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[通过调节RAGE/JAK1/STAT信号通路,沙利德对糖尿病病小鼠损伤的保护作用]

Chang-Long Leng¹, Kuan Lin¹, Mei Zhou¹

¹Wuhan Institute of Biomedical Sciences, Jianghan University Wuhan 430000, China.

Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica

|May 30, 2024

概括

沙利德 (SAL) 通过减少损伤和抑制RAGE/JAK1/STAT3通路,有效地治疗小鼠的糖尿病病 (DN). 这种天然化合物减轻氧化应激和纤维化,为DN提供了潜在的治疗策略.

科学领域:

药理学药理学是指药理学的学科.
腎臟病學 (nephrology) 是一種醫學專業.
生物化学生化学

背景情况:

糖尿病病 (DN) 是糖尿病的严重并发症,其特征是逐渐的损伤.
先进的糖化终产品 (RAGE) /Janus激活激酶1 (JAK1) /转录3 (STAT3) 信号传感器和激活器信号通路的受体参与了DN的发病.
沙利化物 (SAL) 是一种具有潜在治疗功能的天然化合物.

研究的目的:

在糖尿病病 (DN) 的小鼠模型中研究沙利德 (SAL) 对损伤的保护作用.
阐明RAGE/JAK1/STAT3信号通路在SAL的脏保护机制中的作用.

主要方法:

通过使用高脂肪/高糖饮食和注射 estreptozotocin (STZ) 来建立 DN 的小鼠模型.
在10周的时间里,小鼠接受了不同剂量的SAL或甲福林治疗.
评估的参数包括体重,血糖,功能标志物 (Scr,BUN,24小时-UTP),脂质样本,氧化应激标志物 (SOD,CAT,GSH-PX,MDA),组织病理以及RAGE,JAK1,STAT3,α-SMA,维丁的蛋白质表达和AGE通过西斑和免疫组织化学.

主要成果:

盐酸治疗显著逆转了DN诱导的血糖,水摄入量,指数,尿道总蛋白质,血清肌素,BUN,脂质,氧化应激标志物和纤维化指标的增加.
在脏组织中,SAL显著降低了AGE,RAGE,酸化JAK1,酸化STAT3,α-SMA和维门的表达.
与低剂量组相比,高剂量SAL表现出更明显的保护作用.

结论:

在糖尿病病 (DN) 的小鼠模型中,沙利德 (SAL) 显示出显著的保护作用.
盐酸通过抑制AGE介导的RAGE/JAK1/STAT3信号通路来缓解氧化应激和纤维化.
盐酸盐作为治疗糖尿病病的潜在治疗剂具有前途.

关键词:

在 RAGE/JAK1/STAT3 信号轴上糖尿病性脏病糖尿病性脏病氧化应激是一种氧化应激.脏纤维化脏纤维化沙利德化物是什么

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