Dexmedetomidine inhibits systemic inflammatory response induced by renal ischemia reperfusion via mediating macrophage polarization

Autor: HE Xinhai, CHEN Xintong, YANG Ziheng, GU Li, ZHOU Li, QUAN Junxian, LU Kaizhi, GU Jianteng
Jazyk: čínština
Rok vydání: 2020
Předmět:
Zdroj: Di-san junyi daxue xuebao, Vol 42, Iss 6, Pp 611-615 (2020)
Druh dokumentu: article
ISSN: 1000-5404
DOI: 10.16016/j.1000-5404.201911107
Popis: Objective To explore the effects of dexmedetomidine (Dex) on systemic inflammatory response induced by renal ischemia reperfusion (rIRI) and the possible mechanism. Methods Fifteen C57BL/6J mice were randomly divided into 3 groups, that is, sham operation group (laparotomy without renal pedicle occlusion), rIRI group (bilateral renal pedicles was clamped for 60 min with a microvascular clamp), and rIRI+Dex group (intraperitoneal injection of 25 μg/ml Dex in 15 min prior to bilateral renal ischemia). In 24 h after surgery or reperfusion, the blood samples were harvested and analyzed for counts of neutrophils, monocytes and lymphocytes by blood analyzer and for the serum levels of inflammatory cytokines (TNF-α, IL-1β and IL-10) by ELISA. Western blotting was used to detect iNOS and Arg 1 in the harvested peritoneal macrophages for the polarization. Results Compared with the mice in the sham group, the counts of neutrophils, monocytes and lymphocytes were significantly elevated (P < 0.01), the serum levels of TNF-α and IL-1β were increased (P < 0.01), and the expression of M1 marker iNOS was enhanced while that of M2 marker Arg 1 was decreased (P < 0.01). Dex pretreatment resulted in no significant changes in the counts of neutrophils, monocytes and lymphocytes (P>0.05), reduced serum levels of TNF-α and IL-1β (P < 0.01) and increased level of IL-10 (P < 0.01), and decreased expression of iNOS (P < 0.01) as well as increase of Arg 1 (P < 0.05) when compared with the indicators in the rIRI group. Conclusion Dex inhibits the systemic inflammatory response induced by rIRI, which may be associated with modulation of macrophage polarization.
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