p-Cymene inhibits pro-fibrotic and inflammatory mediators to prevent hepatic dysfunction

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Abstract This study evaluated the hepatoprotective potential of p-cymene (p-CYM) against two models of liver damage: ethanol (EtOH)-induced hepatocellular injury and diethylnitrosamine-carbon tetrachloride (DEN-CCl 4 )-induced liver fibrosis (LF). HepG2 cells were treated with p-CYM or silymarin (SIL) before exposure to 10% EtOH in order to induce cellular injury. LF was induced in Sprague–Dawley rats using a single dose of DEN followed by increasing doses of CCl 4 over 60 days. Rats were treated twice weekly with p-CYM or SIL from day 21 to day 60. Results showed that p-CYM effectively mitigated EtOH-induced cell death in HepG2 cells by enhancing the activity of superoxide dismutase and glutathione reductase. In vivo findings revealed that p-CYM attenuated DEN– CCl 4 -induced liver damage by preventing weight loss, improving serum biomarkers (e.g., aspartate transaminase, alanine aminotransferase, alkaline phosphatase, and bilirubin), and reducing liver fibrotic changes. It also decreased the expression of pro-inflammatory and pro-fibrotic markers such as TNF-α, IL-1β, IL-6, TGF-β1, COL1A1 , and TIMP-1 . Molecular docking further supported the experimental findings, showing strong interactions between p-CYM and the target proteins. These results indicate that the hepatoprotective effects of p-CYM are likely due to its combined antioxidant, anti-inflammatory, and anti-fibrotic properties.

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