首页> 美国卫生研究院文献>International Journal of Molecular Sciences >Hepatoprotective Effect of Kombucha Tea in Rodent Model of Nonalcoholic Fatty Liver Disease/Nonalcoholic Steatohepatitis
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Hepatoprotective Effect of Kombucha Tea in Rodent Model of Nonalcoholic Fatty Liver Disease/Nonalcoholic Steatohepatitis

机译:康普茶对非酒精性脂肪性肝病/非酒精性脂肪性肝炎的啮齿动物模型的保肝作用

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摘要

Kombucha tea (KT) has emerged as a substance that protects the liver from damage; however, its mechanisms of action on the fatty liver remain unclear. Therefore, we investigated the potential role of KT and its underlying mechanisms on nonalcoholic fatty liver disease (NAFLD). db/db mice that were fed methionine/choline-deficient (MCD) diets for seven weeks were treated for vehicle (M + V) or KT (M + K) and fed with MCD for four additional weeks. Histomorphological injury and increased levels of liver enzymes and lipids were evident in the M + V group, whereas these symptoms were ameliorated in the M + K group. The M + K group had more proliferating and less apoptotic hepatocytic cells than the M + V group. Lipid uptake and lipogenesis significantly decreased, and free fatty acid (FFA) oxidation increased in the M + K, when compared with the M + V group. With the reduction of hedgehog signaling, inflammation and fibrosis also declined in the M + K group. Palmitate (PA) treatment increased the accumulation of lipid droplets and decreased the viability of primary hepatocytes, whereas KT suppressed PA-induced damage in these cells by enhancing intracellular lipid disposal. These results suggest that KT protects hepatocytes from lipid toxicity by influencing the lipid metabolism, and it attenuates inflammation and fibrosis, which contributes to liver restoration in mice with NAFLD.
机译:康普茶(KT)已作为保护肝脏不受损害的物质而出现。然而,其对脂肪肝的作用机制仍不清楚。因此,我们调查了KT在非酒精性脂肪肝疾病(NAFLD)中的潜在作用及其潜在机制。喂食甲硫氨酸/胆碱缺乏(MCD)饮食七个星期的db / db小鼠进行媒介物(M + V)或KT(M + K)治疗,并再喂MCD四个星期。在M + V组中,组织形态学损伤和肝酶和脂质水平升高,而在M + K组中,这些症状得到缓解。 M + K组比M + V组具有更多的增殖和更少的凋亡的肝细胞。与M + V组相比,M + K中的脂质摄取和脂肪生成显着减少,并且游离脂肪酸(FFA)氧化增加。随着刺猬信号的减少,M + K组的炎症和纤维化也减少了。棕榈酸酯(PA)处理可增加脂质液滴的积累并降低原代肝细胞的活力,而KT可通过增强细胞内脂质处理来抑制PA诱导的这些细胞的损伤。这些结果表明,KT通过影响脂质代谢来保护肝细胞免受脂质毒性的影响,并减轻炎症和纤维化,从而有助于NAFLD小鼠的肝脏恢复。

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