| First Author | Alves JN | Year | 2013 |
| Journal | Arch Biochem Biophys | Volume | 537 |
| Issue | 1 | Pages | 72-81 |
| PubMed ID | 23831508 | Mgi Jnum | J:206688 |
| Mgi Id | MGI:5551690 | Doi | 10.1016/j.abb.2013.06.019 |
| Citation | Alves JN, et al. (2013) Critical role for CCR2 and HMGB1 in induction of experimental endotoxic shock. Arch Biochem Biophys 537(1):72-81 |
| abstractText | 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 20 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 (50 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. |
