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收稿:2019-11-13,
纸质出版:2020-03-30
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何心海, 陈星同, 杨子恒, 等. 右美托咪定调节巨噬细胞极化抑制肾缺血再灌注系统炎性反应[J]. 第三军医大学学报, 2020,42(6):611-615.
Xinhai HE, Xintong CHEN, Ziheng YANG, et al. Dexmedetomidine inhibits systemic inflammatory response induced by renal ischemia reperfusion
何心海, 陈星同, 杨子恒, 等. 右美托咪定调节巨噬细胞极化抑制肾缺血再灌注系统炎性反应[J]. 第三军医大学学报, 2020,42(6):611-615. DOI: 10.16016/j.1000-5404.201911107.
Xinhai HE, Xintong CHEN, Ziheng YANG, et al. Dexmedetomidine inhibits systemic inflammatory response induced by renal ischemia reperfusion
Objective
2
To explore the effects of dexmedetomidine (Dex) on systemic inflammatory response induced by renal ischemia reperfusion (rIRI) and the possible mechanism.
Methods
2
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
2
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
2
Dex inhibits the systemic inflammatory response induced by rIRI
which may be associated with modulation of macrophage polarization.
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