PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 30338935-5 2019 In vitro and in vivo experiments showed that Ang II increased intracellular reactive oxygen species (ROS) production and cardiomyocyte apoptosis; these were reversed by administration of the ROS scavenger N-acetylcysteine and by Mst1 deficiency, which suppressed c-Jun N-terminal kinase (JNK) phosphorylation and downstream signaling. Acetylcysteine 205-221 mitogen-activated protein kinase 8 Homo sapiens 263-286 31506575-6 2019 APE downregulated Dusp-1 and induced a significant increase in JNK/c-Jun phosphorylation that were both prevented by NAC. Acetylcysteine 117-120 mitogen-activated protein kinase 8 Homo sapiens 63-66 31176737-10 2019 In addition, the activation of JNK signaling pathway prompted by WZ26 and cisplatin was also reversed by NAC pretreatment. Acetylcysteine 105-108 mitogen-activated protein kinase 8 Homo sapiens 31-34 31396402-8 2019 Inhibition of ROS with N-acetyl cysteine (NAC) significantly decreased pristimerin-induced cell death by inhibiting the phosphorylation of ASK1 and JNK. Acetylcysteine 23-40 mitogen-activated protein kinase 8 Homo sapiens 148-151 31396402-8 2019 Inhibition of ROS with N-acetyl cysteine (NAC) significantly decreased pristimerin-induced cell death by inhibiting the phosphorylation of ASK1 and JNK. Acetylcysteine 42-45 mitogen-activated protein kinase 8 Homo sapiens 148-151 31386885-10 2019 The apoptotic process was probably mediated via ROS overproduction and MAPK (ERK and JNK) activation as N-acetylcysteine, or specific inhibitors of these kinases prevented the XN-induced caspase-3 activity and, hence, apoptosis. Acetylcysteine 104-120 mitogen-activated protein kinase 8 Homo sapiens 85-88 31233063-7 2019 Furthermore, NAC was found to prevent Slp-induced p70 and JNK phosphorylation. Acetylcysteine 13-16 mitogen-activated protein kinase 8 Homo sapiens 58-61 30338935-5 2019 In vitro and in vivo experiments showed that Ang II increased intracellular reactive oxygen species (ROS) production and cardiomyocyte apoptosis; these were reversed by administration of the ROS scavenger N-acetylcysteine and by Mst1 deficiency, which suppressed c-Jun N-terminal kinase (JNK) phosphorylation and downstream signaling. Acetylcysteine 205-221 mitogen-activated protein kinase 8 Homo sapiens 288-291 30055241-9 2018 In addition, NAC also inhibited JNK and ERK activation by Sb exposure. Acetylcysteine 13-16 mitogen-activated protein kinase 8 Homo sapiens 32-35 30584464-5 2018 When treating PC cells with N-acetyl-L-cysteine (NAC), the intracellular ROS generation is repressed, but the expression of phosphorylation of JNK and c-Jun increased. Acetylcysteine 28-47 mitogen-activated protein kinase 8 Homo sapiens 143-146 30584464-5 2018 When treating PC cells with N-acetyl-L-cysteine (NAC), the intracellular ROS generation is repressed, but the expression of phosphorylation of JNK and c-Jun increased. Acetylcysteine 49-52 mitogen-activated protein kinase 8 Homo sapiens 143-146 30359319-9 2018 Pre-treatment with SP600125 or N-acetylcysteine reversed the effects of high glucose on the JNK signaling pathway and autophagy-related proteins. Acetylcysteine 31-47 mitogen-activated protein kinase 8 Homo sapiens 92-95 30662622-7 2018 Furthermore, H2O2-induced proliferation inhibition, apoptosis, and inflammation in HK-2 cells were ameliorated by NAC (N-acetyl cysteine, the ROS scavenger) and SP600125 (the JNK inhibitor). Acetylcysteine 114-117 mitogen-activated protein kinase 8 Homo sapiens 175-178 30662622-7 2018 Furthermore, H2O2-induced proliferation inhibition, apoptosis, and inflammation in HK-2 cells were ameliorated by NAC (N-acetyl cysteine, the ROS scavenger) and SP600125 (the JNK inhibitor). Acetylcysteine 119-136 mitogen-activated protein kinase 8 Homo sapiens 175-178 29754474-8 2018 SP600125 or NAC reduced OMT-induced p-JNK and NAC significantly lowered caspase-4. Acetylcysteine 12-15 mitogen-activated protein kinase 8 Homo sapiens 38-41 29510199-10 2018 ROS scavenger N-acetyl-L-cysteine partially rescued HepG2 cell growth and prevented MPP depolarization, ERK and JNK activation. Acetylcysteine 14-33 mitogen-activated protein kinase 8 Homo sapiens 112-115 29326072-5 2018 Western blot results indicated that BSNQ and OSNQ up-regulated the phosphorylation of p38 and JNK, and down-regulated the phosphorylation of ERK, Akt and STAT3, and that these effects were blocked by N-acetyl-l-cysteine. Acetylcysteine 200-219 mitogen-activated protein kinase 8 Homo sapiens 94-97 29389802-9 2018 N-acetyl-L-cysteine, a scavenger of ROS, significantly reversed dioscin-induced cell death and activation of JNK and p38. Acetylcysteine 0-19 mitogen-activated protein kinase 8 Homo sapiens 109-112 28993908-7 2018 To investigate the crosstalk between different signaling pathways, pretreatment of HepG2 with N-acetylcysteine, an ROS scavenger, attenuated 4-methoxy-TEMPO-induced DNA damage, suppressed JNK activation, and diminished autophagy induction. Acetylcysteine 94-110 mitogen-activated protein kinase 8 Homo sapiens 188-191 29291542-3 2018 Protocatechuic acid, Akt inhibitor, Bay 11-7085 and N-acetylcysteine reduced the lipopolysaccharide-caused production of cytokines and chemokines, expression of cyclooxygenase, increase in the levels and activities of Toll-like receptor-4, p-Akt and mTOR, activation of NF-kappaB, phosphorylation of the JNK and p38-MAPK, and production of reactive oxygen species in keratinocytes. Acetylcysteine 52-68 mitogen-activated protein kinase 8 Homo sapiens 304-307 28681938-6 2018 Moreover, pretreatment of the cells with antioxidant N-acetyl cysteine (NAC) inhibited omega-HUA-induced increased reactive oxygen species (ROS) levels, cleaved caspase-3 and cleaved PARP, and phosphorylated JNK, phosphorylated p38, and increased cell viability and colony-forming ability. Acetylcysteine 53-70 mitogen-activated protein kinase 8 Homo sapiens 208-211 28681938-6 2018 Moreover, pretreatment of the cells with antioxidant N-acetyl cysteine (NAC) inhibited omega-HUA-induced increased reactive oxygen species (ROS) levels, cleaved caspase-3 and cleaved PARP, and phosphorylated JNK, phosphorylated p38, and increased cell viability and colony-forming ability. Acetylcysteine 72-75 mitogen-activated protein kinase 8 Homo sapiens 208-211 28583366-8 2017 Pre-treatment with n-acetyl-l-cysteine (NAC), a ROS scavenger, enhanced PTX-mediated cell cycle arrest, apoptosis and the JNK and ERK MAPK activation, while pre-treatment with SP600125 or PD98509 attenuated PTX-mediated effects in HepG2 cells. Acetylcysteine 19-38 mitogen-activated protein kinase 8 Homo sapiens 122-125 26756900-10 2016 Pre-treatment with a reactive oxygen species (ROS) scavenger, N-acetylcysteine, attenuated DOX-induced Jnk activation and subsequent p53 accumulation. Acetylcysteine 62-78 mitogen-activated protein kinase 8 Homo sapiens 103-106 28758971-9 2017 Moreover, an ROS scavenger, N-acetylcysteine (NAC), reversed tricetin-induced JNK activation and subsequent cell apoptosis. Acetylcysteine 28-44 mitogen-activated protein kinase 8 Homo sapiens 78-81 28758971-9 2017 Moreover, an ROS scavenger, N-acetylcysteine (NAC), reversed tricetin-induced JNK activation and subsequent cell apoptosis. Acetylcysteine 46-49 mitogen-activated protein kinase 8 Homo sapiens 78-81 29050275-8 2017 Moreover, NAC was able to eliminate AB23A-induced JNK phosphorylation. Acetylcysteine 10-13 mitogen-activated protein kinase 8 Homo sapiens 50-53 28393248-7 2017 c-JUN N-terminal kinase (JNK)/insulin receptor substrate 1 (IRS1)/AKT/GSK signaling was explored using western blot analysis in HepG2 cells treated with high glucose and/or EGCG or N-acetyl-cysteine. Acetylcysteine 181-198 mitogen-activated protein kinase 8 Homo sapiens 0-23 28393248-7 2017 c-JUN N-terminal kinase (JNK)/insulin receptor substrate 1 (IRS1)/AKT/GSK signaling was explored using western blot analysis in HepG2 cells treated with high glucose and/or EGCG or N-acetyl-cysteine. Acetylcysteine 181-198 mitogen-activated protein kinase 8 Homo sapiens 25-28 28087840-9 2017 Reactive oxygen species (ROS) inhibitor, N-acetyl cysteine (NAC), suppressed TNF-alpha/Cholix-induced JNK and ERK phosphorylation, resulting in inhibition of PARP cleavage. Acetylcysteine 41-58 mitogen-activated protein kinase 8 Homo sapiens 102-105 28087840-9 2017 Reactive oxygen species (ROS) inhibitor, N-acetyl cysteine (NAC), suppressed TNF-alpha/Cholix-induced JNK and ERK phosphorylation, resulting in inhibition of PARP cleavage. Acetylcysteine 60-63 mitogen-activated protein kinase 8 Homo sapiens 102-105 27650197-7 2017 On the other hand, the increased phosphorylation of mitogen-activated protein kinase (MAPK) proteins (c-Jun N-terminal kinase [JNK], p38, and extracellular signal-regulated kinase [ERK]) by JDA-202 was suppressed by N-acetylcysteine (NAC) or catalase, a known reactive oxygen species (ROS) or H2O2 scavenger. Acetylcysteine 216-232 mitogen-activated protein kinase 8 Homo sapiens 102-125 27650197-7 2017 On the other hand, the increased phosphorylation of mitogen-activated protein kinase (MAPK) proteins (c-Jun N-terminal kinase [JNK], p38, and extracellular signal-regulated kinase [ERK]) by JDA-202 was suppressed by N-acetylcysteine (NAC) or catalase, a known reactive oxygen species (ROS) or H2O2 scavenger. Acetylcysteine 216-232 mitogen-activated protein kinase 8 Homo sapiens 127-130 27650197-7 2017 On the other hand, the increased phosphorylation of mitogen-activated protein kinase (MAPK) proteins (c-Jun N-terminal kinase [JNK], p38, and extracellular signal-regulated kinase [ERK]) by JDA-202 was suppressed by N-acetylcysteine (NAC) or catalase, a known reactive oxygen species (ROS) or H2O2 scavenger. Acetylcysteine 234-237 mitogen-activated protein kinase 8 Homo sapiens 102-125 27650197-7 2017 On the other hand, the increased phosphorylation of mitogen-activated protein kinase (MAPK) proteins (c-Jun N-terminal kinase [JNK], p38, and extracellular signal-regulated kinase [ERK]) by JDA-202 was suppressed by N-acetylcysteine (NAC) or catalase, a known reactive oxygen species (ROS) or H2O2 scavenger. Acetylcysteine 234-237 mitogen-activated protein kinase 8 Homo sapiens 127-130 27484511-11 2016 Western blotting revealed that Z5 markedly stimulated the MAPK pathways, including ERK1/2, JNK and P38, however, the mechanisms were prevented by NAC. Acetylcysteine 146-149 mitogen-activated protein kinase 8 Homo sapiens 91-94 27035222-8 2016 ROS scavenger, N-acetyl-L-cysteine (NAC, 5 mM), was able to hinder the autophagy, apoptosis and phosphorylation of JNK, and JNK inhibitor (SP600125, 10 microM) significantly inhibited the autophagy and apoptosis, and attenuated the sensitivity of MG63 cells to AE-PDT. Acetylcysteine 15-34 mitogen-activated protein kinase 8 Homo sapiens 115-118 27633119-6 2016 In addition, pretreatment with N-acetyl-cysteine (NAC) and SP600125, the inhibitor of ROS and JNK, induced MKN45 cell proliferation, prevented the cell apoptosis and released the cells from cycle arrest. Acetylcysteine 31-48 mitogen-activated protein kinase 8 Homo sapiens 94-97 27633119-6 2016 In addition, pretreatment with N-acetyl-cysteine (NAC) and SP600125, the inhibitor of ROS and JNK, induced MKN45 cell proliferation, prevented the cell apoptosis and released the cells from cycle arrest. Acetylcysteine 50-53 mitogen-activated protein kinase 8 Homo sapiens 94-97 27633119-7 2016 Finally, we found that pretreatment with NAC prevented the JNK, p53, caspase-9 and -3 protein phosphorylation induced by the polysaccharide, however, pretreatment with SP600125 did not affect the generation of ROS, suggesting that ROS is upstream of JNK. Acetylcysteine 41-44 mitogen-activated protein kinase 8 Homo sapiens 59-62 27633119-7 2016 Finally, we found that pretreatment with NAC prevented the JNK, p53, caspase-9 and -3 protein phosphorylation induced by the polysaccharide, however, pretreatment with SP600125 did not affect the generation of ROS, suggesting that ROS is upstream of JNK. Acetylcysteine 41-44 mitogen-activated protein kinase 8 Homo sapiens 250-253 27570977-6 2016 Moreover, the generation of reactive oxygen species (ROS) was detected in bladder cancer cells, upon treatment of vitamin K2 and the anti-oxidant N-acetyl cysteine (NAC) almost blocked the Vitamin K2-triggered apoptosis, loss of mitochondria membrane potential and activation of JNK and p38 MAPK. Acetylcysteine 146-163 mitogen-activated protein kinase 8 Homo sapiens 279-282 27570977-6 2016 Moreover, the generation of reactive oxygen species (ROS) was detected in bladder cancer cells, upon treatment of vitamin K2 and the anti-oxidant N-acetyl cysteine (NAC) almost blocked the Vitamin K2-triggered apoptosis, loss of mitochondria membrane potential and activation of JNK and p38 MAPK. Acetylcysteine 165-168 mitogen-activated protein kinase 8 Homo sapiens 279-282 27253411-6 2016 Moreover, we found that erianin induced activation of c-Jun N-terminal kinase (JNK) signal pathway, which was also blocked by NAC. Acetylcysteine 126-129 mitogen-activated protein kinase 8 Homo sapiens 54-77 27253411-6 2016 Moreover, we found that erianin induced activation of c-Jun N-terminal kinase (JNK) signal pathway, which was also blocked by NAC. Acetylcysteine 126-129 mitogen-activated protein kinase 8 Homo sapiens 79-82 27035222-8 2016 ROS scavenger, N-acetyl-L-cysteine (NAC, 5 mM), was able to hinder the autophagy, apoptosis and phosphorylation of JNK, and JNK inhibitor (SP600125, 10 microM) significantly inhibited the autophagy and apoptosis, and attenuated the sensitivity of MG63 cells to AE-PDT. Acetylcysteine 15-34 mitogen-activated protein kinase 8 Homo sapiens 124-127 27035222-8 2016 ROS scavenger, N-acetyl-L-cysteine (NAC, 5 mM), was able to hinder the autophagy, apoptosis and phosphorylation of JNK, and JNK inhibitor (SP600125, 10 microM) significantly inhibited the autophagy and apoptosis, and attenuated the sensitivity of MG63 cells to AE-PDT. Acetylcysteine 36-39 mitogen-activated protein kinase 8 Homo sapiens 115-118 27035222-8 2016 ROS scavenger, N-acetyl-L-cysteine (NAC, 5 mM), was able to hinder the autophagy, apoptosis and phosphorylation of JNK, and JNK inhibitor (SP600125, 10 microM) significantly inhibited the autophagy and apoptosis, and attenuated the sensitivity of MG63 cells to AE-PDT. Acetylcysteine 36-39 mitogen-activated protein kinase 8 Homo sapiens 124-127 30123617-9 2016 In addition, we found that rasfonin increased the phosphorylation of c-Jun NH2-terminal kinase (JNK), which was inhibited by NAC. Acetylcysteine 125-128 mitogen-activated protein kinase 8 Homo sapiens 69-94 27074555-6 2016 Interestingly, the ROS scavenger NAC attenuated carfilzomib/vorinostat-mediated activation of p38MAPK and JNK. Acetylcysteine 33-36 mitogen-activated protein kinase 8 Homo sapiens 106-109 30123617-9 2016 In addition, we found that rasfonin increased the phosphorylation of c-Jun NH2-terminal kinase (JNK), which was inhibited by NAC. Acetylcysteine 125-128 mitogen-activated protein kinase 8 Homo sapiens 96-99 25204891-8 2015 Profiling of MAPKs revealed activation of JNK upon hesperetin treatment which was abrogated upon NAC pre-treatment. Acetylcysteine 97-100 mitogen-activated protein kinase 8 Homo sapiens 42-45 26625208-7 2016 The generation of ROS in response to TMZ-POH seems to play a crucial role in the cell death process since the blockage of ROS production using the antioxidant N-acetyl-L-cysteine or catalase reversed the TMZ-POH-induced JNK activation, DNA damage, and cancer cell apoptosis. Acetylcysteine 159-178 mitogen-activated protein kinase 8 Homo sapiens 220-223 26235743-10 2015 Pretreatment with the antioxidants N-acetyl cysteine or glutathione attenuated 8m-induced apoptosis and JNK activation in HCT116 cells. Acetylcysteine 35-52 mitogen-activated protein kinase 8 Homo sapiens 104-107 26296767-3 2015 In this study, we showed that the HCV-induced activation and mitochondrial accumulation of Bax were significantly attenuated by treatment with a general antioxidant, N-acetyl cysteine (NAC), or a specific c-Jun N-terminal kinase (JNK) inhibitor, SP600125, with the result suggesting that the reactive oxygen species (ROS)/JNK signalling pathway is upstream of Bax activation in HCV-induced apoptosis. Acetylcysteine 166-183 mitogen-activated protein kinase 8 Homo sapiens 322-325 26296767-5 2015 The HCV-induced increase in the Bim mRNA and protein levels was significantly counteracted by treatment with NAC or SP600125, suggesting that the ROS/JNK signalling pathway is involved in Bim upregulation. Acetylcysteine 109-112 mitogen-activated protein kinase 8 Homo sapiens 150-153 26851027-4 2016 The specificity of ROS-mediated ATM-JNK activation was confirmed by treatment with N-acetylcysteine, a ROS scavenger. Acetylcysteine 83-99 mitogen-activated protein kinase 8 Homo sapiens 36-39 26291278-6 2015 Conversely, arsenite-induced H3S10 phosphorylation and HO-1 expression were blocked by N-acetylcysteine (NAC), the c-Jun N-terminal kinase (JNK) inhibitor SP600125, and JNK knockdown (siJNK). Acetylcysteine 105-108 mitogen-activated protein kinase 8 Homo sapiens 169-172 25607831-8 2015 Pretreatment with N-acetyl-cysteine (NAC), the inhibitor of ROS, or with SP600125, the inhibitor of JNK, prevented the apoptosis and the high expression of p-JNK, p53, caspase-9 and caspase-3 in CDK5RAP1-deficient MCF-7 cells. Acetylcysteine 18-35 mitogen-activated protein kinase 8 Homo sapiens 158-161 26002468-6 2015 The antioxidant N-Acety-l-Cysteine (NAC) was found to attenuate the JNK and p38 MAPK activation with a concomitant reduction of PA-induced autophagy and apoptosis. Acetylcysteine 16-34 mitogen-activated protein kinase 8 Homo sapiens 68-71 25781201-8 2015 AhR antagonists (alpha-naphthoflavone, CH223191) or antioxidants (N-acetyl-l-cysteine, EUK-134) attenuated 5F 203-mediated JNK and p38 activation, depending on the cell type. Acetylcysteine 66-85 mitogen-activated protein kinase 8 Homo sapiens 123-126 25607831-8 2015 Pretreatment with N-acetyl-cysteine (NAC), the inhibitor of ROS, or with SP600125, the inhibitor of JNK, prevented the apoptosis and the high expression of p-JNK, p53, caspase-9 and caspase-3 in CDK5RAP1-deficient MCF-7 cells. Acetylcysteine 37-40 mitogen-activated protein kinase 8 Homo sapiens 158-161 23836369-9 2015 N-acetylcysteine, an ROS scavenger, inhibited 2-ABP-induced activation of ERK and JNK, the cell death and caspase-3 activity, which suggested that oxidative stress plays a crucial role in apoptosis through activation of caspase-3 in a ROS/JNK-dependent signaling cascade. Acetylcysteine 0-16 mitogen-activated protein kinase 8 Homo sapiens 82-85 25178491-8 2015 Moreover, PYDDT-induced apoptosis as well as activation of JNK was abrogated by the pretreatment with antioxidant N-acetylcysteine. Acetylcysteine 114-130 mitogen-activated protein kinase 8 Homo sapiens 59-62 23836369-9 2015 N-acetylcysteine, an ROS scavenger, inhibited 2-ABP-induced activation of ERK and JNK, the cell death and caspase-3 activity, which suggested that oxidative stress plays a crucial role in apoptosis through activation of caspase-3 in a ROS/JNK-dependent signaling cascade. Acetylcysteine 0-16 mitogen-activated protein kinase 8 Homo sapiens 239-242 25473894-5 2015 Significantly, JNK inhibition promoted 5-FU- and GEM-induced increase in intracellular reactive oxygen species (ROS), and scavenging intracellular ROS by use of N-acetylcysteine impaired JNK inhibition-mediated promotion of the cytotoxicity of 5-FU and GEM. Acetylcysteine 161-177 mitogen-activated protein kinase 8 Homo sapiens 187-190 25527729-5 2015 Furthermore, JNK and ERK activation could be inhibited by both DPI and a free radicals scavenger N-acetyl cysteine. Acetylcysteine 97-114 mitogen-activated protein kinase 8 Homo sapiens 13-16 25997958-7 2015 In addition, NAC completely blocked phosphorylation of JNK and p38 MAPK induced by capsaicin. Acetylcysteine 13-16 mitogen-activated protein kinase 8 Homo sapiens 55-58 24905542-10 2014 The clinical antidote N-acetylcysteine offered almost complete protection even if administered 6h after APAP and a partial protection when given at 15 h. CONCLUSION: These data highlight important mechanistic events in APAP toxicity in PHH and indicate a critical role of JNK in the progression of injury after APAP in humans. Acetylcysteine 22-38 mitogen-activated protein kinase 8 Homo sapiens 272-275 25289048-4 2014 Pretreatment with N-acetylcysteine, an antioxidant chemical compound, inhibited the activation of ASK1, JNK and Bim, as well as the apoptosis induced by casticin. Acetylcysteine 18-34 mitogen-activated protein kinase 8 Homo sapiens 104-107 24738081-6 2014 LQ-mediated cell viability reduction, mitochondrial dysfunction, apoptosis related protein abnormal expressions, and JNK and P38 activation were partially abolished by N-Acetyl-L-cysteine (a ROS inhibitor) pretreatment. Acetylcysteine 168-187 mitogen-activated protein kinase 8 Homo sapiens 117-120 24938881-9 2014 Abrin also shown to increase in stress factor associated proteins SAPK/JNK, c-fos and c-jun levels which were effectively suppressed by NAC and trolox. Acetylcysteine 136-139 mitogen-activated protein kinase 8 Homo sapiens 71-74 24915933-14 2014 N-acetyl-L-cysteine (NAC), an antioxidant, can partially attenuate DS/Cu complex-induced apoptosis and block JNK activation in vitro. Acetylcysteine 0-19 mitogen-activated protein kinase 8 Homo sapiens 109-112 24531650-8 2014 RESULTS: In vivo, N-acetylcysteine ameliorated the D-GalN/LPS-induced hepatotoxicity and reduced GSK3beta activity; GSK3beta inhibition increased hepatic superoxide dismutase activity and the glutathione content, decreased malondialdehyde production in the liver tissues; while GSK3beta inhibition suppressed the JNK activation in the liver and decreased cytochrome c release from mitochondria. Acetylcysteine 18-34 mitogen-activated protein kinase 8 Homo sapiens 313-316 23640957-7 2014 Furthermore, ROS scavenger N-acetyl L-cysteine attenuated beta-sitosterol-mediated sub-G1 accumulation, PARP cleavage, JNK and AMPK activation in U266 cells. Acetylcysteine 27-46 mitogen-activated protein kinase 8 Homo sapiens 119-122 24476312-7 2014 CeKD-induced cell apoptosis and ROS generation, as well as JNK activation, were inhibited by the antioxidant N-acetyl-L-cysteine. Acetylcysteine 109-128 mitogen-activated protein kinase 8 Homo sapiens 59-62 24735948-10 2014 In addition, N-acetylcysteine, an antioxidant, attenuated chrysotile asbestos-induced dephosphorylation of P-AKT and completely abolished phosphorylation/activation of JNK. Acetylcysteine 13-29 mitogen-activated protein kinase 8 Homo sapiens 168-171 24651440-10 2014 Moreover, the antioxidant N-acetylcysteine prevented phosphorylation of both JNK and c-Jun. Acetylcysteine 26-42 mitogen-activated protein kinase 8 Homo sapiens 77-80 23776698-10 2013 In addition, NAC completely blocked phosphorylation of JNK and p38 MAPK induced by AGE-BSA. Acetylcysteine 13-16 mitogen-activated protein kinase 8 Homo sapiens 55-58 24211866-6 2014 In addition, OLO-2 provokes the generation of reactive oxygen species (ROS) in HepG2 cells, while the antioxidant N-acetyl cysteine (NAC) almost completely blocks OLO-2-induced apoptosis and the activation of p38 and JNK. Acetylcysteine 114-131 mitogen-activated protein kinase 8 Homo sapiens 217-220 24211866-6 2014 In addition, OLO-2 provokes the generation of reactive oxygen species (ROS) in HepG2 cells, while the antioxidant N-acetyl cysteine (NAC) almost completely blocks OLO-2-induced apoptosis and the activation of p38 and JNK. Acetylcysteine 133-136 mitogen-activated protein kinase 8 Homo sapiens 217-220 24134840-5 2013 c-Jun N-terminal protein kinase (JNK) activation by curcumin was dependent on MST1, since MST1 inhibition by RNAi or NAC largely inhibited curcumin-induced JNK activation. Acetylcysteine 117-120 mitogen-activated protein kinase 8 Homo sapiens 0-31 24134840-5 2013 c-Jun N-terminal protein kinase (JNK) activation by curcumin was dependent on MST1, since MST1 inhibition by RNAi or NAC largely inhibited curcumin-induced JNK activation. Acetylcysteine 117-120 mitogen-activated protein kinase 8 Homo sapiens 33-36 24134840-5 2013 c-Jun N-terminal protein kinase (JNK) activation by curcumin was dependent on MST1, since MST1 inhibition by RNAi or NAC largely inhibited curcumin-induced JNK activation. Acetylcysteine 117-120 mitogen-activated protein kinase 8 Homo sapiens 156-159 24025361-10 2013 BBMD3 increased the production of reactive oxygen species (ROS) and ROS scavenger, N-acetylcysteine (NAC), could block the phosphorylation of JNK and c-Jun induced by BBMD3. Acetylcysteine 83-99 mitogen-activated protein kinase 8 Homo sapiens 142-145 24025361-10 2013 BBMD3 increased the production of reactive oxygen species (ROS) and ROS scavenger, N-acetylcysteine (NAC), could block the phosphorylation of JNK and c-Jun induced by BBMD3. Acetylcysteine 101-104 mitogen-activated protein kinase 8 Homo sapiens 142-145 22906494-9 2012 N-acetyl cysteine prevents GSH depletion and blocks menadione-induced complex dissociation, JNK activation and inhibits menadione-induced cytotoxicity. Acetylcysteine 0-17 mitogen-activated protein kinase 8 Homo sapiens 92-95 23717422-6 2013 In addition, sanguinarine effectively increased the activation of the c-Jun N-terminal kinase (JNK) and the expression of the early growth response gene-1 (Egr-1), which was recovered by pretreatment with NAC. Acetylcysteine 205-208 mitogen-activated protein kinase 8 Homo sapiens 70-93 23717422-6 2013 In addition, sanguinarine effectively increased the activation of the c-Jun N-terminal kinase (JNK) and the expression of the early growth response gene-1 (Egr-1), which was recovered by pretreatment with NAC. Acetylcysteine 205-208 mitogen-activated protein kinase 8 Homo sapiens 95-98 23416263-6 2013 Pretreatment with the antioxidant N-acetyl-cysteine (NAC): reduced the induction of ROS and MDA by CeO2 nanoparticles; recovered the activity of SOD, GSH-px and CAT; reduced the phosphorylation levels of ERK1/2, JNK and p38; and attenuated CeO2 nanoparticles-induced damage and apoptosis in SMMC-7721 cells. Acetylcysteine 34-51 mitogen-activated protein kinase 8 Homo sapiens 212-215 23416263-6 2013 Pretreatment with the antioxidant N-acetyl-cysteine (NAC): reduced the induction of ROS and MDA by CeO2 nanoparticles; recovered the activity of SOD, GSH-px and CAT; reduced the phosphorylation levels of ERK1/2, JNK and p38; and attenuated CeO2 nanoparticles-induced damage and apoptosis in SMMC-7721 cells. Acetylcysteine 53-56 mitogen-activated protein kinase 8 Homo sapiens 212-215 23405080-7 2013 Furthermore, exposure to Cd induced the phosphorylations of c-jun N-terminal kinases (JNK), extracellular signal-regulated kinases (ERK)1/2, and p38-mitogen-activated protein kinase (MAPK), which was prevented by NAC. Acetylcysteine 213-216 mitogen-activated protein kinase 8 Homo sapiens 60-84 22744860-10 2012 The antioxidant N-acetylcysteine and the NADPH inhibitor partially blunted sustained adenosine-induced JNK activation but were ineffective in attenuation of p38 activation or barrier dysfunction. Acetylcysteine 16-32 mitogen-activated protein kinase 8 Homo sapiens 103-106 23222262-7 2013 Removal of intracellular reactive oxygen species by N-acetyl-cysteine reduced the activation of AMP-activated protein kinase, extracellular signal-regulated kinase and Jun N-terminal kinase, and interleukin-8 induction. Acetylcysteine 52-69 mitogen-activated protein kinase 8 Homo sapiens 168-189 23063000-7 2013 In addition, most of the genes, known to be inducible by NF-kappaB or JNK following cytokines stimulation, were less induced by SCE when endothelial cells were pretreated with the antioxidant N-Acetylcysteine (NAC), suggesting a role of ROS in endothelial cell activation by SCE. Acetylcysteine 192-208 mitogen-activated protein kinase 8 Homo sapiens 70-73 23063000-7 2013 In addition, most of the genes, known to be inducible by NF-kappaB or JNK following cytokines stimulation, were less induced by SCE when endothelial cells were pretreated with the antioxidant N-Acetylcysteine (NAC), suggesting a role of ROS in endothelial cell activation by SCE. Acetylcysteine 210-213 mitogen-activated protein kinase 8 Homo sapiens 70-73 22824464-8 2012 Moreover, it was found that antioxidant N-acetylcysteine (NAC) blocked the induction of apoptosis and partly reversed the activation of JNK and p38, up-regulation of Bax, down-regulation of Bcl-2 and the activation of caspase-3 in NG-treated cells. Acetylcysteine 40-56 mitogen-activated protein kinase 8 Homo sapiens 136-139 22824464-8 2012 Moreover, it was found that antioxidant N-acetylcysteine (NAC) blocked the induction of apoptosis and partly reversed the activation of JNK and p38, up-regulation of Bax, down-regulation of Bcl-2 and the activation of caspase-3 in NG-treated cells. Acetylcysteine 58-61 mitogen-activated protein kinase 8 Homo sapiens 136-139 22606295-10 2012 NRG induced elevation in JNK phosphorylation that was inhibited by NAC. Acetylcysteine 67-70 mitogen-activated protein kinase 8 Homo sapiens 25-28 21827635-5 2012 RESULTS: Analysis was conducted on the mitogen-activated protein kinase signalling pathways, demonstrating that NAC infusion blocked the exercise-induced increase in JNK phosphorylation, but not ERK1/2, or p38 MAPK. Acetylcysteine 112-115 mitogen-activated protein kinase 8 Homo sapiens 166-169 21806545-9 2012 Atorvastatin, SP600125, JNK siRNA (small interfering RNA) and NAC (N-acetylcysteine) completely attenuated the leptin and phospho-JNK protein expression induced by Ang II. Acetylcysteine 62-65 mitogen-activated protein kinase 8 Homo sapiens 130-133 21806545-9 2012 Atorvastatin, SP600125, JNK siRNA (small interfering RNA) and NAC (N-acetylcysteine) completely attenuated the leptin and phospho-JNK protein expression induced by Ang II. Acetylcysteine 67-83 mitogen-activated protein kinase 8 Homo sapiens 130-133 22575515-8 2012 Meanwhile, results also showed that N-acetylcysteine (a reactive oxygen species scavenger) suppressed the proliferation and the ERK1/2 and JNK activation induced by 5-HT. Acetylcysteine 36-52 mitogen-activated protein kinase 8 Homo sapiens 139-142 21453688-5 2011 Activation of ERK and JNK, but not p38, via phosphorylation induction was identified in EPO1- but not EPO- or EPO2-treated U87 and C6 cells, and this was blocked by adding NAC. Acetylcysteine 172-175 mitogen-activated protein kinase 8 Homo sapiens 22-25 20919940-4 2011 Pretreatment with apocynin (NADPH oxidase inhibitor) or N-acetyl cysteine (antioxidant) significantly attenuated OSS-induced JNK activation. Acetylcysteine 56-73 mitogen-activated protein kinase 8 Homo sapiens 125-128 20674153-4 2010 In addition, icariin provoked the generation of reactive oxygen species (ROS) in SMMC-7721 cells, while the antioxidant N-acetyl cysteine almost completely blocked icariin-induced JNK activation and apoptosis. Acetylcysteine 120-137 mitogen-activated protein kinase 8 Homo sapiens 180-183 21385609-9 2011 The antioxidant N-acetylcysteine prevented JNK activation by trans-2-hexadecenal. Acetylcysteine 16-32 mitogen-activated protein kinase 8 Homo sapiens 43-46 21532338-8 2011 N-acetyl-cysteine (NAC; 10 mM) pre-treatment rescued cell viability of RKS262 (23 microM)-treated SMSKCNR cells, and pre-treatment with ascorbic acid (100 muM) and a MAPK inhibitor SB203580 (20 muM) reversed SAPK/JNK, caspase-3 activation, PARP-1 cleavage, and suppression of IGF-1R, PI3K, and PKC phosphorylation. Acetylcysteine 0-17 mitogen-activated protein kinase 8 Homo sapiens 213-216 21532338-8 2011 N-acetyl-cysteine (NAC; 10 mM) pre-treatment rescued cell viability of RKS262 (23 microM)-treated SMSKCNR cells, and pre-treatment with ascorbic acid (100 muM) and a MAPK inhibitor SB203580 (20 muM) reversed SAPK/JNK, caspase-3 activation, PARP-1 cleavage, and suppression of IGF-1R, PI3K, and PKC phosphorylation. Acetylcysteine 19-22 mitogen-activated protein kinase 8 Homo sapiens 213-216 21378396-7 2011 Iron or N-acetylcysteine supplementation reversed Dp44mT-induced up-regulation of phospho-JNK, but only iron was able to reverse the effect of DFO on JNK. Acetylcysteine 8-24 mitogen-activated protein kinase 8 Homo sapiens 90-93 21391979-10 2011 Generation of ROS induced phosphorylation of p42/p44 mitogen-activated protein kinase (MAPK), p38 MAPK and JNK1/2, which was attenuated by DPI and APO and the ROS scavenger N-acetylcysteine. Acetylcysteine 173-189 mitogen-activated protein kinase 8 Homo sapiens 107-113 21569548-9 2011 JNK phosphorylation induced by celastrol was suppressed by NAC and JNK inhibitor SP600125 (SP). Acetylcysteine 59-62 mitogen-activated protein kinase 8 Homo sapiens 0-3 21254278-0 2011 N-acetyl-L-cysteine counteracts oxidative stress and prevents H2O2 induced germ cell apoptosis through down-regulation of caspase-9 and JNK/c-Jun. Acetylcysteine 0-19 mitogen-activated protein kinase 8 Homo sapiens 136-139 20868662-4 2011 Carnosine exhibited better protection against MDA-induced cell injury than antioxidant N-acetyl-cysteine (NAC) with its multi-potency, which alleviated MDA-induced protein cross-linking, Deltapsim decrease, reactive oxygen species burst, JNK and ERK activation. Acetylcysteine 87-104 mitogen-activated protein kinase 8 Homo sapiens 238-241 20868662-4 2011 Carnosine exhibited better protection against MDA-induced cell injury than antioxidant N-acetyl-cysteine (NAC) with its multi-potency, which alleviated MDA-induced protein cross-linking, Deltapsim decrease, reactive oxygen species burst, JNK and ERK activation. Acetylcysteine 106-109 mitogen-activated protein kinase 8 Homo sapiens 238-241 20868662-6 2011 Carnosine alleviated all these alterations induced by MDA, but NAC merely inhibited Bcl-2 family-related activation of JNK and ERK. Acetylcysteine 63-66 mitogen-activated protein kinase 8 Homo sapiens 119-122 20920557-5 2010 The same results were obtained in the cells treated with N-acetyl-L-cysteine, suggesting that the prolonged activation of JNK and p38 by ISA is mediated by reactive oxygen species generated from mitochondria. Acetylcysteine 57-76 mitogen-activated protein kinase 8 Homo sapiens 122-125 20653470-0 2010 N-acetylcysteine protects alveolar epithelial cells from hydrogen peroxide-induced apoptosis through scavenging reactive oxygen species and suppressing c-Jun N-terminal kinase. Acetylcysteine 0-16 mitogen-activated protein kinase 8 Homo sapiens 152-175 20932751-5 2010 Pretreatment with the antioxidant N-acetyl-L-cysteine (NAC) markedly inhibited the CWJ-081-induced JNK activation and apoptosis. Acetylcysteine 34-53 mitogen-activated protein kinase 8 Homo sapiens 99-102 20443032-5 2010 At the same time, ERK and c-Jun N-terminal kinase (JNK) as well as cell division control protein 2 homolog (Cdc2) were found to be highly phosphorylated, which could be counteracted with the antioxidant N-acetylcysteine (NAC). Acetylcysteine 203-219 mitogen-activated protein kinase 8 Homo sapiens 26-49 20443032-5 2010 At the same time, ERK and c-Jun N-terminal kinase (JNK) as well as cell division control protein 2 homolog (Cdc2) were found to be highly phosphorylated, which could be counteracted with the antioxidant N-acetylcysteine (NAC). Acetylcysteine 203-219 mitogen-activated protein kinase 8 Homo sapiens 51-54 20443032-5 2010 At the same time, ERK and c-Jun N-terminal kinase (JNK) as well as cell division control protein 2 homolog (Cdc2) were found to be highly phosphorylated, which could be counteracted with the antioxidant N-acetylcysteine (NAC). Acetylcysteine 221-224 mitogen-activated protein kinase 8 Homo sapiens 26-49 20443032-5 2010 At the same time, ERK and c-Jun N-terminal kinase (JNK) as well as cell division control protein 2 homolog (Cdc2) were found to be highly phosphorylated, which could be counteracted with the antioxidant N-acetylcysteine (NAC). Acetylcysteine 221-224 mitogen-activated protein kinase 8 Homo sapiens 51-54 21038848-10 2010 N-Acetylcysteine (NAC), a known antioxidant, also decreased ROS generation, effectively blocked apoptosis, and decreased DADS-induced phosphorylated JNK levels. Acetylcysteine 0-16 mitogen-activated protein kinase 8 Homo sapiens 149-152 21038848-10 2010 N-Acetylcysteine (NAC), a known antioxidant, also decreased ROS generation, effectively blocked apoptosis, and decreased DADS-induced phosphorylated JNK levels. Acetylcysteine 18-21 mitogen-activated protein kinase 8 Homo sapiens 149-152 20632440-14 2010 Peak JNK activation occurred at 12 h post-treatment and this activation persisted for up to 24 h. The expression of phosphorylated JNK and c-Jun protein after 12 h with BrMC-treated cells was inhibited by N-acetylcysteine and SP600125 pre-treatment, but GW9662 had no effect. Acetylcysteine 205-221 mitogen-activated protein kinase 8 Homo sapiens 5-8 20632440-14 2010 Peak JNK activation occurred at 12 h post-treatment and this activation persisted for up to 24 h. The expression of phosphorylated JNK and c-Jun protein after 12 h with BrMC-treated cells was inhibited by N-acetylcysteine and SP600125 pre-treatment, but GW9662 had no effect. Acetylcysteine 205-221 mitogen-activated protein kinase 8 Homo sapiens 131-134 20121705-6 2010 Spermine-induced JNK activation was prevented by 200 microg/ml of both NAC and F1, while iNOS induction was blocked only by F1. Acetylcysteine 71-74 mitogen-activated protein kinase 8 Homo sapiens 17-20 20138622-6 2010 N-acetylcysteine that downregulated TNF-alpha-induced reactive oxygen species (ROS) inhibited JNK activation, but not p38 MAPK. Acetylcysteine 0-16 mitogen-activated protein kinase 8 Homo sapiens 94-97 20144638-5 2010 BAPTA-AM or NAC abrogated CMS-9-elicited p38 MAPK and JNK activation, and rescued viability of CMS-9-treated K562 cells. Acetylcysteine 12-15 mitogen-activated protein kinase 8 Homo sapiens 54-57 19468286-3 2009 The reducing agent, N-acetylcysteine (NAC), effectively inhibited the sustained activation of JNK, release of Endo G, and cell death in Jurkat cells treated by AD5-10. Acetylcysteine 20-36 mitogen-activated protein kinase 8 Homo sapiens 94-97 19540902-4 2009 N-Acetylcysteine (ROS scavenger) pretreatment reduced the dissipation of DeltaPsim, but insignificantly affected AA-induced p38 MAPK and JNK activation. Acetylcysteine 0-16 mitogen-activated protein kinase 8 Homo sapiens 137-140 19954742-7 2010 However, the phosphorylation of JNK rather than ERK1/2 activation by surfactin was blocked by NAC/catalase. Acetylcysteine 94-97 mitogen-activated protein kinase 8 Homo sapiens 32-35 19468286-3 2009 The reducing agent, N-acetylcysteine (NAC), effectively inhibited the sustained activation of JNK, release of Endo G, and cell death in Jurkat cells treated by AD5-10. Acetylcysteine 38-41 mitogen-activated protein kinase 8 Homo sapiens 94-97 19210339-11 2009 Cigarette smoke condensate-stimulated urokinase production was dependent on the activity of ERK/JNK pathways and was inhibited by the reactive oxygen species scavenger, N-acetyl cysteine. Acetylcysteine 169-186 mitogen-activated protein kinase 8 Homo sapiens 96-99 19176594-0 2009 N-acetyl cysteine mediates protection from 2-hydroxyethyl methacrylate induced apoptosis via nuclear factor kappa B-dependent and independent pathways: potential involvement of JNK. Acetylcysteine 0-17 mitogen-activated protein kinase 8 Homo sapiens 177-180 19292871-5 2009 ROS in turn exerted feedback regulation on JNK activation, as shown by the observations that cyclosporin A and the antioxidant N-acetylcysteine significantly inhibited the phosphorylation of JNK induced by morphine. Acetylcysteine 127-143 mitogen-activated protein kinase 8 Homo sapiens 43-46 19292871-5 2009 ROS in turn exerted feedback regulation on JNK activation, as shown by the observations that cyclosporin A and the antioxidant N-acetylcysteine significantly inhibited the phosphorylation of JNK induced by morphine. Acetylcysteine 127-143 mitogen-activated protein kinase 8 Homo sapiens 191-194 19176594-8 2009 NAC mediated prevention of HEMA induced cell death in NF-kappaB knockdown cells was correlated with a decreased induction of c-Jun N-terminal kinase (JNK) activity since NAC inhibited HEMA mediated increase in JNK levels. Acetylcysteine 0-3 mitogen-activated protein kinase 8 Homo sapiens 125-148 19176594-8 2009 NAC mediated prevention of HEMA induced cell death in NF-kappaB knockdown cells was correlated with a decreased induction of c-Jun N-terminal kinase (JNK) activity since NAC inhibited HEMA mediated increase in JNK levels. Acetylcysteine 0-3 mitogen-activated protein kinase 8 Homo sapiens 150-153 19176594-8 2009 NAC mediated prevention of HEMA induced cell death in NF-kappaB knockdown cells was correlated with a decreased induction of c-Jun N-terminal kinase (JNK) activity since NAC inhibited HEMA mediated increase in JNK levels. Acetylcysteine 0-3 mitogen-activated protein kinase 8 Homo sapiens 210-213 19176594-8 2009 NAC mediated prevention of HEMA induced cell death in NF-kappaB knockdown cells was correlated with a decreased induction of c-Jun N-terminal kinase (JNK) activity since NAC inhibited HEMA mediated increase in JNK levels. Acetylcysteine 170-173 mitogen-activated protein kinase 8 Homo sapiens 125-148 19176594-8 2009 NAC mediated prevention of HEMA induced cell death in NF-kappaB knockdown cells was correlated with a decreased induction of c-Jun N-terminal kinase (JNK) activity since NAC inhibited HEMA mediated increase in JNK levels. Acetylcysteine 170-173 mitogen-activated protein kinase 8 Homo sapiens 150-153 19176594-8 2009 NAC mediated prevention of HEMA induced cell death in NF-kappaB knockdown cells was correlated with a decreased induction of c-Jun N-terminal kinase (JNK) activity since NAC inhibited HEMA mediated increase in JNK levels. Acetylcysteine 170-173 mitogen-activated protein kinase 8 Homo sapiens 210-213 19176594-11 2009 Moreover, our data suggest the potential involvement of JNK pathway in NAC mediated protection. Acetylcysteine 71-74 mitogen-activated protein kinase 8 Homo sapiens 56-59 18569013-7 2008 In addition, Cr(VI) treatment induced endoplasmic reticulum (ER) stress and JNK activation and these effects were diminished by N-acetylcysteine. Acetylcysteine 128-144 mitogen-activated protein kinase 8 Homo sapiens 76-79 18805632-5 2009 ROS activated almost immediately in a time- and concentration-dependent manner the MAPK pathways p38, ERK and JNK (their activation was abrogated by the antioxidant N-acetylcysteine). Acetylcysteine 165-181 mitogen-activated protein kinase 8 Homo sapiens 110-113 18840412-6 2008 Pretreatment with antioxidant N-acetyl-l-cysteine (NAC) prevented glibenclamide-induced JNK activation, apoptosis and cellular viability decline. Acetylcysteine 30-49 mitogen-activated protein kinase 8 Homo sapiens 88-91 18718914-8 2008 Pretreatment with antioxidant N-acetylcysteine prevented the p53 accumulation, the phosphorylations of JNK and p38 MAPK, the inhibition of NF-kappaB activity, as well as the apoptosis induced by 15d-PGJ(2). Acetylcysteine 30-46 mitogen-activated protein kinase 8 Homo sapiens 103-106 18032928-8 2007 Furthermore, pretreatment of K562/A02 cells with NAC eliminated P-gp downregulation, JNK phosphorylation and c-Jun activation induced by salvicine. Acetylcysteine 49-52 mitogen-activated protein kinase 8 Homo sapiens 85-88 18728404-8 2008 Moreover, NAC effectively blocked apoptosis and decreased the levels of phosphorylated JNK induced by selenite. Acetylcysteine 10-13 mitogen-activated protein kinase 8 Homo sapiens 87-90 18038907-7 2007 In addition, NAC prevented LPS-induced activation of p38 MAPK and JNK but not phosphorylation and subsequent degradation of IkB. Acetylcysteine 13-16 mitogen-activated protein kinase 8 Homo sapiens 66-69 18038907-8 2007 These results indicate that NAC exerts anti-inflammatory effects in LPS-stimulated gingival fibroblasts, functioning at least in part via down-regulation of JNK and p38 MAPK activation. Acetylcysteine 28-31 mitogen-activated protein kinase 8 Homo sapiens 157-160 17481858-11 2007 Among various antioxidants used in this study, only thiol-containing antioxidants such as NAC or GSH inhibited both JNK and p38 MAPK activation and apoptosis, indicating the unique protective capacity of thiol compounds. Acetylcysteine 90-93 mitogen-activated protein kinase 8 Homo sapiens 116-119 17296806-7 2007 It is noteworthy that suppression of ROS accumulation by ROS scavengers butylated hydroxyanisole, and N-acetyl-L-cysteine prevented the luteolin-induced suppression of NF-kappaB and potentiation of JNK and significantly suppressed the synergistic cytotoxicity seen with cotreatment of luteolin and TNF. Acetylcysteine 102-121 mitogen-activated protein kinase 8 Homo sapiens 198-201 16648577-8 2006 Whereas the antioxidant N-acetyl-l-cysteine blocked the generation of reactive oxygen species and activation of JNK and AMPK, it did not block immunotoxin-induced apoptosis. Acetylcysteine 24-43 mitogen-activated protein kinase 8 Homo sapiens 112-115 16973888-2 2006 Addition of antioxidants such as N-acetyl-l-cysteine or catalase attenuates G-Rh2-induced ROS generation, JNK1 activation, and apoptosis. Acetylcysteine 33-52 mitogen-activated protein kinase 8 Homo sapiens 106-110 16515547-7 2006 Furthermore, suppression of the 6-OHDA-generated reactive oxygen species (ROS) by pre-incubation of cells with N-acetyl-L-cysteine effectively inhibited the 6-OHDA-induced activation of ASK1, p38 and JNK, and protected the cells from apoptosis. Acetylcysteine 111-130 mitogen-activated protein kinase 8 Homo sapiens 200-203 15965068-10 2005 N-acetylcysteine reduced the stimulatory effect of celecoxib on stress kinase activities, suggesting an involvement of JNK in HO-1 expression. Acetylcysteine 0-16 mitogen-activated protein kinase 8 Homo sapiens 119-122 15817678-4 2005 Application of N-acetylcysteine (NAC) or blocking the activity of Nox, a protein leading to the formation of ROS, with diphenylene iodonium (DPI) inhibits the responses of BMM cells to RANKL, including ROS production, activation of c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein (MAP) kinase, and extracellular signal-regulated kinase (ERK), and osteoclast differentiation. Acetylcysteine 15-31 mitogen-activated protein kinase 8 Homo sapiens 232-255 15817678-4 2005 Application of N-acetylcysteine (NAC) or blocking the activity of Nox, a protein leading to the formation of ROS, with diphenylene iodonium (DPI) inhibits the responses of BMM cells to RANKL, including ROS production, activation of c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein (MAP) kinase, and extracellular signal-regulated kinase (ERK), and osteoclast differentiation. Acetylcysteine 15-31 mitogen-activated protein kinase 8 Homo sapiens 257-260 15670787-3 2005 Both Cd-induced JNK and c-Jun phosphorylation and apoptosis were inhibited dramatically by N-acetyl-L-cysteine, a free radical scavenger. Acetylcysteine 91-110 mitogen-activated protein kinase 8 Homo sapiens 16-19 15197348-5 2004 The reduction in cell growth and enhancement in cell killing by the combination of GST-MDA-7 and radiation were blocked by an ROS scavenger, N-acetyl cysteine (NAC), a JNK1/2/3 inhibitor SP600125, a pan-caspase inhibitor (zVAD) and by an inhibitor of caspase 9 (LEHD), but not by an inhibitor of caspase 8 (IETD). Acetylcysteine 160-163 mitogen-activated protein kinase 8 Homo sapiens 168-176 14647418-7 2004 Lastly, antioxidants (e.g., L-N-acetylcysteine; L-NAC) opposed adaphostin-mediated mitochondrial dysfunction, Raf-1/MEK/ERK downregulation, JNK activation, and apoptosis. Acetylcysteine 28-46 mitogen-activated protein kinase 8 Homo sapiens 140-143 15197348-9 2004 In contrast, incubation with NAC blocked JNK1/2/3 activation and cell killing, but not the increases in BAD and BAX expression. Acetylcysteine 29-32 mitogen-activated protein kinase 8 Homo sapiens 41-49 15203191-13 2004 TGF-beta-stimulated ERK and JNK phosphorylation was also inhibited by NAC. Acetylcysteine 70-73 mitogen-activated protein kinase 8 Homo sapiens 28-31 15093752-6 2004 Lastly, the antioxidant N-acetyl-l-cysteine (LNAC) attenuated Bortezomib-mediated reactive oxygen species (ROS) generation, ERK inactivation, JNK activation, mitochondrial dysfunction, and apoptosis. Acetylcysteine 24-43 mitogen-activated protein kinase 8 Homo sapiens 142-145 12819184-10 2003 EGCG-induced JNK activation was blocked by the antioxidants glutathione and N-acetyl-l-cysteine, suggesting that the cell death signaling was potentially triggered by oxidative stress. Acetylcysteine 76-95 mitogen-activated protein kinase 8 Homo sapiens 13-16 14967008-8 2004 Moreover, exposure of PAECs to NAC alleviated the arsenite-induced JNK/AP-1 activation and apoptosis, whereas exposure of PAECs to BSO enhanced the arsenite-induced JNK/AP-1 activation and apoptosis. Acetylcysteine 31-34 mitogen-activated protein kinase 8 Homo sapiens 67-70 14614324-7 2003 Lastly, the free radical scavenger L-N-acetylcysteine (LNAC) attenuated HDI-mediated ROS generation, JNK activation, and apoptosis. Acetylcysteine 35-53 mitogen-activated protein kinase 8 Homo sapiens 101-104 14614324-7 2003 Lastly, the free radical scavenger L-N-acetylcysteine (LNAC) attenuated HDI-mediated ROS generation, JNK activation, and apoptosis. Acetylcysteine 55-59 mitogen-activated protein kinase 8 Homo sapiens 101-104 12414812-6 2003 N-Acetylcysteine and PP2 also partially inhibited JNK and p38 MAPK activation. Acetylcysteine 0-16 mitogen-activated protein kinase 8 Homo sapiens 50-53 12898340-6 2003 Meanwhile, compared to that of the controls, our results showed decreased level of ROS, less JNK activity and lower expression of cleaved caspase-3 in pretreated NAC groups and in Rg1 pretreated groups. Acetylcysteine 162-165 mitogen-activated protein kinase 8 Homo sapiens 93-96 11597988-6 2001 Ang II, as well as exogenous H(2)O(2), activated ERK, p38 MAPK, and JNK, which were significantly inhibited by N-acetylcysteine and DPI. Acetylcysteine 111-127 mitogen-activated protein kinase 8 Homo sapiens 68-71 12206715-11 2002 Taken together these results strongly suggest that EGCG executed apoptotic cell death via an ASK1, MKK and JNK/p38 cascade which is triggered by NAC-sensitive intracellular oxidative events in a manner distinct from chemically induced or receptor-mediated apoptosis. Acetylcysteine 145-148 mitogen-activated protein kinase 8 Homo sapiens 107-110 12206715-7 2002 The JNK/p38 activation by EGCG was also potently inhibited by NAC, whereas those by VP16 and TNF were either not or only minimally affected by NAC. Acetylcysteine 62-65 mitogen-activated protein kinase 8 Homo sapiens 4-7 12023963-6 2002 In addition, a fusion between p47(phox) and the TRAF4 C terminus constitutively activated JNK, and this activation was decreased by the antioxidant N-acetyl cysteine. Acetylcysteine 148-165 mitogen-activated protein kinase 8 Homo sapiens 90-93 11740866-2 2002 We found that activation of ECV-304 cells by TNFalpha was accompanied by a transient burst of oxidants and activation of JNK, both of which were suppressed by two distinct inhibitors of the phagocyte NADPH oxidase and the thiol antioxidant N-acetyl cysteine (NAC). Acetylcysteine 240-257 mitogen-activated protein kinase 8 Homo sapiens 121-124 11740866-2 2002 We found that activation of ECV-304 cells by TNFalpha was accompanied by a transient burst of oxidants and activation of JNK, both of which were suppressed by two distinct inhibitors of the phagocyte NADPH oxidase and the thiol antioxidant N-acetyl cysteine (NAC). Acetylcysteine 259-262 mitogen-activated protein kinase 8 Homo sapiens 121-124 11448159-6 2001 Both oxidase inhibitors and the thiol antioxidant N-acetyl cysteine decreased Tat-induced JNK1 activation in parallel with reduction in oxidant levels. Acetylcysteine 50-67 mitogen-activated protein kinase 8 Homo sapiens 90-94 11768769-7 2001 Free radical scavengers N-acetyl-L-cysteine (NAC), or glutathione (GSH), inhibited ERK2 activation and, to a much lesser extent, JNK1 activation by BHA/tBHQ, implicating the role of oxidative stress. Acetylcysteine 24-43 mitogen-activated protein kinase 8 Homo sapiens 129-133 10970698-3 2000 We extend these findings and show that the stimulation of JNK and apoptosis by antagonist G is dependent upon the generation of reactive oxygen species (ROS) being inhibited either by anoxia or the presence of N-acetyl cysteine (n-AC). Acetylcysteine 210-227 mitogen-activated protein kinase 8 Homo sapiens 58-61 11454688-10 2001 In contrast with partial protection by the caspase-3 inhibitor, the antioxidant N-acetyl-L-cysteine gave marked protection from As2O3-induced apoptosis and eliminated the activation of p38, JNK, and caspase-3, and the generation of ROS. Acetylcysteine 80-99 mitogen-activated protein kinase 8 Homo sapiens 190-193 11384840-7 2001 The free radical scavenging thiol antioxidant N-acetylcysteine (NAC) alleviated partially JNK-1 activation in amino acid-deprived cells. Acetylcysteine 46-62 mitogen-activated protein kinase 8 Homo sapiens 90-95 11384840-7 2001 The free radical scavenging thiol antioxidant N-acetylcysteine (NAC) alleviated partially JNK-1 activation in amino acid-deprived cells. Acetylcysteine 64-67 mitogen-activated protein kinase 8 Homo sapiens 90-95 11306679-8 2001 The stimulatory effect of Zn(2+) on both PI3K and JNK was repressed by the free-radical scavenging agent N-acetylcysteine. Acetylcysteine 105-121 mitogen-activated protein kinase 8 Homo sapiens 50-53 11350834-4 2001 Here we show that in a serum-depleted environment (0.1% fetal bovine serum), NAC substantially inhibited lipopolysaccharide (LPS) activation of the mitogen-activated protein kinases (MAPKs), namely extracellular signal-regulated kinase (ERK), p38mapk, and c-Jun NH2-terminal kinase (JNK). Acetylcysteine 77-80 mitogen-activated protein kinase 8 Homo sapiens 256-281 11350834-4 2001 Here we show that in a serum-depleted environment (0.1% fetal bovine serum), NAC substantially inhibited lipopolysaccharide (LPS) activation of the mitogen-activated protein kinases (MAPKs), namely extracellular signal-regulated kinase (ERK), p38mapk, and c-Jun NH2-terminal kinase (JNK). Acetylcysteine 77-80 mitogen-activated protein kinase 8 Homo sapiens 283-286 11350834-5 2001 By contrast, in the presence of 10% serum, NAC had no effect on LPS activation of p42 and p44 ERK and in fact enhanced LPS induction of p38mapk and JNK phosphorylation. Acetylcysteine 43-46 mitogen-activated protein kinase 8 Homo sapiens 148-151 10970698-3 2000 We extend these findings and show that the stimulation of JNK and apoptosis by antagonist G is dependent upon the generation of reactive oxygen species (ROS) being inhibited either by anoxia or the presence of N-acetyl cysteine (n-AC). Acetylcysteine 229-233 mitogen-activated protein kinase 8 Homo sapiens 58-61 10026227-4 1999 NAC inhibited agonist-induced ERK2, JNK1, and p38 MAP kinase activation and c-Fos, c-Jun, and JunB expression except for platelet-derived growth factor BB-induced ERK2 activation. Acetylcysteine 0-3 mitogen-activated protein kinase 8 Homo sapiens 36-40 10873716-7 2000 Media supplementation with the glutathione precursor N-acetyl-cysteine (NAC) reduced PCB 77-induced JNK/SAPK. Acetylcysteine 53-70 mitogen-activated protein kinase 8 Homo sapiens 100-108 10873716-7 2000 Media supplementation with the glutathione precursor N-acetyl-cysteine (NAC) reduced PCB 77-induced JNK/SAPK. Acetylcysteine 72-75 mitogen-activated protein kinase 8 Homo sapiens 100-108 10734112-4 2000 Interestingly, pretreatment with the antioxidants, N-acetyl-L-cysteine, dithiothreitol, and glutathione, impaired chelerythrine-induced JNK1 and p38 activation. Acetylcysteine 51-70 mitogen-activated protein kinase 8 Homo sapiens 136-140 10464319-5 1999 N-acetyl cysteine (a scavenger of reactive oxygen intermediates) abolished the ability of all oxidative stressors tested to activate JNK1, but failed to affect the activation of JNK1 by UV-B or by another ribotoxic stressor, the antibiotic anisomycin. Acetylcysteine 0-17 mitogen-activated protein kinase 8 Homo sapiens 133-137 10400652-7 1999 Both vanadate-induced degradation of IkappaBalpha and activation of JNK were potently inhibited by pretreatment of cells with N-acetylcysteine or dimercaprol. Acetylcysteine 126-142 mitogen-activated protein kinase 8 Homo sapiens 68-71 9670954-6 1998 The activation of JNK by HIV-tat appears to be mediated through generation of free radical species, since pretreatment of cells with N-acetylcysteine (NAC) abolished the effect. Acetylcysteine 133-149 mitogen-activated protein kinase 8 Homo sapiens 18-21 9670954-6 1998 The activation of JNK by HIV-tat appears to be mediated through generation of free radical species, since pretreatment of cells with N-acetylcysteine (NAC) abolished the effect. Acetylcysteine 151-154 mitogen-activated protein kinase 8 Homo sapiens 18-21 12671299-5 1998 Pretreatment with free radical scavengers N-acetyl-L-cysteine (NAC), glutathione (GSH), or vitamin E, inhibited ERK2 activation and, to a much lesser extent, JNK 1 activation by BHA and tBHQ, implicating the role of oxidative stress. Acetylcysteine 42-61 mitogen-activated protein kinase 8 Homo sapiens 158-163 9182816-7 1997 The antioxidant N-acetylcysteine impaired the UVB- and EGF-induced activation of JNK1. Acetylcysteine 16-32 mitogen-activated protein kinase 8 Homo sapiens 81-85 9430725-6 1998 Isothiocyanate-induced JNK activation was blocked by the antioxidants 2-mercaptoethanol and N-acetyl-L-cysteine, suggesting that the death signaling was triggered by oxidative stress. Acetylcysteine 92-111 mitogen-activated protein kinase 8 Homo sapiens 23-26 9452508-7 1998 Anti-oxidants N-acetylcysteine and catalase, which serve as scavengers of reactive oxygen species generated by metabolic DA oxidation, effectively block DA-induced JNK activation and subsequent apoptosis. Acetylcysteine 14-30 mitogen-activated protein kinase 8 Homo sapiens 164-167 9360968-9 1997 Pretreatment with N-acetyl-L-cysteine, glutathione, or vitamin E attenuated ERK2 but not JNK1 activation by BHA and tBHQ. Acetylcysteine 18-37 mitogen-activated protein kinase 8 Homo sapiens 89-93 9354637-5 1997 The sodium nitroprusside-induced stimulation of JNK1 activity was abolished by treatment of cells with N-acetylcysteine. Acetylcysteine 103-119 mitogen-activated protein kinase 8 Homo sapiens 48-52 33806765-7 2021 Pre-treatment with N-acetylcysteine significantly abrogated the expression of nuclear HIF-1alpha, JNK transduction components and fibrotic marker proteins. Acetylcysteine 19-35 mitogen-activated protein kinase 8 Homo sapiens 98-101 8824287-3 1996 In this study we show that the structurally unrelated antioxidant agents pyrrolidine dithiocarbamate (PDTC), butylated hydroxyanisole, and Nacetylcysteine activated JNK (c-Jun NH2-terminal kinase) in Jurkat T cells. Acetylcysteine 139-154 mitogen-activated protein kinase 8 Homo sapiens 165-168 8824287-3 1996 In this study we show that the structurally unrelated antioxidant agents pyrrolidine dithiocarbamate (PDTC), butylated hydroxyanisole, and Nacetylcysteine activated JNK (c-Jun NH2-terminal kinase) in Jurkat T cells. Acetylcysteine 139-154 mitogen-activated protein kinase 8 Homo sapiens 170-195 9234735-5 1997 We identified the intracellular glutathione (GSH) level as critical for JNK/SAPK activation by MMS: enhancing the GSH level by pretreatment of the cells with GSH or N-acetylcysteine inhibits, whereas depletion of the cellular GSH pool causes hyperinduction of JNK/SAPK activity by MMS. Acetylcysteine 165-181 mitogen-activated protein kinase 8 Homo sapiens 72-80 9234735-5 1997 We identified the intracellular glutathione (GSH) level as critical for JNK/SAPK activation by MMS: enhancing the GSH level by pretreatment of the cells with GSH or N-acetylcysteine inhibits, whereas depletion of the cellular GSH pool causes hyperinduction of JNK/SAPK activity by MMS. Acetylcysteine 165-181 mitogen-activated protein kinase 8 Homo sapiens 72-75 34763314-11 2022 Moreover, these elevated levels of the proteins were inhibited by the antioxidant N-acetylcysteine and the JNK inhibitor SP600125, suggesting the involvement of ROS/JNK-dependent mechanisms in AGS-30-induced apoptosis. Acetylcysteine 82-98 mitogen-activated protein kinase 8 Homo sapiens 165-168 34681610-5 2021 Further study revealed that OTA increased reactive oxygen species (ROS) levels, and N-acetyl cysteine (NAC) could reduce OTA-induced JNK-related apoptosis and ROS levels in HK-2 cells. Acetylcysteine 84-101 mitogen-activated protein kinase 8 Homo sapiens 133-136 34468764-11 2021 Eliminating ROS by N-acetyl-l-cysteine abrogated Cd-induced PP2A-JNK pathway disruption and concurrently reinforced MgIG-conferred protective effects, which could be further slightly strengthened by PP2A overexpression. Acetylcysteine 19-38 mitogen-activated protein kinase 8 Homo sapiens 65-68 34481340-13 2021 Treatment with the ROS scavenger N-acetyl cysteine, effectively reversed the induction of apoptosis, autophagy, JNK activation and DNA damage elicited by RA. Acetylcysteine 33-50 mitogen-activated protein kinase 8 Homo sapiens 112-115 34776955-5 2021 This was confirmed by which the JNK inhibitor SP600125 partially rescued CRC cells from chaetocin induced apoptosis and the ROS scavenger N-acetyl-L-cysteine (NAC) reversed both the chaetocin induced apoptosis and the JNK/c-Jun pathway activation. Acetylcysteine 138-157 mitogen-activated protein kinase 8 Homo sapiens 218-221 34776955-5 2021 This was confirmed by which the JNK inhibitor SP600125 partially rescued CRC cells from chaetocin induced apoptosis and the ROS scavenger N-acetyl-L-cysteine (NAC) reversed both the chaetocin induced apoptosis and the JNK/c-Jun pathway activation. Acetylcysteine 159-162 mitogen-activated protein kinase 8 Homo sapiens 218-221 34644184-8 2021 Mancozeb reduced viability and increased the level of intracellular ROS, p38 and c-Jun N-terminal kinases (JNK) MAPK proteins phosphorylation, and apoptotic cell death, which could be blocked by NAC as an inhibitor of oxidative stress. Acetylcysteine 195-198 mitogen-activated protein kinase 8 Homo sapiens 81-105 34644184-8 2021 Mancozeb reduced viability and increased the level of intracellular ROS, p38 and c-Jun N-terminal kinases (JNK) MAPK proteins phosphorylation, and apoptotic cell death, which could be blocked by NAC as an inhibitor of oxidative stress. Acetylcysteine 195-198 mitogen-activated protein kinase 8 Homo sapiens 107-110 34681610-5 2021 Further study revealed that OTA increased reactive oxygen species (ROS) levels, and N-acetyl cysteine (NAC) could reduce OTA-induced JNK-related apoptosis and ROS levels in HK-2 cells. Acetylcysteine 103-106 mitogen-activated protein kinase 8 Homo sapiens 133-136 33900847-10 2021 Pre-treatment with the antioxidant N-acetyl-L-cysteine could ameliorate HUA-activated JNK and hepatic steatosis. Acetylcysteine 35-54 mitogen-activated protein kinase 8 Homo sapiens 86-89 34475984-5 2021 The inhibition of ROS generation by N-acetyl-l-cysteine not only recovered cell migration and viability, but also reduced beta-catenin accumulation and JNK and ERK activation. Acetylcysteine 36-55 mitogen-activated protein kinase 8 Homo sapiens 152-155 35571453-11 2022 BBR-induced, dose-dependent induction of apoptosis was accompanied by sustained phosphorylation of c-jun-NH2-kinase (JNK) and the JNK inhibitor (SP600125) significantly suppressed BBR-induced apoptosis, N-acetyl cysteine (NAC), a ROS scavenger, was sufficient to both suppress apoptosis signal-regulating kinase 1 (ASK1) and JNK activation and disrupt apoptotic induction. Acetylcysteine 203-220 mitogen-activated protein kinase 8 Homo sapiens 99-115 35571453-11 2022 BBR-induced, dose-dependent induction of apoptosis was accompanied by sustained phosphorylation of c-jun-NH2-kinase (JNK) and the JNK inhibitor (SP600125) significantly suppressed BBR-induced apoptosis, N-acetyl cysteine (NAC), a ROS scavenger, was sufficient to both suppress apoptosis signal-regulating kinase 1 (ASK1) and JNK activation and disrupt apoptotic induction. Acetylcysteine 203-220 mitogen-activated protein kinase 8 Homo sapiens 117-120 35571453-11 2022 BBR-induced, dose-dependent induction of apoptosis was accompanied by sustained phosphorylation of c-jun-NH2-kinase (JNK) and the JNK inhibitor (SP600125) significantly suppressed BBR-induced apoptosis, N-acetyl cysteine (NAC), a ROS scavenger, was sufficient to both suppress apoptosis signal-regulating kinase 1 (ASK1) and JNK activation and disrupt apoptotic induction. Acetylcysteine 203-220 mitogen-activated protein kinase 8 Homo sapiens 130-133 35571453-11 2022 BBR-induced, dose-dependent induction of apoptosis was accompanied by sustained phosphorylation of c-jun-NH2-kinase (JNK) and the JNK inhibitor (SP600125) significantly suppressed BBR-induced apoptosis, N-acetyl cysteine (NAC), a ROS scavenger, was sufficient to both suppress apoptosis signal-regulating kinase 1 (ASK1) and JNK activation and disrupt apoptotic induction. Acetylcysteine 222-225 mitogen-activated protein kinase 8 Homo sapiens 99-115 35571453-11 2022 BBR-induced, dose-dependent induction of apoptosis was accompanied by sustained phosphorylation of c-jun-NH2-kinase (JNK) and the JNK inhibitor (SP600125) significantly suppressed BBR-induced apoptosis, N-acetyl cysteine (NAC), a ROS scavenger, was sufficient to both suppress apoptosis signal-regulating kinase 1 (ASK1) and JNK activation and disrupt apoptotic induction. Acetylcysteine 222-225 mitogen-activated protein kinase 8 Homo sapiens 117-120 35571453-11 2022 BBR-induced, dose-dependent induction of apoptosis was accompanied by sustained phosphorylation of c-jun-NH2-kinase (JNK) and the JNK inhibitor (SP600125) significantly suppressed BBR-induced apoptosis, N-acetyl cysteine (NAC), a ROS scavenger, was sufficient to both suppress apoptosis signal-regulating kinase 1 (ASK1) and JNK activation and disrupt apoptotic induction. Acetylcysteine 222-225 mitogen-activated protein kinase 8 Homo sapiens 130-133 33959604-9 2021 In addition, the activation of ER stress and the JNK signaling pathway prompted by IATL and cisplatin was also reversed by NAC pretreatment. Acetylcysteine 123-126 mitogen-activated protein kinase 8 Homo sapiens 49-52 32658869-7 2020 Decrease of mtROS with N-acetyl-L-cysteine attenuated the activation of JNK and the increase of SOD2 transcription. Acetylcysteine 23-42 mitogen-activated protein kinase 8 Homo sapiens 72-75 33632046-8 2021 The antioxidant N-acetyl cysteine (NAC) also showed similar effects on JNK and NF-kappaB-P65 phosphorylation and inflammatory cytokines (p < .00). Acetylcysteine 16-33 mitogen-activated protein kinase 8 Homo sapiens 71-74 33632046-8 2021 The antioxidant N-acetyl cysteine (NAC) also showed similar effects on JNK and NF-kappaB-P65 phosphorylation and inflammatory cytokines (p < .00). Acetylcysteine 35-38 mitogen-activated protein kinase 8 Homo sapiens 71-74 32922532-8 2020 ROS exclusive inhibitor antioxidant N-acetyl cysteine (NAC) weakens the phosphorylation of JNK proteins induced by Propranolol. Acetylcysteine 36-53 mitogen-activated protein kinase 8 Homo sapiens 91-94 32922532-8 2020 ROS exclusive inhibitor antioxidant N-acetyl cysteine (NAC) weakens the phosphorylation of JNK proteins induced by Propranolol. Acetylcysteine 55-58 mitogen-activated protein kinase 8 Homo sapiens 91-94 32985606-7 2020 Notably, all these events were reverted by N-acetyl-L-cysteine and JNK inhibitor SP600125 furnishing evidence that APE exerted its effects through the activation of ROS/JNK signaling. Acetylcysteine 43-62 mitogen-activated protein kinase 8 Homo sapiens 169-172 31934265-11 2019 After pretreatment with NAC, the phosphorylation of P38MAPK, JNK, and NF-kappaB and TGF-beta expressions in ECs under stretch was suppressed; similar results were observed in simvastatin-treated ECs. Acetylcysteine 24-27 mitogen-activated protein kinase 8 Homo sapiens 61-64 32131874-9 2020 RESULTS: Low-dose NAC (1000 muM) increased the expression of Nrf2 and phospho-p62 in MH7A cells, activating antioxidant genes, suppressing the expression of MMP-3, and inhibiting the phosphorylation of JNK. Acetylcysteine 18-21 mitogen-activated protein kinase 8 Homo sapiens 202-205 31756635-6 2020 The elevation of Drp1 phosphorylation was partly dependent on the reactive oxygen species (ROS)-mediated activation of c-Jun-N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK), as N-acetyl-l-cysteine (NAC) pretreatment inhibited the activation of JNK and p38 MAPK while attenuating Drp1 phosphorylation in acetaldehyde-treated cells. Acetylcysteine 201-220 mitogen-activated protein kinase 8 Homo sapiens 119-142 31756635-6 2020 The elevation of Drp1 phosphorylation was partly dependent on the reactive oxygen species (ROS)-mediated activation of c-Jun-N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK), as N-acetyl-l-cysteine (NAC) pretreatment inhibited the activation of JNK and p38 MAPK while attenuating Drp1 phosphorylation in acetaldehyde-treated cells. Acetylcysteine 222-225 mitogen-activated protein kinase 8 Homo sapiens 119-142 31617221-9 2020 In addition, ARG increased the generation of reactive oxygen species (ROS) in HepG2 cells, while the antioxidant N-acetyl cysteine almost reversed ARG-induced JNK and p38 activation, and dramatically decreased cell apoptosis. Acetylcysteine 113-130 mitogen-activated protein kinase 8 Homo sapiens 159-162