Protective Effects of Combined Ischemic Preconditioning and Ascorbic Acid on Mitochondrial Injury in Hepatic Ischemia/Reperfusion

2007 ◽  
Vol 142 (1) ◽  
pp. 45-52 ◽  
Author(s):  
Woo-Yong Lee ◽  
Jun-Seok Lee ◽  
Sun-Mee Lee
Keyword(s):  
Ascorbic Acid ◽  
Ischemic Preconditioning ◽  
Ischemia Reperfusion ◽  
Protective Effects ◽  
Hepatic Ischemia ◽  
Mitochondrial Injury ◽  
Hepatic Ischemia Reperfusion

scholarly journals Mild Hypothermia Attenuates Hepatic Ischemia–Reperfusion Injury through Regulating the JAK2/STAT3-CPT1a-Dependent Fatty Acid β-Oxidation

2020 ◽  
Vol 2020 ◽  
pp. 1-16
Author(s):  
Wei Wang ◽  
Xiaoyan Hu ◽  
Zhiping Xia ◽  
Zhongzhong Liu ◽  
Zibiao Zhong ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Fatty Acid ◽  
Mild Hypothermia ◽  
Ischemia Reperfusion ◽  
Protective Effects ◽  
Hepatic Enzyme ◽  
Hepatocyte Apoptosis ◽  
Hepatic Ischemia ◽  
Mitochondrial Injury ◽  
Hepatic Ischemia Reperfusion

Hepatic ischemia–reperfusion (IR) injury is a clinical issue that can result in poor outcome and lacks effective therapies at present. Mild hypothermia (32–35°C) is a physiotherapy that has been reported to significantly alleviate IR injury, while its protective effects are attributed to multiple mechanisms, one of which may be the regulation of fatty acid β-oxidation (FAO). The aim of the present study was to investigate the role and underlying mechanisms of FAO in the protective effects of mild hypothermia. We used male mice to establish the experimental models as previously described. In brief, before exposure to in situ ischemia for 1 h and reperfusion for 6 h, mice received pretreatment with mild hypothermia for 2 h and etomoxir (inhibitor of FAO) or leptin (activator of FAO) for 1 h, respectively. Then, tissue and blood samples were collected to evaluate the liver injury, oxidative stress, and changes in hepatic FAO. We found that mild hypothermia significantly reduced the hepatic enzyme levels and the score of hepatic pathological injury, hepatocyte apoptosis, oxidative stress, and mitochondrial injury. In addition, the expression of the rate-limiting enzyme (CPT1a) of hepatic FAO was downregulated almost twofold by IR, while this inhibition could be significantly reversed by mild hypothermia. Experiments with leptin and etomoxir confirmed that activation of FAO could also reduce the hepatic enzyme levels and the score of hepatic pathological injury, hepatocyte apoptosis, oxidative stress, and mitochondrial injury induced by IR, which had the similar effects to mild hypothermia, while inhibition of FAO had negative effects. Furthermore, mild hypothermia and leptin could promote the phosphorylation of JAK2/STAT3 and upregulate the ratio of BCL-2/BAX to suppress hepatocyte apoptosis. Thus, we concluded that FAO played an important role in hepatic IR injury and mild hypothermia attenuated hepatic IR injury mainly via the regulation of JAK2/STAT3-CPT1a-dependent FAO.

scholarly journals Comparison of the protective effects of desflurane and propofol anesthesia in rats: a hepatic ischemia-reperfusion injury model

2013 ◽  
Vol 43 ◽  
pp. 592-598
Author(s):  
Ayca TAŞ TUNA ◽  
Cengiz Bekir DEMİREL ◽  
Yusuf ÜNAL ◽  
Aslıhan ÇAVUNT BAYRAKTAR ◽  
Demet YILMAZER ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Protective Effects ◽  
Hepatic Ischemia ◽  
Injury Model ◽  
Hepatic Ischemia Reperfusion

scholarly journals Fenofibrate Ameliorates Hepatic Ischemia/Reperfusion Injury in Mice: Involvements of Apoptosis, Autophagy, and PPAR-α Activation

PPAR Research ◽  
2021 ◽  
Vol 2021 ◽  
pp. 1-16
Author(s):  
Jie Zhang ◽  
Ping Cheng ◽  
Weiqi Dai ◽  
Jie Ji ◽  
Liwei Wu ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Protective Effects ◽  
Hepatocyte Apoptosis ◽  
Ischemia And Reperfusion Injury ◽  
Hepatic Ischemia ◽  
Tissue Samples ◽  
Hepatic Ischemia Reperfusion ◽  
And Oxidative Stress

Hepatic ischemia and reperfusion injury is characterized by hepatocyte apoptosis, impaired autophagy, and oxidative stress. Fenofibrate, a commonly used antilipidemic drug, has been verified to exert hepatic protective effects in other cells and animal models. The purpose of this study was to identify the function of fenofibrate on mouse hepatic IR injury and discuss the possible mechanisms. A segmental (70%) hepatic warm ischemia model was established in Balb/c mice. Serum and liver tissue samples were collected for detecting pathological changes at 2, 8, and 24 h after reperfusion, while fenofibrate (50 mg/kg, 100 mg/kg) was injected intraperitoneally 1 hour prior to surgery. Compared to the IR group, pretreatment of FF could reduce the inflammatory response and inhibit apoptosis and autophagy. Furthermore, fenofibrate can activate PPAR-α, which is associated with the phosphorylation of AMPK.

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