Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8290712 | Archives of Biochemistry and Biophysics | 2013 | 10 Pages |
Abstract
Our aim was to investigate CCR2 and HMGB1 involvement in a murine model of endotoxic shock. We used C57BL/6 CCR2 knockout (KO) mice and wild-type (WT) littermates to establish an optimal dose of LPS. CCR2 KO mice survived more frequently than WT mice after 80, 40 and 20Â mg/kg of LPS i.p. Inflammation and redox markers were high in WT mice than in CCR2 KO mice. HMGB1 expression was reduced in CCR2 KO mice in parallel to ERK 1/2 activation. Therefore, we used glycyrrhizic acid (50Â mg/kg), an HMGB1 inhibitor in WT mice injected with LPS, and mortality was fully abolished. Thus, drugs targeting CCR2 and HMGB1 could represent future resources for sepsis treatment.
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Authors
Jackson Nogueira Alves, Karla Maria Pereira Pires, Manuella Lanzetti, Marina Valente Barroso, Cláudia Farias Benjamim, Cristiane Aguiar Costa, Angela Castro Resende, Juliana Carvalho Santos, Marcelo Lima Ribeiro, LuÃs Cristóvão Porto,