ArticleFrontiers in pharmacology2025
Protective effects of shikimic acid against thioacetamide-induced hepatic fibrosis: role of Nrf2/NF-κB signaling pathways.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- β-Caryophyllene Mitigates Thioacetamide-Induced Liver Fibrosis Through CB2-Mediated Suppression of Necroptosis: A Therapeutic Investigation.Pharmacology research & perspectives · 2026Article
- Article
- Ivabradine Attenuates Experimental Hepatic Fibrosis by Modulating Inflammatory and Apoptotic Signaling Pathways.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Molecular insights of a Unani formulation in targeting fibrosis-associated diseases.Frontiers in pharmacology · 2026Review
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Abstract
Background: Liver fibrosis is a chronic condition marked by scar tissue accumulation in the liver that impairs function. Shikimic acid (SA) has demonstrated significant antioxidant and anti-inflammatory properties and is a hydroaromatic natural product found in various plant sources, including star anise. Thioacetamide (TAA) is commonly used as an experimental model to induce liver fibrosis. This study was designed to investigate the protective effects of SA against TAA-induced liver fibrosis in rats. Methods: Fifty male Wistar rats were divided into five groups (n = 10): control, TAA (200 mg/kg), SA (50 mg/kg), and two combination groups receiving TAA plus SA (50 and 100 mg/kg). Treatments were administered intraperitoneally for 6 weeks. Liver function, oxidative stress markers, inflammatory mediators, apoptotic proteins, fibrogenic factors, and histopathology were assessed. Results: SA treatment significantly attenuated liver fibrosis induced by TAA through improved liver enzymes, including alkaline phosphatase (ALP) and aspartate transaminase (AST), serum alanine transaminase (ALT) and antioxidant parameters, including catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), and superoxide dismutase (SOD). SA-enhanced nuclear factor erythroid 2-related factor-2 (Nrf2) expression while reducing oxidative stress markers, including nitric oxide (NO), malondialdehyde (MDA) and reduced glutathione (GSH), and inflammatory mediators, including tumour necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β) and nuclear factor kappa-light-chain-enhancer of activated B-cells (NF-κB). Furthermore, SA demonstrated anti-apoptotic effects by modulating Bax, Bcl2, and caspase-3 levels and exhibited anti-fibrotic properties through suppression of transforming growth factor beta (TGF-β) and collagen type I alpha-1 chain (COL1A1) expressions. Notably, SA improved histopathological alterations with a slight presence of fibroplasia. These protective effects were more pronounced at the higher dose (100 mg/kg). Conclusion: SA effectively protected against TAA-induced liver fibrosis through multiple mechanisms, including the normalisation of liver enzymes, enhancement of antioxidant defences via Nrf2 activation, suppression of inflammatory mediators, and modulation of apoptotic and fibrogenic pathways.
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