AKT抑制剂通过阻断EndoMT转换来延缓STZ诱导的糖尿病病
Yue Chen1, Yuanjing Li2, Xing Wen3
1Department of Oncology, Chongqing University Jiangjin Hospital, Chongqing, China.
Pakistan journal of pharmaceutical sciences
|February 1, 2026
概括
一种AKT抑制剂通过减少炎症和氧化压力来治疗糖尿病病 (DN) 是有前途的. 这种干预可以通过抑制内皮质-介质酶过渡 (EndoMT) 来减缓DN进展.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學專業.
- 内分泌学 在内分泌学.
- 分子生物学分子生物学
背景情况:
- 糖尿病病 (DN) 是糖尿病的一个主要并发症,导致末期病.
- 了解DN病原体对于开发有效的治疗方法至关重要.
研究的目的:
- 研究AKT抑制剂在糖尿病病中调节内皮 - 介质细胞过渡 (EndoMT) 的作用.
- 为了确定AKT抑制是否可以减轻DN进展.
主要方法:
- 威斯塔鼠被分为对照组,DN模型和AKT抑制剂治疗组.
- 生物化学标记物 (血清肌素,BUN,尿蛋白),氧化应激标记物 (ROS,SOD),炎症因子 (IL-6,IL-1β) 和EndoMT标记物 (VE-cadherin,CD31,α-SMA,原I) 进行了评估.
主要成果:
- 用AKT抑制剂治疗显著降低了血清肌素,BUN,尿蛋白,ROS,IL-6,IL-1β,α-SMA和原I水平.
- 抑制剂增加了SOD活性和VE-Cadherin和CD31的表达.
- 通过AKT抑制剂,p-AKT水平也降低了.
结论:
- 抑制AKT可能会延迟糖尿病病的进展.
- 抑制EndoMT,炎症和氧化应激是潜在的机制.
- AKT 抑制剂代表了对DN的潜在治疗策略.
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