PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32871518-9 2020 Importantly, the anti-apoptotic property of NAC could be attributed to inactivation of MAPK signaling molecules; p38 and JNK, and enhancement of the ovarian vascular endothelial growth factor (VEGF) expression. Acetylcysteine 44-47 mitogen-activated protein kinase 8 Rattus norvegicus 121-124 33262689-0 2020 N-Acetylcysteine Rescues Hippocampal Oxidative Stress-Induced Neuronal Injury via Suppression of p38/JNK Signaling in Depressed Rats. Acetylcysteine 0-16 mitogen-activated protein kinase 8 Rattus norvegicus 101-104 29315209-8 2018 Pin-activated ERK/JNK were significantly reduced after the administration of NAC; however, the inhibition of ERK/JNK failed to change the Pin-induced ROS production. Acetylcysteine 77-80 mitogen-activated protein kinase 8 Rattus norvegicus 18-21 32810585-11 2020 Further investigation of the underlying mechanisms revealed that the ROS scavenger N-acetyl-l-cysteine inhibited CRS-induced JNK activation. Acetylcysteine 83-102 mitogen-activated protein kinase 8 Rattus norvegicus 125-128 30633982-0 2019 N-acetylcysteine alleviates fluoride-induced testicular apoptosis by modulating IRE1alpha/JNK signaling and nuclear Nrf2 activation. Acetylcysteine 0-16 mitogen-activated protein kinase 8 Rattus norvegicus 90-93 29410271-8 2018 In addition, a ROS scavenger N-acetyl-l-cysteine (NAC) down-regulated the protein level of p-p38, p-JNK and Prdx1, and H9c2 cell apoptosis. Acetylcysteine 29-48 mitogen-activated protein kinase 8 Rattus norvegicus 100-103 29410271-8 2018 In addition, a ROS scavenger N-acetyl-l-cysteine (NAC) down-regulated the protein level of p-p38, p-JNK and Prdx1, and H9c2 cell apoptosis. Acetylcysteine 50-53 mitogen-activated protein kinase 8 Rattus norvegicus 100-103 32398966-10 2020 By using ROS scavenger N-acetyl-cysteine (NAC) could reverse the effects of nicotine by down-regulation the phosphorylation of p38MAPK and JNK pathways, and pretreatment of specific inhibitors of p38MAPK and JNK could restore the autophagy impairment and cardiomyocytes hypertrophy induced by nicotine. Acetylcysteine 23-40 mitogen-activated protein kinase 8 Rattus norvegicus 139-142 32398966-10 2020 By using ROS scavenger N-acetyl-cysteine (NAC) could reverse the effects of nicotine by down-regulation the phosphorylation of p38MAPK and JNK pathways, and pretreatment of specific inhibitors of p38MAPK and JNK could restore the autophagy impairment and cardiomyocytes hypertrophy induced by nicotine. Acetylcysteine 23-40 mitogen-activated protein kinase 8 Rattus norvegicus 208-211 32398966-10 2020 By using ROS scavenger N-acetyl-cysteine (NAC) could reverse the effects of nicotine by down-regulation the phosphorylation of p38MAPK and JNK pathways, and pretreatment of specific inhibitors of p38MAPK and JNK could restore the autophagy impairment and cardiomyocytes hypertrophy induced by nicotine. Acetylcysteine 42-45 mitogen-activated protein kinase 8 Rattus norvegicus 139-142 32398966-10 2020 By using ROS scavenger N-acetyl-cysteine (NAC) could reverse the effects of nicotine by down-regulation the phosphorylation of p38MAPK and JNK pathways, and pretreatment of specific inhibitors of p38MAPK and JNK could restore the autophagy impairment and cardiomyocytes hypertrophy induced by nicotine. Acetylcysteine 42-45 mitogen-activated protein kinase 8 Rattus norvegicus 208-211 30633982-9 2019 Simultaneously, NAC pretreatment downregulated XBP1 splicing, reduced JNK phosphorylation and further blocked cleavage of caspase-3, all these might contribute to the inhibition of testicular cell apoptosis. Acetylcysteine 16-19 mitogen-activated protein kinase 8 Rattus norvegicus 70-73 30633982-10 2019 Collectively, the present results suggested that prolonged administration of NAC preserved testicular function and normalized sex hormonal disruption induced by NaF via the inhibition of Nrf2-associated oxidative damage and Ire1alpha-JNK-mediated apoptosis in rat testis. Acetylcysteine 77-80 mitogen-activated protein kinase 8 Rattus norvegicus 234-237 25681429-8 2015 The reactive oxygen species (ROS) inhibitors N-acetylcysteine (NAC), diphenyleneiodonium (DPI), and Tempol also diminished MCP-1 upregulation and JNK activation induced by ADP. Acetylcysteine 45-61 mitogen-activated protein kinase 8 Rattus norvegicus 146-149 26804764-10 2016 Moreover, The activation of AMPK/mTOR/p70s6k/4EBP1 and JNK signalling pathways induced by NP could be efficiently reversed by pretreatment of N-acetylcysteine or 3-MA. Acetylcysteine 142-158 mitogen-activated protein kinase 8 Rattus norvegicus 55-58 26891662-5 2016 In the amygdala, JNK was increased in diabetics treated with saline or NAC. Acetylcysteine 71-74 mitogen-activated protein kinase 8 Rattus norvegicus 17-20 25769956-7 2015 Pretreatment with the ROS inhibitor N-acetylcysteine abrogated the phosphorylation of p38 and JNK induced by high glucose. Acetylcysteine 36-52 mitogen-activated protein kinase 8 Rattus norvegicus 94-97 25681429-8 2015 The reactive oxygen species (ROS) inhibitors N-acetylcysteine (NAC), diphenyleneiodonium (DPI), and Tempol also diminished MCP-1 upregulation and JNK activation induced by ADP. Acetylcysteine 63-66 mitogen-activated protein kinase 8 Rattus norvegicus 146-149 22085843-9 2012 Furthermore, Cu(2+)/PDTC complex was capable of increasing the phosphorylations of ERK1/2 and JNK, and its upstream kinase MEK1/2 and MKK4, which could be reversed by NAC. Acetylcysteine 167-170 mitogen-activated protein kinase 8 Rattus norvegicus 94-97 24824652-6 2014 An antioxidant, N-acetyl-L-cysteine (NAC), prevented IH-induced hepatic insulin resistance in parallel with prevention of decreased IkappaBalpha content, increased JNK phosphorylation (markers of IKKbeta and JNK activation, respectively), increased serine phosphorylation of IRS-1 and IRS-2, and impaired insulin signaling in the liver without affecting IH-induced hepatic PKCdelta activation. Acetylcysteine 16-35 mitogen-activated protein kinase 8 Rattus norvegicus 164-167 24824652-6 2014 An antioxidant, N-acetyl-L-cysteine (NAC), prevented IH-induced hepatic insulin resistance in parallel with prevention of decreased IkappaBalpha content, increased JNK phosphorylation (markers of IKKbeta and JNK activation, respectively), increased serine phosphorylation of IRS-1 and IRS-2, and impaired insulin signaling in the liver without affecting IH-induced hepatic PKCdelta activation. Acetylcysteine 16-35 mitogen-activated protein kinase 8 Rattus norvegicus 208-211 24824652-6 2014 An antioxidant, N-acetyl-L-cysteine (NAC), prevented IH-induced hepatic insulin resistance in parallel with prevention of decreased IkappaBalpha content, increased JNK phosphorylation (markers of IKKbeta and JNK activation, respectively), increased serine phosphorylation of IRS-1 and IRS-2, and impaired insulin signaling in the liver without affecting IH-induced hepatic PKCdelta activation. Acetylcysteine 37-40 mitogen-activated protein kinase 8 Rattus norvegicus 164-167 24824652-6 2014 An antioxidant, N-acetyl-L-cysteine (NAC), prevented IH-induced hepatic insulin resistance in parallel with prevention of decreased IkappaBalpha content, increased JNK phosphorylation (markers of IKKbeta and JNK activation, respectively), increased serine phosphorylation of IRS-1 and IRS-2, and impaired insulin signaling in the liver without affecting IH-induced hepatic PKCdelta activation. Acetylcysteine 37-40 mitogen-activated protein kinase 8 Rattus norvegicus 208-211 24162829-4 2014 GA activated calcium/calmodulin-dependent protein kinase II (CaMKII), c-Jun N-terminal kinase (JNK) and P38; but these activating effects were attenuated by pretreatment with N-acetyl-L-cysteine, a ROS inhibitor. Acetylcysteine 175-194 mitogen-activated protein kinase 8 Rattus norvegicus 70-93 23271287-12 2012 The elevated ROS was strongly associated with the activation of JNK and ERK1/2 signal pathways after MPP(+) exposure, since the pretreatment of NAC significantly reduced the upregulation of p-JNK and p-ERK1/2. Acetylcysteine 144-147 mitogen-activated protein kinase 8 Rattus norvegicus 64-67 23271287-12 2012 The elevated ROS was strongly associated with the activation of JNK and ERK1/2 signal pathways after MPP(+) exposure, since the pretreatment of NAC significantly reduced the upregulation of p-JNK and p-ERK1/2. Acetylcysteine 144-147 mitogen-activated protein kinase 8 Rattus norvegicus 192-195 22336129-10 2012 The administration of NAC increased GSH, attenuated ROS, cytokines, MPO, JNK, pAKT and caspase-3 and lung permeability associated with decreased activation of nuclear factor-kappaB. Acetylcysteine 22-25 mitogen-activated protein kinase 8 Rattus norvegicus 73-76 22554771-9 2012 An antioxidant drug, N-acetyl-l-cysteine significantly inhibited TNF-alpha-induced phosphorylation of p38 and JNK. Acetylcysteine 21-40 mitogen-activated protein kinase 8 Rattus norvegicus 110-113 22470108-10 2012 NAC administration attenuated JNK activation, but had no effect on ERK. Acetylcysteine 0-3 mitogen-activated protein kinase 8 Rattus norvegicus 30-33 21856376-6 2012 Taken together, the above findings indicate that the specificity of NAC action was not restricted to regulating marker proteins in the extrinsic and JNK pathways as seen in vitro but extended to include intrinsic pathway of metazoan apoptosis as well. Acetylcysteine 68-71 mitogen-activated protein kinase 8 Rattus norvegicus 149-152 21627650-8 2012 The phosphorylated JNK protein was induced by hypoxia and was abolished by pretreatment with SP600125, losartan (an angiotensin II receptor antagonist) or N-acetylcysteine. Acetylcysteine 155-171 mitogen-activated protein kinase 8 Rattus norvegicus 19-22 21843499-5 2011 We found the treatment of SP600125 or NAC could decrease the activation of Ask1 during ischemia/reperfusion and suppress the assembly of the Fas Daxx Ask1 signaling module, and in succession inhibit JNK activation and c-Jun phosphorylation. Acetylcysteine 38-41 mitogen-activated protein kinase 8 Rattus norvegicus 199-202 20037173-10 2010 However, NAC pretreatment significantly improved renal function and decreased the activation of ERK, JNK, Bax and Bad, whereas it increased Bcl-2 and Bcl-xL. Acetylcysteine 9-12 mitogen-activated protein kinase 8 Rattus norvegicus 101-104 20824644-0 2010 N-acetylcysteine counteracts oxidative stress and prevents hCG-induced apoptosis in rat Leydig cells through down regulation of caspase-8 and JNK. Acetylcysteine 0-16 mitogen-activated protein kinase 8 Rattus norvegicus 142-145 20824644-7 2010 NAC treatment induced down-regulation of upstream JNK/pJNK and down-stream caspase-3 in the target cells. Acetylcysteine 0-3 mitogen-activated protein kinase 8 Rattus norvegicus 50-53 20824644-8 2010 Taken together, the above findings indicate that NAC counteracted the oxidative stress in Leydig cells induced as a result of repeated hCG stimulation, and inhibited apoptosis by mainly regulating the extrinsic and JNK pathways of metazoan apoptosis. Acetylcysteine 49-52 mitogen-activated protein kinase 8 Rattus norvegicus 215-218 20571742-10 2010 The phosphorylation of c-jun N-terminal protein kinase (JNK) was increased markedly when stimulated with high glucose for 30 and 60 min, which was abolished when pretreated with CLT or NAC. Acetylcysteine 185-188 mitogen-activated protein kinase 8 Rattus norvegicus 23-54 20571742-10 2010 The phosphorylation of c-jun N-terminal protein kinase (JNK) was increased markedly when stimulated with high glucose for 30 and 60 min, which was abolished when pretreated with CLT or NAC. Acetylcysteine 185-188 mitogen-activated protein kinase 8 Rattus norvegicus 56-59 9832211-5 1998 Furthermore, N-acetylcysteine, an antioxidant, prevented the auto-oxidized dopamine-induced JNK/SAPK activation and DNA fragmentation. Acetylcysteine 13-29 mitogen-activated protein kinase 8 Rattus norvegicus 92-100 20179891-6 2010 Furthermore, NAC increased the protein expression of p-ERK, while inhibited protein expression of p-JNK, NF-kappaB in gastric mucosa. Acetylcysteine 13-16 mitogen-activated protein kinase 8 Rattus norvegicus 100-103 12524169-4 2003 Concomitantly, the late activation of apoptosis signal-regulating kinase 1 (ASK1) and c-Jun N-terminal protein kinase (JNK) was also prevented by Naspm or NAC. Acetylcysteine 155-158 mitogen-activated protein kinase 8 Rattus norvegicus 86-117 12524169-4 2003 Concomitantly, the late activation of apoptosis signal-regulating kinase 1 (ASK1) and c-Jun N-terminal protein kinase (JNK) was also prevented by Naspm or NAC. Acetylcysteine 155-158 mitogen-activated protein kinase 8 Rattus norvegicus 119-122 10807739-6 2000 JNK and ERK were activated by ET-1 binding to a single receptor (ET-1A) but differed in their downstream mechanisms: only JNK activation was sensitive to the radical scavenger N-acetylcysteine and diphenylene iodonium, an inhibitor of NADPH oxidase, indicating a role for ROS. Acetylcysteine 176-192 mitogen-activated protein kinase 8 Rattus norvegicus 0-3 10807739-6 2000 JNK and ERK were activated by ET-1 binding to a single receptor (ET-1A) but differed in their downstream mechanisms: only JNK activation was sensitive to the radical scavenger N-acetylcysteine and diphenylene iodonium, an inhibitor of NADPH oxidase, indicating a role for ROS. Acetylcysteine 176-192 mitogen-activated protein kinase 8 Rattus norvegicus 122-125 19202317-9 2009 We also confirmed that PDGF-induced JNK and Akt activations were inhibited by antioxidants, N-acetylcysteine and diphenyleneiodonium chloride, in RASMCs. Acetylcysteine 92-108 mitogen-activated protein kinase 8 Rattus norvegicus 36-39 17041759-11 2006 Antioxidants such as vitamin C and N-acetyl cysteine inhibited NE-induced ROS production, JNK phosphorylation, caspase activation and apoptosis. Acetylcysteine 35-52 mitogen-activated protein kinase 8 Rattus norvegicus 90-93 15917250-8 2005 Only Yes and JNK activation were sensitive to N-acetylcysteine, inhibitors of NADPH oxidase, PKCzeta, or sphingomyelinase, indicating that the CD95L-induced ROS response is upstream of Yes and JNK but not of Fyn and c-Src activation. Acetylcysteine 46-62 mitogen-activated protein kinase 8 Rattus norvegicus 13-16 9890986-10 1999 This and the findings that (i) HNE strongly induced intracellular peroxide production, (ii) HNE-induced JNK activation was inhibited by pretreatment of the cells with a thiol antioxidant, N-acetylcysteine, and (iii) H2O2 significantly activated JNK support the hypothesis that pro-oxidants play a crucial role in the HNE-induced activation of stress signaling pathways. Acetylcysteine 188-204 mitogen-activated protein kinase 8 Rattus norvegicus 104-107 9890986-10 1999 This and the findings that (i) HNE strongly induced intracellular peroxide production, (ii) HNE-induced JNK activation was inhibited by pretreatment of the cells with a thiol antioxidant, N-acetylcysteine, and (iii) H2O2 significantly activated JNK support the hypothesis that pro-oxidants play a crucial role in the HNE-induced activation of stress signaling pathways. Acetylcysteine 188-204 mitogen-activated protein kinase 8 Rattus norvegicus 245-248 9351437-10 1997 Pretreatment of cells with 500 mumol/L NAC for 1 hour attenuated approximately 50% of Aug II-induced JNK activation, suggesting that ROIs, at least partially, mediate Ang II-induced JNK activation. Acetylcysteine 39-42 mitogen-activated protein kinase 8 Rattus norvegicus 101-104 9351437-10 1997 Pretreatment of cells with 500 mumol/L NAC for 1 hour attenuated approximately 50% of Aug II-induced JNK activation, suggesting that ROIs, at least partially, mediate Ang II-induced JNK activation. Acetylcysteine 39-42 mitogen-activated protein kinase 8 Rattus norvegicus 182-185 9351437-11 1997 Furthermore, 12-HETE-induced JNK activation was reduced by approximately 90% by NAC. Acetylcysteine 80-83 mitogen-activated protein kinase 8 Rattus norvegicus 29-32 35270009-10 2022 Furthermore, pretreatment of cells with SP600125 (JNK inhibitor; 10 muM) or NAC (1 mM) or transfection with JNK-specific siRNA obviously attenuated the MeHg-induced JNK phosphorylation, CHOP and XBP-1 protein expression, apoptotic events, and insulin secretion dysfunction. Acetylcysteine 76-79 mitogen-activated protein kinase 8 Rattus norvegicus 165-168 35270009-11 2022 NAC significantly inhibited MeHg-activated JNK signaling, but SP600125 could not effectively reduce MeHg-induced ROS generation. Acetylcysteine 0-3 mitogen-activated protein kinase 8 Rattus norvegicus 43-46 35582415-9 2022 Furthermore, NAC could effectively reverse VCM-associated increased P38 MAPK/JNK phosphorylation. Acetylcysteine 13-16 mitogen-activated protein kinase 8 Rattus norvegicus 77-80 35582415-10 2022 Conclusions: The results demonstrated that NAC had a protective effect against nephrotoxicity from VCM by inhibiting oxidative stress and apoptosis via P38 MAPK/JNK. Acetylcysteine 43-46 mitogen-activated protein kinase 8 Rattus norvegicus 161-164