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Hepatoprotective effects of cirsimaritin against CCl4-induced oxidative stress, inflammation, and apoptosis in rats.

Y. Bseiso,B. S. Alotaibi,Alaa A. A. Aljabali,O. Gammoh,M. Oqal,E. Qnais,A. Alqudah

Published 2025 in Drug and chemical toxicology (New York, N.Y. 1978)

ABSTRACT

BACKGROUND Carbon tetrachloride (CCl4) induces hepatotoxicity through oxidative stress, inflammation, and apoptosis. Cirsimaritin, a natural flavonoid with antioxidant and anti-inflammatory activity, has not been extensively investigated for hepatoprotection. METHODS Male Wistar rats were allocated into four groups (n = 6): control, cirsimaritin-only (80 mg/kg/day), CCl4-only (1 mL/kg of 1:1 CCl4: olive oil, i.p., twice weekly), and cirsimaritin + CCl4. After four weeks, serum liver function markers, oxidative stress indices, cytokines, apoptotic markers, histology, and hepatic expression of Nrf2, HO-1, and NF-κB p65 were assessed. RESULTS CCl4 significantly elevated ALT, AST, ALP, bilirubin, MDA, TNF-α, IL-6, caspase-3, and caspase-9, while reducing albumin, total protein, SOD, CAT, GPx, IL-4, and IL-10 (p < 0.05-0.001). Cirsimaritin co-treatment reversed these alterations by normalizing liver enzymes, restoring antioxidant activity, lowering lipid peroxidation and pro-inflammatory cytokines, elevating anti-inflammatory cytokines, and attenuating apoptosis. Histology confirmed preservation of hepatic architecture. qPCR analysis showed that CCl4 downregulated Nrf2/HO-1 and upregulated NF-κB p65, whereas cirsimaritin significantly counteracted these molecular changes. CONCLUSION Cirsimaritin protects against CCl4-induced hepatotoxicity by enhancing antioxidant defenses, correcting cytokine imbalance, and inhibiting apoptosis, at least partly via activation of Nrf2/HO-1 and suppression of NF-κB signaling. These findings highlight cirsimaritin as a promising natural hepatoprotective candidate.

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