医学
丙二醛
切梅林
肺
再灌注损伤
超氧化物歧化酶
髓过氧化物酶
水肿
生理盐水
缺血
麻醉
药理学
内科学
内分泌学
氧化应激
炎症
脂肪因子
胰岛素抵抗
胰岛素
作者
Run Zou,Mao-Hua Wang,Ye Chen,Xin Fan,Bo Yang,Juan Du,Xiaobin Wang,Ke‐Xuan Liu,Jun Zhou
出处
期刊:Shock
[Lippincott Williams & Wilkins]
日期:2018-05-31
卷期号:52 (1): 134-141
被引量:38
标识
DOI:10.1097/shk.0000000000001194
摘要
Limb ischemia/reperfusion (LI/R) injury is associated with high morbidity and mortality. The hypothesis of this study is that hydrogen-rich solution could attenuateacute lung injury and improve mortality via chemerin and NLRP3 after LI/R in rats. A rat model of LI/R was performed by clamping the bilateral femoral arteries for 3 h followed by reperfusion. Hydrogen-rich saline (HRS) was administered intraperitoneally (10 mL/kg or 2.5 mL/kg) when the atraumatic micro clips were released. The rats were euthanized at 2 h after reperfusion and then the arterial blood and lung specimens were harvested for further analyses. Meanwhile, survival rate was observed. The results showed that HRS improved the survival rate and attenuated pulmonary edema, injury, and apoptosis. HRS also decreased the levels of tumor necrosis factor-α, interleukin-6, myeloperoxidase and malondialdehyde, and increased the activity of superoxide dismutase in serum and lung after the LI/R event. HRS downregulated the expression of chemerin and NLRP3 in lung. The study demonstrated that chemerin and NLRP3 could serve as important response factors that were involved in the lung injury following LI/R. HRS could significantly attenuate LI/R-mediated acute lung injury, at least in part, by inhibiting the activated chemerin/NLRP3 signaling pathway.
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