n -乙酰半胱氨酸对雄性大鼠脑缺血再灌注海马组织凋亡及NGF-Akt/Bad通路的影响。

IF 3.5 3区 医学 Q2 ENDOCRINOLOGY & METABOLISM
Hamed Saniei, Roya Naderi
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引用次数: 0

摘要

细胞凋亡是脑缺血再灌注(I/R)神经元损伤的主要病理特征。具体的分子介质仍在争论中。本研究旨在探讨脑缺血再灌注对大鼠海马细胞凋亡和NGF-Akt/Bad轴的影响,并与NAC (n -乙酰半胱氨酸)联用。大鼠颈总动脉闭塞(CCAO) 20 min,再灌注24 h。NAC (150mg /kg)于缺血前1小时、再灌注前5分钟腹腔注射。海马神经元TUNEL染色显示再灌注24 h后凋亡神经元数量增加。在分子水平上,I/R损伤导致cleaved caspase3/procaspase3的蛋白表达和细胞色素c水平升高,同时NGF、p-AKT/AKT、p-Bad/Bad和p-Trk/Trk比值下调。NAC处理可显著降低I/R大鼠海马神经元的凋亡损伤,逆转NGF、p-AKT/AKT、p-Bad/Bad和p-Trk/Trk比值。综上所述,我们的数据表明,NGF-Akt/Bad轴可能在海马细胞死亡中发挥调节作用,为过境性缺血性卒中的新治疗策略提供了新的靶点。NAC已被证明可以逆转分子改变,这表明它可能是一种有效的抗急性I/R损伤后海马细胞凋亡的药物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The effect of N-acetylcysteine on apoptosis and NGF-Akt/Bad pathway in the hippocampus tissue of cerebral ischemia-reperfusion in male rats.

Apoptosis is the primary pathological feature of neuronal injury caused by cerebral ischemia-reperfusion (I/R). The detailed molecular mediators are still being debated. This study aims to examine the effects of cerebral ischemia-reperfusion on apoptosis and NGF-Akt/Bad axis in rat hippocampus alone and in combination with NAC (N-Acetylcysteine). Rats were subjected to common carotid artery occlusion (CCAO) for 20 min followed by 24 h reperfusion. NAC (150 mg/kg) was given intraperitoneally (ip) one hour before ischemia and five minutes before reperfusion. TUNEL staining of hippocampus neurons revealed that the number of apoptotic neurons was elevated 24 h after reperfusion. At the molecular levels, I/R injury resulted in an increased protein expression of cleaved caspase3/procaspase3 ratio and cytochrome c level with a concomitant down-regulation of NGF, p-AKT/AKT, p-Bad/Bad and p-Trk/Trk ratio. NAC treatment significantly reduced the apoptotic damage and also reversed NGF, p-AKT/AKT, p-Bad/Bad, and p-Trk/Trk ratio in hippocampus neurons in I/R rats. In conclusion, our data showed that NGF-Akt/Bad axis may play a regulatory role in hippocampus cell death, providing a new target for a novel therapeutic strategy during transit ischemic stroke. NAC has been shown to reverse molecular alterations, suggesting its potential as an effective agent against hippocampal apoptosis following acute I/R injury.

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来源期刊
Metabolic brain disease
Metabolic brain disease 医学-内分泌学与代谢
CiteScore
5.90
自引率
5.60%
发文量
248
审稿时长
6-12 weeks
期刊介绍: Metabolic Brain Disease serves as a forum for the publication of outstanding basic and clinical papers on all metabolic brain disease, including both human and animal studies. The journal publishes papers on the fundamental pathogenesis of these disorders and on related experimental and clinical techniques and methodologies. Metabolic Brain Disease is directed to physicians, neuroscientists, internists, psychiatrists, neurologists, pathologists, and others involved in the research and treatment of a broad range of metabolic brain disorders.
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