Protective Role of trans-Chalcone against the Progression from Simple Steatosis to Non-alcoholic Steatohepatitis: Regulation of miR-122, 21, 34a, and 451
Autor: | Abbas Ebrahimi-Kalan, Elham Karimi-Sales, Sajad Jeddi, Mohammad Reza Alipour |
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Jazyk: | angličtina |
Rok vydání: | 2022 |
Předmět: |
medicine.medical_specialty
Chalcone Liquid diet trans-chalcone mirnas Pharmaceutical Science RM1-950 liver chemistry.chemical_compound Insulin resistance Internal medicine medicine MiR-122 rat General Pharmacology Toxicology and Pharmaceutics Liver injury business.industry Fatty liver nutritional and metabolic diseases medicine.disease Endocrinology chemistry non-alcoholic steatohepatitis Therapeutics. Pharmacology Steatosis Steatohepatitis business |
Zdroj: | Advanced Pharmaceutical Bulletin, Vol 12, Iss 1, Pp 200-205 (2022) |
ISSN: | 2251-7308 2228-5881 |
Popis: | 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 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. |
Databáze: | OpenAIRE |
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