Elham Karimi-Sales
1 
, Sajad Jeddi
2, Abbas Ebrahimi-Kalan
3, Mohammad Reza Alipour
1,4* 1 Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
2 Endocrine Physiology Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
3 Neurosciences Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
4 Department of Physiology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Abstract
Purpose: Non-alcoholic steatohepatitis (NASH) is an inflammatory disorder and an aggressiveform of fatty liver disease. Certain microRNAs, including miR-122, 21, 34a, and 451, areinvolved in the transition from steatosis to NASH. This study examined how trans-chalcone (thecore of chalcone derivatives) affects non-alcoholic fatty liver disease (NAFLD) progression byregulating miRNAs.Methods: Male rats were divided into three groups (n = 7/group) as follows: control, rats weregavaged with 10% tween 80 (for two weeks); NASH, rats were gavaged with a high-fat liquiddiet (HFD; for six weeks) and 10% tween 80 (for two weeks); NASH + Chal, rats were gavagedwith the HFD (for six weeks) and trans-chalcone (for two weeks). Hepatic expression levels ofmiR-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 increasedthe 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 themodulation of miR-122, 21, 34a, and 451 expression levels in the liver.