奥梅普拉在老鼠脏中诱导了profibrotic基因表达:TGF-β/Smad信号通路的含义
Albatoul Allam1, Azza A Ali1, Naira A Abdel Baky1
1Pharmacology and Toxicology Department, Faculty of Pharmacy (Girls), Al-Azhar University, Cairo, Egypt.
Drug and chemical toxicology
|November 20, 2023
概括
像奥梅普拉这样的质子抑制剂可以通过激活profibrotic基因来损害脏. 同时服用反应性氧物种清除剂可能会减轻这种损伤.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學.
- 药理学 药理学是指药理学的学科.
- 分子生物学分子生物学
背景情况:
- 质子抑制剂 (PPI) 被广泛使用,但与损伤有关.
- 造成PPI引起的损伤背后的机制尚不清楚.
研究的目的:
- 为了研究梅诱导的损伤的分子机制.
- 探索反应性氧物种 (ROS) 和TGF-β信号在PPI毒性中的作用.
主要方法:
- 在老鼠中使用奥梅普拉来诱导损伤.
- 对TGF-β/Smad信号通路激活的评估.
- 测量益纤维素基因表达 (CTGF,TIMP-1). 测量益纤维素基因表达的方法.
- 评估ROS水平,SOD活动和MDA水平.
- 用TGF-β抑制剂 (迪赛特) 和ROS清除剂 (N-乙囊) 治疗.
主要成果:
- 奥梅普拉激活了TGF-β/Smad信号传递,并增加了CTGF和TIMP-1的表达.
- 迪赛特化物抑制了欧梅普拉诱导的信号传递和基因表达.
- N-乙囊 (NAC) 降低了TGF-β水平和氧化应激标志物 (MDA),同时恢复了SOD活性.
- 奥梅普拉的益菌效应取决于ROS和TGF-β.
结论:
- 奥梅普拉通过ROS和TGF-β通路促进CTGF和TIMP-1的表达.
- 同时服用ROS清除剂可能会提高梅治疗的安全性.
- 这项研究阐明了PPI诱导的毒性机制.
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