Huazhi Rougan Granule Alleviates Liver and Intestinal Damage in Non-Alcoholic Fatty Liver Disease by Regulating miR-122 Expression and TLR4/MyD88/NF-κB Pathway Activation

脂肪肝 内科学 内分泌学 肝损伤 TLR4型 下调和上调 酒精性肝病 脂质代谢 化学 生物 医学 炎症 肝硬化 生物化学 疾病 基因
作者
Ping Xie,Xiaowei Jin,Chan Li,Kun Lv,Ming Deng
出处
期刊:Combinatorial Chemistry & High Throughput Screening [Bentham Science]
卷期号:28
标识
DOI:10.2174/0113862073290372240603090844
摘要

Purpose: miR-122 is upregulated in non-alcoholic fatty liver disease (NAFLD) liver tissue, and knockdown of miR-122 protects hepatocytes from lipid metabolism disorders. This study aimed to investigate whether Huazhi Rougan Granule (HRG) alleviates NAFLD liver and intestinal injury by regulating the miR-122-mediated TLR4/MyD88/NF-κB pathway. Methods: Rats with NAFLD were constructed by high-fat feeding. Serum levels of total cholesterol (TC), triglycerides (TG), aspartate aminotransferase (AST), and alanine aminotransferase (ALT) were measured using a fully automated biochemical instrument. Histopathological changes in the liver and small intestine were observed by HE staining. QRT-PCR detected the expression level of miR-122 in the liver tissues. The protein expression of TLR4, MyD88, NF- κB p65, and p-p65 in liver tissues was detected by western blotting. Results: HRG slowed down the weight gain of NAFLD rats, decreased (P<0.05) the levels of TC, TG, ALT, AST, TNF-α, IL-1β, IL-6, LPS, and Hpt, improved the pathological status of liver and small intestine tissues, upregulated (P<0.05) the expression of ZO-1 and Occludin, downregulated (P<0.05) the protein expression of TLR4, MyD88, and p-p65, and inhibited (P<0.05) the expression of miR-122. Conclusion: HRG may alleviate hepatic and intestinal injuries in rats with NAFLD by regulating the miR-122-mediated TLR4/MyD88/NF-κB pathway. result: HRG slowed down the weight gain of NAFLD rats, decreased the levels of TC, TG, ALT, AST, TNF-α, IL-1β, IL-6, LPS and Hpt, improved the pathological status of liver and small intestine tissues, up-regulated the expression of ZO-1 and Occludin, down-regulated the protein expression of TLR4, MyD88 and p-p65, and inhibited the expression of miR-122.
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