过高血糖应激会通过触发 redoxosomes/p66SHC 激活诱导肠道质细胞的氧化损伤
Yanmin Jiang1,2, Lan Xu2, Xue Zhu3
1Department of Endocrinology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, People's Republic of China.
Redox report : communications in free radical research
|March 6, 2024
概括
过高血糖应激会通过复原酶/p66SHC信号传递损害糖尿病胃肠功能障碍 (DGD) 中的肠质细胞 (EGC). 抑制这种途径可能为DGD提供治疗点.
科学领域:
- 胃肠病学 胃肠病学
- 内分泌学 在内分泌学.
- 神经科学是一个神经科学.
背景情况:
- 糖尿病胃肠道功能障碍 (DGD) 是糖尿病 (DM) 的严重并发症.
- 糖尿病胃肠道功能障碍 (DGD) 显著影响肠道神经系统 (ENS),特别是肠道质细胞 (EGC).
研究的目的:
- 研究高血糖应激对肠道质细胞 (EGC) 的影响.
- 阐明糖尿病胃肠道功能障碍 (DGD) 中高血糖压力诱导的EGC损伤的潜在分子机制.
主要方法:
- 在体外研究中,EGC暴露于高血糖症,评估活力,亡和氧化损伤.
- 在体内研究中,利用链毒素 (STZ) 诱导的糖尿病小鼠来评估EGC亡和十二指肠的氧化损伤.
主要成果:
- 高血糖应激诱导了EGC的显著氧化损伤,无论是体外还是体内.
- 这种损伤涉及回氧体,包括SRC,Vav2,RAC1和NADPH氧化酶 (NOX) 的激活.
- 红氧体抑制剂 (NSC23766,VAS2870) 和p66SHC减弱了高血糖应激诱导的EGC氧化损伤.
结论:
- 红氧体/p66SHC信号通路在糖尿病胃肠道功能障碍 (DGD) 中介于EGCs的氧化损伤.
- 这种信号级联为治疗糖尿病胃肠功能障碍 (DGD) 提供了潜在的治疗目标.
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