Blocking CXCR1/2 contributes to amelioration of lipopolysaccharide-induced sepsis by downregulating substance P.

摘要: Objectives C-X-C chemokine receptor types 1/2 (CXCR1/2) is known to be activated in liver damage acute-on-chronic failure; however, the role lipopolysaccharide (LPS)-induced sepsis unknown. The current study was designed determine whether or not CXCR1/2 blockade with reparixin ameliorates acute lung injury (ALI) by affecting neuropeptides a LPS-induced mouse model. Materials and methods Male C57BL/6 mice (10 14-week old) were divided into sham, LPS, sham-R, LPS-R groups. Bronchoalveolar lavage fluid (BALF) collected evaluated. histopathology assessed immunocytochemistry staining. Western blot analysis used measure myeloperoxidase, substance P (SP), vasoactive intestinal peptide. Results animal models ameliorated cotreatment antagonist. Moreover, protective effects of antagonists attributed increased secretion pro-opiomelanocortin decreased SP. Reparixin expression necroptosis cell death markers induced LPS. Conclusion results this indicate that may represent promising therapeutic strategy for treatment sepsis-associated ALI through regulation necroptosis.