Hydrogen-Rich Saline Attenuates Acute Lung Injury Induced by Limb Ischemia/Reperfusion via Down-Regulating Chemerin and NLRP3 in Rats.

Hydrogen-Rich Saline Attenuates Acute Lung Injury Induced by Limb Ischemia/Reperfusion via Down-Regulating Chemerin and NLRP3 in Rats.
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DOI:
10.1097/shk.0000000000001194
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发表时间:
2019-07
期刊:
影响因子:
3.1
通讯作者:
R. Zou;Maohua Wang;Ye Chen;Xin Fan;Bo Yang;Juan Du;Xiao-bin Wang;Ke-xuan Liu;Jun Zhou
R. Zou;Maohua Wang;Ye Chen;Xin Fan;Bo Yang;Juan Du;Xiao-bin Wang;Ke-xuan Liu;Jun Zhou
中科院分区:
医学2区
文献类型:
--
作者:
R. Zou;Maohua Wang;Ye Chen;Xin Fan;Bo Yang;Juan Du;Xiao-bin Wang;Ke-xuan Liu;Jun Zhou

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肢体缺血/再灌注(LI/R)损伤与高发病率和死亡率相关。本研究的假设是富氢溶液可通过chemerin和NLRP 3减轻LI/R后大鼠的急性肺损伤并提高死亡率。采用夹闭双侧股动脉3 h后再灌注的方法建立LI/R大鼠模型。释放无创微型夹时,腹腔内给予富氢盐水(HRS)(10 mL/kg或2.5 mL/kg)。再灌注后2 h处死大鼠,取动脉血和肺标本进行进一步分析。同时观察存活率。结果表明,HRS可提高小鼠存活率,减轻肺水肿、肺损伤和细胞凋亡。HRS还可降低LI/R后血清和肺组织中肿瘤坏死因子-α、白细胞介素-6、髓过氧化物酶和丙二醛的水平,升高超氧化物歧化酶的活性。HRS下调肺组织chemerin和NLRP 3的表达。本研究表明chemerin和NLRP 3可能是LI/R后肺损伤的重要反应因子。HRS可显著减轻LI/R介导的急性肺损伤,至少部分是通过抑制激活的chemerin/NLRP 3信号通路。
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.