过氧化物酶体增殖物激活受体通过AMPK/mTOR信号通路在急性肝缺血再灌注损伤中发挥重要作用。
PPAR Plays an Important Role in Acute Hepatic Ischemia-Reperfusion Injury via AMPK/mTOR Pathway.
作者信息
Wu Liwei, Yu Qiang, Cheng Ping, Guo Chuanyong
机构信息
Department of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, China.
Department of Gerontology, Shanghai Minhang District Central Hospital, Shanghai 201100, China.
出版信息
PPAR Res. 2021 Jul 3;2021:6626295. doi: 10.1155/2021/6626295. eCollection 2021.
BACKGROUND
Hepatic ischemia-reperfusion (IR) injury is one of the severe complications associated with liver surgery and leads to liver dysfunction. PPAR is always linked with various physiologic pathways, and it can alleviate liver damage in IR injury.
AIM
In this study, we explored the potential mechanism of PPAR in the pathogenesis of hepatic IR injury by mice model.
METHODS
After treated with si-PPAR or rosiglitazone, mice were subjected to hepatic ischemia-reperfusion. Liver tissue and blood samples were collected to evaluate liver injury and detected relative mRNA and protein expressions.
RESULTS
The expression of PPAR was increased after reperfusion. And the alleviation of PPAR aggravated the liver damage in IR; at the same time, upregulation of the expression of PPAR released the liver damage. And these effects of PPAR in IR were related to the AMPK/mTOR/autophagy signaling pathway.
CONCLUSION
PPAR plays an important role in hepatic IR injury at least partly via the AMPK/mTOR/autophagy pathway.
背景
肝缺血再灌注（IR）损伤是肝手术相关的严重并发症之一，可导致肝功能障碍。过氧化物酶体增殖物激活受体（PPAR）总是与各种生理途径相关联，并且它可以减轻IR损伤中的肝损伤。
目的
在本研究中，我们通过小鼠模型探索PPAR在肝IR损伤发病机制中的潜在机制。
方法
用小干扰RNA（si-PPAR）或罗格列酮处理后，对小鼠进行肝缺血再灌注。收集肝组织和血液样本以评估肝损伤，并检测相关的信使核糖核酸（mRNA）和蛋白质表达。
结果
再灌注后PPAR的表达增加。PPAR表达的降低加重了IR中的肝损伤；同时，PPAR表达的上调减轻了肝损伤。PPAR在IR中的这些作用与腺苷酸活化蛋白激酶（AMPK）/雷帕霉素靶蛋白（mTOR）/自噬信号通路有关。
结论
PPAR至少部分通过AMPK/mTOR/自噬途径在肝IR损伤中起重要作用。
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