article · Journal of Cellular and Molecular Medicine
Liver fibrosis is a common chronic condition affecting the liver. This animal study investigated the protective effects of pitavastatin against liver fibrosis chemically induced by thioacetamide in rats. Exposure to thioacetamide caused liver injury characterised by elevated liver enzymes, reduced albumin levels, tissue damage, increased oxidative stress markers, and elevated inflammatory signals. Oral administration of pitavastatin at doses of 0.4 and 0.8 mg per kg daily over two weeks improved liver enzyme and albumin levels while preventing structural liver alterations. Pitavastatin reduced markers of oxidative damage and suppressed key inflammatory factors and pathways, including NF-kappaB and PI3K/Akt signalling. Simultaneously, it increased antioxidant defences and enhanced Nrf2 and HO-1 expression. These findings indicate that pitavastatin counteracts early-stage liver fibrosis by reducing oxidative stress and inflammation through specific cellular pathways.
Liver fibrosis is a widespread chronic condition that can progress to severe organ damage. Identifying existing drugs that can protect hepatic tissue offers potential therapeutic avenues. This research demonstrates how pitavastatin reduces liver injury and inflammation in a laboratory model, explaining the cellular mechanisms that could inform future strategies for treating early-stage liver disease.
This research highlights the potential repurposing of pitavastatin as a treatment for early-stage liver fibrosis. Potential users include pharmaceutical developers and clinical researchers investigating hepatoprotective therapies. Because the findings are derived exclusively from an in vivo rat model, the work is at an early preclinical research stage and would require extensive clinical testing to determine safety and therapeutic efficacy in humans.
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Liver fibrosis is a common chronic hepatic disease. This study aimed to investigate the effect of pitavastatin (Pit) against thioacetamide (TAA)-induced liver fibrosis. Rats were divided into four groups: (1) control group; (2) TAA group (100 mg/kg, i.p.) three times weekly for 2 weeks; (3 and 4) TAA/Pit-treated group, in which Pit was administered orally (0.4 and 0.8 mg/kg/day) for 2 weeks following TAA injections. TAA caused liver damage manifested by elevated serum transaminases, reduced albumin and histological alterations. Hepatic malondialdehyde (MDA) was increased, and glutathione (GSH) and superoxide dismutase (SOD) were decreased in TAA-administered rats. TAA upregulated the inflammatory markers NF-κB, NF-κB p65, TNF-α and IL-6. Treatment with Pit ameliorated serum transaminases, elevated serum albumin and prevented histopathological changes in TAA-intoxicated rats. Pit suppressed MDA, NF-κB, NF-κB p65, the inflammatory cytokines and PI3K mRNA in TAA-intoxicated rats. In addition, Pit enhanced hepatic antioxidants and boosted the nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) mRNA. Moreover, immunohistological studies supported the ability of Pit to reduce liver fibrosis via suppressing p-AKT expression. In conclusion, Pit effectively prevents TAA-induced liver fibrosis by attenuating oxidative stress and the inflammatory response. The hepatoprotective efficacy of Pit was associated with the upregulation of Nrf2/HO-1 and downregulation of NF-κB and PI3K/Akt signalling pathways.
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DOI: 10.1111/jcmm.18116
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