Diethylcarbamazine (dec) protects against acute hepatotoxicity induced by carbon tetrachloride (ccl4) in mice by modulating pro-inflammatory markers through autophagy activation

Authors

  • Sura Wanessa Santos Rocha Laboratory of Ultrastructure, Instituto Aggeu Magalhães, Fundação Oswaldo Cruz, Brazil, Postgraduate Program in Biological Science, Universidade Federal de Pernambuco, Brazil, Postgraduate Program in Applied Cellular and Molecular Biology, Universidade de Pernambuco, Brazil
  • Maria Eduarda de Rocha França Laboratory of Ultrastructure, Instituto Aggeu Magalhães, Fundação Oswaldo Cruz, Brazil, Postgraduate Program in Biological Science, Universidade Federal de Pernambuco, Brazil,
  • Wilma Helena Oliveira Laboratory of Ultrastructure, Instituto Aggeu Magalhães, Fundação Oswaldo Cruz, Brazil, Postgraduate Program in Biological Science, Universidade Federal de Pernambuco, Brazil
  • Deniele Bezerra Lós Postgraduate Program in Biotechnology (RENORBIO), Universidade Federal de Pernambuco, Brazil
  • Débora Dantas Nucci Cerqueira Graduate Student in Biological Science, Instituto de Ciências Biológicas, Universidade de Pernambuco, Brazil
  • Amanda Mota Vieira Postgraduate Program in Applied Cellular and Molecular Biology, Universidade de Pernambuco, Brazil
  • Bruno Melo Carvalho Postgraduate Program in Applied Cellular and Molecular Biology, Universidade de Pernambuco, Brazil
  • Christina Alves Peixoto Laboratory of Ultrastructure, Instituto Aggeu Magalhães, Fundação Oswaldo Cruz, Brazil, Postgraduate Program in Biological Science, Universidade Federal de Pernambuco, Brazil

DOI:

https://doi.org/10.1590/s2175-97902025e23935

Keywords:

Diethylcarbamazine, Hepatoprotective, Anti-inflammatory, Carbon tetrachloride, Autophagy

Abstract

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.

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Published

2025-11-10

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How to Cite

Diethylcarbamazine (dec) protects against acute hepatotoxicity induced by carbon tetrachloride (ccl4) in mice by modulating pro-inflammatory markers through autophagy activation. (2025). Brazilian Journal of Pharmaceutical Sciences, 61, e23935. https://doi.org/10.1590/s2175-97902025e23935