scholarly journals Iron overload as a risk factor for hepatic ischemia‐reperfusion injury in liver transplantation: Potential role of ferroptosis

2020 ◽  
Vol 20 (6) ◽  
pp. 1606-1618 ◽  
Author(s):  
Naoya Yamada ◽  
Tadayoshi Karasawa ◽  
Taiichi Wakiya ◽  
Ai Sadatomo ◽  
Homare Ito ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Risk Factor ◽  
Iron Overload ◽  
Reperfusion Injury ◽  
Potential Role ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Hepatic Ischemia ◽  
Hepatic Ischemia Reperfusion

The role of HMGB-1 on the development of necrosis during hepatic ischemia and hepatic ischemia/reperfusion injury in mice

2005 ◽  
Vol 124 (1) ◽  
pp. 59-66 ◽  
Author(s):  
Taiji Watanabe ◽  
Sunao Kubota ◽  
Masaki Nagaya ◽  
Shoichi Ozaki ◽  
Hiroko Nagafuchi ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Hepatic Ischemia ◽  
Hepatic Ischemia Reperfusion

scholarly journals Sevoflurane relieves hepatic ischemia–reperfusion injury by inhibiting the expression of Grp78

2018 ◽  
Vol 38 (5) ◽  
Author(s):  
Di Liu ◽  
Xin Jin ◽  
Chunqi Zhang ◽  
You Shang
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Regulatory Protein ◽  
Liver Homogenate ◽  
Hepatic Ischemia ◽  
Damage Degree ◽  
Tnf Α ◽  
Hepatic Ischemia Reperfusion

Purpose: This article aimed to study the role of sevoflurane pre-conditioning in hepatic ischemia–reperfusion and its potential mechanism. Methods: Rat liver ischemia–reperfusion model was constructed. Serum TNF-α, IL-1β, IL-10, and IL-6 concentrations were detected by ELISA. Malondialdehyde (MDA), superoxide dismutase (SOD), and nitric oxide (NO) in liver homogenate were determined. Hematoxylin–Eosin (HE) staining, Tunel, and immunohistochemistry were performed. Ischemia–reperfusion hepatocyte model was established. Cells transfection was conducted. Apoptosis was observed by flow cytometry. Quantitative real-time PCR (qRT-PCR) and Western blotting analysis were used. Results: Compared with I/R group, liver damage degree, liver cell apoptosis, and glucose regulatory protein 78 (Grp78) expression was obviously reduced in rats of SEV group. TNF-α, IL-1β, and IL-6 concentrations were also significantly increased (P<0.01). MDA and NO concentrations were dramatically lower (P<0.01) and SOD concentration was significantly higher (P<0.01). Apoptosis rate, Grp78, PERK, eIF2α, and p-c-JNK/JNK expression was also significantly decreased (P<0.01). Sevoflurane significantly reduced apoptosis and expression of PERK, eIF2α, p-c-JNK/JNK by inhibiting the expression of Grp78 (P<0.01). Conclusion: Sevoflurane relieves hepatic ischemia–reperfusion injury by inhibiting the expression of Grp78.

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