Abstract
Background Hepatic ischemia-reperfusion (IR) injury is one of the severe complications associated with liver surgery and leads to liver dysfunction. PPARγ 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 PPARγ in the pathogenesis of hepatic IR injury by mice model. Methods After treated with si-PPARγ 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 PPARγ was increased after reperfusion. And the alleviation of PPARγ aggravated the liver damage in IR; at the same time, upregulation of the expression of PPARγ released the liver damage. And these effects of PPARγ in IR were related to the AMPK/mTOR/autophagy signaling pathway. Conclusion PPARγ plays an important role in hepatic IR injury at least partly via the AMPK/mTOR/autophagy pathway.
Highlights
Ischemia-reperfusion (IR) is a phenomenon occurring after the restoration of arterial blood flow to a specific organ or tissue [1]
The adenosine monophosphateactivated protein kinase/mammalian target of rapamycin (AMPK/mTOR) signaling pathway has been confirmed that it is a critical regulator of cellular processes, including cell growth, viability, differentiation, survival, and metabolism [16,17,18]; mTOR has been identified as a key modulator of autophagy [19]; and its dysregulation has been implicated in a variety of pathological disorders, including playing critical roles in regulating liver IR injury
To confirm the activation of peroxisome proliferator-activated receptor-γ (PPARγ) during the hepatic ischemiareperfusion injury, we detected the expression of PPARγ by western blot and Quantitative Real-Time- (qRT-)PCR
Summary
Ischemia-reperfusion (IR) is a phenomenon occurring after the restoration of arterial blood flow to a specific organ or tissue [1]. PPARγ has an important role in regulating the inflammatory response and oxidative stress in hepatic IR injury [7,8,9]. The protecting effects of PPARγ agonists, such as telmisartan [10], irbesartan [11], darglitazone [12], rosiglitazone [13], and pioglitazone [14], in IR injury have been reported [15] These evidences suggested that PPARγ agonists can modulate inflammatory responses, oxidative stress, and metabolism in IR. The alleviation of PPARγ aggravated the liver damage in IR; at the same time, upregulation of the expression of PPARγ released the liver damage These effects of PPARγ in IR were related to the AMPK/mTOR/autophagy signaling pathway. PPARγ plays an important role in hepatic IR injury at least partly via the AMPK/mTOR/autophagy pathway
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