scholarly journals Protective effects of cordycepin on the histopathological changes and oxidative stress induced by hepatic ischemia/reperfusion in rats

2018 ◽  
Vol 1 (1) ◽  
pp. 17-24
Author(s):  
Mehmet Hanifi Okur ◽  
Hikmet Zeytun ◽  
Erol Basuguy ◽  
Gulay Aydogdu ◽  
Ulas Alabalık ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ischemia Reperfusion ◽  
Protective Effects ◽  
Histopathological Changes ◽  
Hepatic Ischemia ◽  
Hepatic Ischemia Reperfusion ◽  
And Oxidative Stress

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.

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 Hyperglycemia Aggravates Hepatic Ischemia Reperfusion Injury by Inducing Chronic Oxidative Stress and Inflammation

2016 ◽  
Vol 2016 ◽  
pp. 1-16 ◽  
Author(s):  
Yihan Zhang ◽  
Dongdong Yuan ◽  
Weifeng Yao ◽  
Qianqian Zhu ◽  
Yue Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
High Glucose ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Diabetic Rats ◽  
Nuclear Factor ◽  
Hepatic Ischemia ◽  
Chronic Oxidative Stress ◽  
Hepatic Ischemia Reperfusion ◽  
And Oxidative Stress

Aim. To investigate whether hyperglycemia will aggravate hepatic ischemia reperfusion injury (HIRI) and the underlying mechanisms.Methods. Control and streptozotocin-induced diabetic Sprague-Dawley rats were subjected to partial hepatic ischemia reperfusion. Liver histology, transferase, inflammatory cytokines, and oxidative stress were assessed accordingly. Similarly, BRL-3A hepatocytes were subjected to hypoxia/reoxygenation (H/R) after high (25 mM) or low (5.5 mM) glucose culture. Cell viability, reactive oxygen species (ROS), and activation of nuclear factor-erythroid 2-related factor 2 (Nrf2) and nuclear factor of kappa light polypeptide gene enhancer in B-cells (NF-κB) were determined.Results. Compared with control, diabetic rats presented more severe hepatic injury and increased hepatic inflammatory cytokines and oxidative stress. HIRI in diabetic rats could be ameliorated by pretreatment of N-acetyl-L-cysteine (NAC) or apocynin. Excessive ROS generation and consequent Nrf2 and NF-κB translocation were determined after high glucose exposure. NF-κB translocation and its downstream cytokines were further increased in high glucose cultured group after H/R. While proper regulation of Nrf2 to its downstream antioxidases was observed in low glucose cultured group, no further induction of Nrf2 pathway by H/R after high glucose culture was identified.Conclusion. Hyperglycemia aggravates HIRI, which might be attributed to chronic oxidative stress and inflammation and potential malfunction of antioxidative system.

scholarly journals Blocking the Hepatic Branch of the Vagus Aggravates Hepatic Ischemia-Reperfusion Injury via Inhibiting the Expression of IL-22 in the Liver

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Heng Zhou ◽  
Juling Xu ◽  
Sanxiong Huang ◽  
Ying He ◽  
Xiaowei He ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Underlying Mechanism ◽  
Protective Effects ◽  
Histopathological Changes ◽  
Hepatic Ischemia ◽  
Stat3 Pathway ◽  
Hepatic Ischemia Reperfusion ◽  
Hepatic Branch

Liver ischemia-reperfusion injury (IRI) is an inevitable process during liver transplantation, hemorrhagic shock, resection, and other liver surgeries. It is an important cause of postoperative liver dysfunction and increased medical costs. The protective effects of the vagus nerve on hepatic IRI have been reported, but the underlying mechanism has not been fully understood. We established a hepatic vagotomy (Hv) mouse model to study the effect of the vagus on liver IRI and to explore the underlying mechanism. Liver IRI was more serious in mice with Hv, which showed higher serum ALT and AST activities and histopathological changes. Further experiments confirmed that Hv significantly downregulated the expression of IL-22 protein and mRNA in the liver, blocking the activation of the STAT3 pathway. The STAT3 pathway in the livers of Hv mice was significantly activated, and liver injury was clearly alleviated after treatment with exogenous IL-22 recombinant protein. In conclusion, Hv can aggravate hepatic IRI, and its mechanism may be related to inhibition of IL-22 expression and downregulation of the STAT3 pathway in the liver.

scholarly journals Agaricoglycerides Protect against Hepatic Ischemia/Reperfusion Injury by Attenuating Inflammatory Response, Oxidative Stress, and Expression of NF-κB

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Xiang-qian Zhao ◽  
Bin Liang ◽  
Yang Liu ◽  
Xiao-qiang Huang
Keyword(s):  
Oxidative Stress ◽  
Ischemia Reperfusion Injury ◽  
Inflammatory Diseases ◽  
Ischemia Reperfusion ◽  
Interleukin 1 ◽  
Hepatic Ischemia ◽  
Protective Strategy ◽  
Hepatic Ischemia Reperfusion ◽  
And Oxidative Stress ◽  
Necrosis Factor

We have investigated the effects of agaricoglycerides (AG) in a mouse model of hepatic I/R injury. I/R triggered increases/changes in markers of liver injury, hepatic oxidative stress, tumor necrosis factor-α(TNF-α), interleukin-1β(IL-1β), and nuclear factorκB (NF-κB). AG significantly reduced the extent of liver inflammation and oxidative stress and also attenuated the NF-κB activation as well as TNF-αand IL-1βproduction. Our results indicate that AG may represent a novel protective strategy against I/R-induced injury and inflammatory diseases.

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