Experimental Studies on Protective Effects of FK506 Against Hepatic Ischemia-Reperfusion Injury

Sawada, Toshihiko; Inoue, Katsuhiko; Tanabe, Dairou; Kawamoto, Shunji; Tsuji, Tatsuya; Tashiro, Seiki

doi:10.2152/jmi.63.262

Cited by 2 publications

(1 citation statement)

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“…Vinpocetine inhibits the release of IL‐1β and IL‐6 but enhances the expression of GSH in warm hepatic IR rat models . As a strong immunosuppressive agent, FK506 decreases apoptosis in sinusoidal endothelial cells and inhibits the activation of inflammation, consequently maintaining normal microcirculation in hepatic IR animals .…”

Section: Pharmacological Pre‐conditioning Before Hepatic Irmentioning

confidence: 99%

Pre‐conditions for eliminating mitochondrial dysfunction and maintaining liver function after hepatic ischaemia reperfusion

Hu¹

2017

J Cellular Molecular Medi

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The liver, the largest organ with multiple synthesis and secretion functions in mammals, consists of hepatocytes and Kupffer, stem, endothelial, stellate and other parenchymal cells. Because of early and extensive contact with the external environment, hepatic ischaemia reperfusion (IR) may result in mitochondrial dysfunction, autophagy and apoptosis of cells and tissues under various pathological conditions. Because the liver requires a high oxygen supply to maintain normal detoxification and synthesis functions, it is extremely susceptible to ischaemia and subsequent reperfusion with blood. Consequently, hepatic IR leads to acute or chronic liver failure and significantly increases the total rate of morbidity and mortality through multiple regulatory mechanisms. An increasing number of studies indicate that mitochondrial structure and function are impaired after hepatic IR, but that the health of liver tissues or liver grafts can be effectively rescued by attenuation of mitochondrial dysfunction. In this review, we mainly focus on the subsequent therapeutic interventions related to the conservation of mitochondrial function involved in mitigating hepatic IR injury and the potential mechanisms of protection. Because mitochondria are abundant in liver tissue, clarification of the regulatory mechanisms between mitochondrial dysfunction and hepatic IR should shed light on clinical therapies for alleviating hepatic IR‐induced injury.

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Section: Pharmacological Pre‐conditioning Before Hepatic Irmentioning

confidence: 99%