Abstract
Liver fibrosis is characterized by a series of events including activation of quiescent hepatic stellate cells (HSCs) into proinflammatory, contractile, and fibrogenic myofibroblasts, which is the primary trigger for the fibrogenesis process. HSC activation involves many signaling pathways such as the TGF-β/smads pathway. Specific microRNAs have been identified to play a crucial role in the activation of HSCs via various signaling pathways. Piperine has recently been studied as a promising anti-fibrotic agent against pancreatic fibrosis through altering the TGF-β1/Smad pathway. Hence, the current study evaluated the beneficial effects of piperine in thioacetamide-induced liver fibrosis in mice through the modulation of miRNA-17 and TGF-β/smads pathways. Mice were allocated into three groups randomly. Thioacetamide was used to induce liver fibrosis for 6 weeks. Starting from the fourth week of the experiment, mice were treated with piperine daily for 21 days. Piperine treatment resulted in a significant downregulation of miRNA-17 expression, leading to the restoration of smad-7 accompanied with marked inhibition of TGF-β/smads signaling with further suppression of the activated HSCs and collagen deposition in the hepatocytes. In conclusion, piperine has the potential to be a promising therapeutic drug for the treatment of liver fibrosis through inhibiting the TGF-β/smads pathway.
Highlights
Hepatic fibrosis is a long-term and consequent event of chronic liver injury and inflammation
The current study aims to evaluate the potential efficacy of piperine in the treatment of liver fibrosis induced with thioacetamide in mice through the modulation of miR-17 and TGF-/Smad pathways
Alanine transaminase (ALT) was increased by 1.7 fold and aspartate transaminase was increased by 2.4 fold in the mice with liver fibrosis compared to the control group
Summary
Hepatic fibrosis is a long-term and consequent event of chronic liver injury and inflammation (hepatitis). Liver injury can be induced by hepatotropic viruses, drug toxicity, alcohol, lipocyte deposition (steatosis), aflatoxin B1, and tobacco (Boyer and Lindor, 2016; McGlynn et al, 2021). Factors leads to the development of chronic inflammation of the liver, which is expressed by necrosis and apoptosis of hepatocytes. These processes induce a series of events including activation of quiescent hepatic stellate cells (HSCs) into proinflammatory, contractile, and fibrogenic myofibroblasts, which is the primary trigger for the fibrogenesis process (Bataller and Brenner, 2005; Boyer and Lindor, 2016)
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