The current study examined the effects of Diethylcarbamazine (DEC) on CCl4-induced liver toxicity and the autophagic process in mice. A dose of 50mg/kg of DEC was intragastrically administered for 12 days before the CCl4 (10%,v/v in olive oil, 2ml/kg) was administered via injection. Mice were euthanized 24h after the CCl4 injection. The rise in serum levels of NO and activity of glutathione reductase in CCl4-intoxicated mice were suppressed by DEC. Liver histopathology showed that DEC reduced the incidence of liver lesions induced by CCl4. In addition, DEC reduced the expression of TNF-α,IL-1β,IL-6,IL-22,NF-κB, MMP-9, COX-2 and iNOS in CCl4-treated mice. There was also a reduction in the expression of AKT and apoptotic cells. The expression of IL-10, IFN-γ, LC3 and PI3K increased in the DEC pre-treated group. The hepatoprotective mechanisms of DEC may be related to the attenuation of oxidative stress and anti-inflammatory activity. Thus, the impact of DEC on inflammatory and autophagic mechanisms becomes apparent, underscoring the importance of analyzing this drug's ability to induce improvements in acute toxin-induced hepatitis. Therefore, the conduct of this study is justified, as the development of new treatments and access to healthcare are paramount for the care of patients with hepatitis.
Diethylcarbamazine (dec) protects against acute hepatotoxicity induced by carbon tetrachloride (ccl4) in mice by modulating pro-inflammatory markers through autophagy activation
S. W. Rocha,M. R. França,W. Oliveira,D. Lós,D. Cerqueira,Amanda Mota Vieira,B. Carvalho,C. Peixoto
Published 2025 in Brazilian Journal of Pharmaceutical Sciences
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Brazilian Journal of Pharmaceutical Sciences
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