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Suppression of nonalcoholic fatty liver disease by thymoquinone associated with inhibition of miRNA-155/ROS/p53/TIMP-1-mediated fibrosis and autophagy upregulation
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DOI：10.1515/tjb-2025-0102.png)
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Abstract
En 中文
Objective liver fibrosis is a hallmark of non-alcoholic fatty liver disease (NAFLD; complication, and dysregulation of microRNA-155 (miRNA-155) is connected with hepatic fibrosis. We sought to investigate the link between hepatic miRNA-155/oxidative stress (ROS)/apoptosis (p53)/profibrosis (TIMP-1) axis-mediated liver fibrosis in NAFLD-induced hepatic injury in association with the inhibition of the autophagosome marker, LC3 with and without the incorporation of the plant phytochemical compound thymoquinone (TQ). Methods NAFLD was induced by feeding rats with a high fat and carbohydrate diets (HFCD) until being culled at day 28 (model group). The protective group received both, thymoquinone 10 mg/kg, i.p and HFCD until day 28. Results We documented in the model group hepatic induction of injury and fibrosis associated with the increase of tissue and blood levels of miRNA-155, ROS, p53, TIMP-1, and dyslipidemia. Whereas, inhibition of LC3 and the antioxidant enzymes by HFCD was observed. All these parameters were protected (p<0.01) by TQ. In addition, we observed a significant (p<0.001) correlation between hepatic fibrosis and liver injury parameters. Conclusions NAFLD is associated with the modulation of hepatic miRNA-155/ROS/p53/TIMP-1 axis as well as LC3, liver fibrosis, and dyslipidemia while being protected by thymoquinone.
Keywords:
fatty liver disease
miRNA-155/ROS/p53/TIMP-1 axis
autophagosome
liver fibrosis
thymoquinone
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