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首页> 外文期刊>Alcohol >Therapeutic potential of interleukin-6 in preventing obesity- and alcohol-associated fatty liver transplant failure.
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Therapeutic potential of interleukin-6 in preventing obesity- and alcohol-associated fatty liver transplant failure.

机译：IL-6预防肥胖和酒精相关的脂肪肝移植失败的治疗潜力。

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Donor organ shortage significantly hinders orthotopic liver transplantation therapy, the only effective treatment for chronic end-stage liver disease and acute liver failure. Further complicating this matter is the prevalence of steatosis in 13% to 50% of donor livers obtained from obese and alcoholic individuals. When transplanted, these livers are associated with primary nonfunction and an elevated risk of dysfunction. New therapeutic approaches to render marginal fatty livers worthy for clinical transplantation are actively being sought. Study findings obtained from my group show that in vitro treatment with interleukin-6 (IL-6) dramatically reduces mortality, liver injury, and necrapoptosis in steatotic Zucker rat liver isografts. Findings of additional studies indicate that IL-6 induces hepatoprotection of steatotic liver isografts by preventing sinusoidal endothelial cell damage and, consequently, the amelioration of hepatic microcirculation, and by protecting against hepatocyte death, which is likely mediated through activation of signal transducer and activator of transcription 3/Bcl-x(L). Finally, in vitro IL-6 treatment also prevents mortality associated with alcoholic fatty liver transplants. Relative to the protective effect of IL-6 on steatotic Zucker rat liver, IL-6 is less effective in alcoholic fatty livers, which may be due to the inhibitory effects of ethanol on IL-6 activation of signal transducer and activator of transcription 3 in hepatocytes and sinusoidal endothelial cells. Collectively, these results support the assertion that in vitro IL-6 treatment of steatotic livers may render allografts usable for clinical transplantation, thereby decreasing the gap between the short supply of cadaver liver allografts and high demands for replacement livers. Higher concentrations of IL-6 may be required to protect against alcoholic fatty liver isograft injury because alcohol inhibits IL-6 signaling in the liver.
机译：供体器官短缺严重阻碍了原位肝移植治疗，这是慢性终末期肝病和急性肝衰竭的唯一有效治疗方法。使该问题进一步复杂化的是，肥胖和酒精中毒者中有13％至50％的供体肝脏中有脂肪变性。移植后，这些肝脏与原发性无功能和功能障碍的风险增加有关。积极寻求使边缘性脂肪肝值得临床移植的新治疗方法。从我的研究小组获得的研究结果表明，白细胞介素6（IL-6）的体外治疗可显着降低脂肪变性祖克大鼠肝同种异体移植的死亡率，肝损伤和肾小管坏死。其他研究发现表明，IL-6通过防止肝窦内皮细胞损伤，从而改善肝微循环，防止肝细胞死亡来诱导脂肪变性肝同种异体的肝保护作用，这很可能是通过激活信号转导子和激活子来介导的。转录3 / Bcl-x（L）。最后，体外IL-6治疗还可以预防酒精性脂肪肝移植的死亡率。相对于IL-6对Zucker脂肪肝大鼠的保护作用，IL-6在酒精性脂肪肝中的疗效较差，这可能是由于乙醇对IL-6激活信号转导子和转录激活子3的抑制作用所致。肝细胞和窦状内皮细胞。总体而言，这些结果支持这样的主张，即体外IL-6治疗脂肪变性肝脏可能使同种异体移植物可用于临床移植，从而缩小了尸体同种异体肝脏供不应求与替换肝脏的高需求之间的差距。由于酒精会抑制肝脏中的IL-6信号传导，因此可能需要更高浓度的IL-6来预防酒精性脂肪肝的同种异体移植损伤。

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