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首页> 外文期刊>Liver international : >Yo Jyo Hen Shi Ko, a novel Chinese herbal, prevents nonalcoholic steatohepatitis in ob/ob mice fed a high fat or methionine-choline-deficient diet.
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Yo Jyo Hen Shi Ko, a novel Chinese herbal, prevents nonalcoholic steatohepatitis in ob/ob mice fed a high fat or methionine-choline-deficient diet.

机译:Yo Jyo Hen Shi Ko是一种新型中草药,可以预防高脂或蛋氨酸-胆碱缺乏饮食的ob / ob小鼠的非酒精性脂肪性肝炎。

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Background: Oxidative stress plays a role in the pathogenesis of nonalcoholic steatohepatitis (NASH). Yo Jyo Hen Shi Ko (YHK) is a complex compound purported to reduce reactive oxygen species (ROS) by blocking the propagation of radical-induced reactions. The aim of this study was to evaluate the role of the effect of YHK in experimental NASH. Methods: NASH was induced in male ob/ob mice by a high-fat (HF) diet or methionine/choline-deficient (MCD) diet for 4 weeks. YHK-treated animals received YHK solution orally (20 mg/kg/day) in both experimental diets (n=6; each group) while control animals received only vehicle. Results: The MCD and HF groups developed moderate diffuse macrosteatosis, hepatocellular ballooning, and a diffuse inflammatory infiltrate. With the addition of YHK, there was a marked reduction in macrosteatosis in both groups. This was associated with decreased lipoperoxide and reduced glutathione-GSH concentrations as well as reduced serum aminotransferases and improved histological markers of inflammation. These changes were also associated with weight loss in the MCD+YHK group and diminished weight gain in the HF+YHK group. Conclusion: YHK therapy blunts the development of macrosteatosis in these models of NASH and significantly reduces markers of oxidative stress. YHK also diminishes weight gain in this obesity prone model. Our findings warrant further study on the mechanisms involved with these effects.
机译:背景:氧化应激在非酒精性脂肪性肝炎(NASH)的发病机理中起作用。 Yo Jyo Hen Shi Ko(YHK)是一种复杂的化合物,旨在通过阻止自由基诱导的反应的传播来减少活性氧(ROS)。这项研究的目的是评估YHK在NASH实验中的作用。方法:雄性ob / ob小鼠通过高脂饮食或蛋氨酸/胆碱缺乏症(MCD)饮食诱导NASH 4周。接受YHK处理的动物在两种实验饮食(n = 6;每组)中口服YHK溶液(20 mg / kg /天),而对照动物仅接受赋形剂。结果:MCD和HF组出现中度弥漫性大脂肪变性,肝细胞球囊扩张和弥漫性炎症浸润。随着YHK的加入,两组的宏观脂肪变性明显减少。这与降低脂过氧化物和降低谷胱甘肽-GSH浓度以及降低血清氨基转移酶和改善炎症的组织学标志有关。这些变化还与MCD + YHK组的体重减轻和HF + YHK组的体重增加减少有关。结论:YHK疗法在这些NASH模型中钝化了巨大脂肪变性,并显着降低了氧化应激指标。 YHK还减少了这种肥胖倾向模型中的体重增加。我们的发现值得进一步研究与这些作用有关的机制。

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