在db/db小鼠中,acteoside通过调节AKT/GSK-3β信号通路来保护podocyte免受亡
Xiaoya Li1,2,3, Zhilong Liu3,4, Zhixiu He1,2,3
1Department of Nephrology, Shanxi Provincial People's Hospital, Taiyuan, China.
BMC endocrine disorders
|October 23, 2023
概括
乙酸盐 (Act) 通过防止 podocyte 亡,减少糖尿病小鼠的白蛋白尿和损伤. 这种天然化合物抑制AKT/GSK-3β通路,为糖尿病病提供了潜在的治疗方法.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學專業.
- 药理学 药理学是指药理学的学科.
- 糖尿病学 糖尿病学
背景情况:
- 足细胞亡是糖尿病病 (DKD) 进展的关键因素.
- 乙酸 (Act),源自Rehmannia glutinosa,表现出已知的保护作用.
研究的目的:
- 在糖尿病病 (DKD) 的小鼠模型中研究Acteoside (Act) 的保护作用.
- 阐明ACT对细胞亡和功能作用的潜在机制.
主要方法:
- 使用C57BLKS/J db/db小鼠作为DKD模型.
- 用于8周的行为,评估尿蛋白,功能和血液脂质.
- 通过HE和PAS染色评估病理;通过免疫组织化学,西部斑点和TUNEL染色检查细胞亡和信号通路.
主要成果:
- 在db/db小鼠中,Act的使用显著降低了albuminuria (391至152ug/24h),并改善了病理.
- 作用上调的 podocyte 标记物 (synaptopodin, podocin) 和抑制的 podocyte 亡 (减少分离的 caspase-3 和 Bax,增加 Bcl-2).
- 这种行为抑制了AKT/GSK-3β信号通路.
结论:
- 乙酸 (Act) 通过抑制AKT/GSK-3β信号通路来保护细胞免受亡.
- 在小鼠中,Act治疗改善了白蛋白尿和延迟了糖尿病病 (DKD) 的进展.
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