Antioxidant N-acetylcysteine inhibits the activation of JNK3 mediated by the GluR6–PSD95–MLK3 signaling module during cerebral ischemia in rat hippocampus
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Acknowledgement
This work was supported by a grant from the Key Project of the National Natural Science Foundation of China (No. 30330190).
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2015, NeuropharmacologyCitation Excerpt :NO, derived from nNOS, activated the JNK3 signaling pathway via S-nitrosylation, triggering ischemic neuronal cell death (Pei et al., 2008; Yu et al., 2008). Antioxidant therapy with N-acetylcysteine inhibited the activation of JNK3 and attenuated neural damage in experimental cerebral ischemic models (Qi et al., 2010; Zhang et al., 2006). In present study, we found that both pre- and post-ischemic treatments of MCP remarkably suppressed the phosphorylation of JNK3 at the CA1 region of ischemic brains.
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2013, SteroidsCitation Excerpt :At the time of ovariectomy (STED) or 10 weeks later (LTED), placebo (20% β-Cyclodextrin) or 17β-estradiol osmotic mini-pumps (0.0167 mg E2 in 20% β-Cyclodextrin, 0.5 μL/h, 14-day release; Alzet, Cupertino, CA) were implanted subcutaneously between the scapulae to mimic physiological E2 levels during Diestrus I (10–15 pg/mL) [30]. All animals (except sham control) underwent global cerebral ischemia (GCI) via 4-vessel occlusion as described previously [44,37,45]. The day before GCI, animals were anesthetized using chloral hydrate (350 mg/kg, ip), and both vertebral arteries (VA) were permanently occluded at the level of the alar foramina via electrocauterization.
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2011, Archives of Biochemistry and BiophysicsCitation Excerpt :This finding extended our former observations showing the Ask1-MKK4-JNK activation cascade was selectively inhibited by administration of NAC [37]. Given the fact above, in our present study, we gave rats N-acetylcysteine (NAC) before cerebral ischemia as previous described [12,27], then we detected the translocation of Daxx, and interaction among Fas, Daxx and Ask1. We found an interesting phenomenon that NAC played a role in both diminishing Daxx trafficking and disturbing the Fas-Daxx-Ask1 signal module.
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The first two authors contributed equally to this work.