophages were converted, including lipid storage and pyroptosis.	3,3',4,5'-tetrahydroxystilbene	96-107	microRNA 200a	Mus musculus	51-59
32886103-10	2020	Collectively, our findings demonstrate that piceatannol exerts anti-atherosclerotic activity on RAW264.7 cells by regulating miR-200a/Nrf2/GSDMD signaling.	3,3',4,5'-tetrahydroxystilbene	44-55	microRNA 200a	Mus musculus	125-133
32802189-10	2020	AAV9-induced overexpression of miR-17 and lentivirus-mediated silencing of miR-200a in skeletal muscle ameliorated whole-body insulin resistance in DEHP-exposed mice.	Diethylhexyl Phthalate	148-152	microRNA 200a	Mus musculus	75-83
32802189-11	2020	Conclusions: The miR-17/Keap1-Nrf2/miR-200a axis contributed to DEHP-induced insulin resistance.	Diethylhexyl Phthalate	64-68	microRNA 200a	Mus musculus	35-43
31863770-5	2020	LF, CR, Que and Ex significantly ameliorated HF-induced hepatic steatosis to varying degrees, inhibited T4 production via differentially elevating miR-339, miR-383 and miR-146b to decrease NIS expression and regulating miR-200a/Nrf2 to maintain redox status in the thyroid.	Quercetin	8-11	microRNA 200a	Mus musculus	219-227
31733831-0	2020	Isorhynchophylline exerts anti-asthma effects in mice by inhibiting the proliferation of airway smooth muscle cells: The involvement of miR-200a-mediated FOXC1/NF-kappaB pathway.	rhyncophylline	0-18	microRNA 200a	Mus musculus	136-144
32802189-0	2020	Epigenetic repression of miR-17 contributed to di(2-ethylhexyl) phthalate-triggered insulin resistance by targeting Keap1-Nrf2/miR-200a axis in skeletal muscle.	Diethylhexyl Phthalate	47-73	microRNA 200a	Mus musculus	127-135
32031966-6	2020	In aortic endothelial cells (ECs) isolated from C57BL/6 wild-type (WT) mice, high glucose (HG) reduced miR-200a level and increased the expression of kelch-like ECH-associated protein 1 (Keap1) - a target of miR-200a and a negative regulator of NRF2.	Glucose	82-89	microRNA 200a	Mus musculus	103-111
32031966-6	2020	In aortic endothelial cells (ECs) isolated from C57BL/6 wild-type (WT) mice, high glucose (HG) reduced miR-200a level and increased the expression of kelch-like ECH-associated protein 1 (Keap1) - a target of miR-200a and a negative regulator of NRF2.	Glucose	82-89	microRNA 200a	Mus musculus	208-216
31896068-11	2020	The expression of miR-200a was upregulated both in the peri-infarcted region of mice myocardium and H2O2-treated cardiomyocytes.	Water	100-104	microRNA 200a	Mus musculus	18-26
31781322-0	2019	miR-200a Attenuated Doxorubicin-Induced Cardiotoxicity through Upregulation of Nrf2 in Mice.	Doxorubicin	20-31	microRNA 200a	Mus musculus	0-8
31781322-4	2019	Our study is aimed at investigating the effect of miR-200a on DOX-induced cardiotoxicity in mice.	Doxorubicin	62-65	microRNA 200a	Mus musculus	50-58
31781322-7	2019	In our study, we found that miR-200a mRNA was the only microRNA that was significantly decreased in DOX-treated mice and H9c2 cells.	Doxorubicin	100-103	microRNA 200a	Mus musculus	28-36
31781322-9	2019	Moreover, miR-200a reduced oxidative stress and cardiac apoptosis without affecting matrix metalloproteinase and inflammatory factors in mice with acute DOX injection.	Doxorubicin	153-156	microRNA 200a	Mus musculus	10-18
31781322-10	2019	miR-200a also attenuated DOX-induced oxidative injury and cell loss in vitro.	Doxorubicin	25-28	microRNA 200a	Mus musculus	0-8
31781322-12	2019	miR-200a also provided cardiac benefits in a chronic model of DOX-induced cardiotoxicity.	Doxorubicin	62-65	microRNA 200a	Mus musculus	0-8
31781322-13	2019	In conclusion, miR-200a protected against DOX-induced cardiotoxicity via activation of the Nrf2 signaling pathway.	Doxorubicin	42-45	microRNA 200a	Mus musculus	15-23
31781322-14	2019	Our data suggest that miR-200a may represent a new cardioprotective strategy against DOX-induced cardiotoxicity.	Doxorubicin	85-88	microRNA 200a	Mus musculus	22-30