ArticleMolecular biology reports2026
Hepatoprotective effects of cinnamic acid against carbon tetrachloride-induced liver injury in a mouse model.
Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundCinnamic acid (CA), a natural phenolic compound with antioxidant and anti-inflammatory properties, has recently attracted attention for its potential protective effects on liver function. This study aimed to evaluate the hepatoprotective effects of CA against carbon tetrachloride (CCl₄)-induced toxicity in mice.
methodsThirty NMRI mice were randomly divided into five groups: control, CCl₄, and three groups treated with CA (50, 100, and 200 mg/kg). CA was administered orally for seven days prior to CCl₄ injection. Serum biochemical parameters and total antioxidant capacity (TAC) were measured. Gene expression levels of Nrf2, Foxo3, IL-6, and TNF-α, as well as liver histology, were also assessed.
resultsCCl₄ exposure markedly elevated hepatic enzymes, bilirubin, urea, and C-reactive protein (CRP) levels while reducing albumin and total protein concentrations. Pretreatment with CA improved several of these parameters, particularly at higher doses (100-200 mg/kg). Although CA treatment did not significantly restore TAC levels, higher CA doses (100-200 mg/kg) upregulated Nrf2 and Foxo3, suggesting activation of antioxidant-related signaling pathways, and downregulated IL-6 and TNF-α expression, indicating reduced inflammatory marker expression. TNF-α. Histopathological analysis confirmed these biochemical findings, showing reduced necrosis and inflammation in CA-treated mice.
conclusionCinnamic acid may exert hepatoprotective effects against CCl₄-induced liver injury, with secondary favorable effects on renal biochemical markers of CCl₄-induced systemic toxicity, by modulating oxidative and inflammatory pathways. Its association with increased Nrf2 and Foxo3 expression and reduced inflammatory mediator expression supports further investigation of CA as a potential hepatoprotective compound.
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