Protective Role of trans-Chalcone against the Progression from Simple Steatosis to Non-alcoholic Steatohepatitis: Regulation of miR-122, 21, 34a, and 451

被引:5
|
作者
Karimi-Sales, Elham [1 ]
Jeddi, Sajad [2 ]
Ebrahimi-Kalan, Abbas [3 ]
Alipour, Mohammad Reza [1 ,4 ]
机构
[1] Tabriz Univ Med Sci, Drug Appl Res Ctr, Tabriz, Iran
[2] Shahid Beheshti Univ Med Sci, Res Inst Endocrine Sci, Endocrine Physiol Res Ctr, Tehran, Iran
[3] Tabriz Univ Med Sci, Neurosci Res Ctr, Tabriz, Iran
[4] Tabriz Univ Med Sci, Dept Physiol, Fac Med, Tabriz, Iran
关键词
Non-alcoholic steatohepatitis; trans-chalcone; miRNAs; Liver; Rat; FATTY LIVER-DISEASE; INSULIN SENSITIVITY; DOWN-REGULATION; MICRORNAS; EXPRESSION; ACID; HOMEOSTASIS; RESISTANCE; SIRT1; MODEL;
D O I
10.34172/apb.2022.022
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Purpose: Non-alcoholic steatohepatitis (NASH) is an inflammatory disorder and an aggressive form of fatty liver disease. Certain microRNAs, including miR-122, 21, 34a, and 451, are involved in the transition from steatosis to NASH. This study examined how trans-chalcone (the core of chalcone derivatives) affects non-alcoholic fatty liver disease (NAFLD) progression by regulating miRNAs. Methods: Male rats were divided into three groups (n = 7/group) as follows: control, rats were gavaged with 10% tween 80 (for two weeks); NASH, rats were gavaged with a high-fat liquid diet (HFD; for six weeks) and 10% tween 80 (for two weeks); NASH + Chal, rats were gavaged with the HFD (for six weeks) and trans-chalcone (for two weeks). Hepatic expression levels of miR-122, 21, 34a, and 451 were determined. Results: trans-Chalcone reversed histological abnormalities, reduced liver injury markers, and attenuated insulin resistance in HFD-fed rats. In the liver, HFD-induced NASH increased the expression level of miR-34a and decreased expression levels of miR-122, 21, and 451. However, trans-chalcone inhibited HFD-induced changes in expression levels of these miRNAs. Conclusion: trans-Chalcone could inhibit the transition from steatosis to NASH through the modulation of miR-122, 21, 34a, and 451 expression levels in the liver.
引用
收藏
页码:200 / 205
页数:6
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