Cobra Venom Factor-induced complement depletion protects against lung ischemia reperfusion injury through alleviating blood-air barrier damage.
Cobra Venom Factor-induced complement depletion protects against lung ischemia reperfusion injury through alleviating blood-air barrier damage.
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眼镜蛇毒因子诱导的补体耗竭通过减轻血气屏障损伤来预防肺缺血再灌注损伤
DOI：
10.1038/s41598-018-28724-z
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发表时间：
2018-07-09
影响因子：
4.6
通讯作者：
Fei L
中科院分区：
文献类型：
--
作者：
Haihua C;Wei W;Kun H;Yuanli L;Fei L
本研究旨在研究眼镜蛇毒因子(CVF)诱导的补体耗竭对大鼠肺缺血再灌注损伤(LIRI)的保护作用，并探讨其分子机制。成年SD大鼠随机分为5组(n = 6)：对照组、假手术组、I/R组、 + 组、I/R CVF组。麻醉前24 μ经尾静脉注射脑血管紧张素(50 g/kg)。夹闭左肺门60 ，再灌流4 小时，造成肺缺血再灌注(I/R)。测定补体活性、病理组织学肺损伤评分、炎症介质、肺通透性、肺水肿、紧密连接完整性和血-气屏障。结果表明，CVF可显著降低血浆和BALF中补体活性。组织学评价表明，CVF引起的补体耗竭可明显减轻肺组织的损伤，抑制肺组织和BALF的炎症反应。此外，CVF预处理还具有改善肺通透性和保护IR状态下紧密连接完整性的作用。综上所述，CVF诱导的补体耗竭可抑制I/R诱导的炎症反应，减轻肺I/R损伤。其保护作用的机制可能与改善血-气屏障损伤有关。
The purpose of this study was to study whether complement depletion induced by pretreatment with Cobra Venom Factor (CVF) could protect against lung ischemia reperfusion injury (LIRI) in a rat model and explore its molecular mechanisms. Adult Sprague-Dawley rats were randomly assigned to five groups (n = 6): Control group, Sham-operated group, I/R group, CVF group, I/R + CVF group. CVF (50 μg/kg) was injected through the tail vein 24 h before anesthesia. Lung ischemia reperfusion (I/R) was induced by clamping the left hilus pulmonis for 60 minutes followed by 4 hours of reperfusion. Measurement of complement activity, pathohistological lung injury score, inflammatory mediators, pulmonary permeability, pulmonary edema, integrity of tight junction and blood-air barrier were performed. The results showed that pretreatment with CVF significantly reduced complement activity in plasma and BALF. Evaluation in histomorphology showed that complement depletion induced by CVF significantly alleviated the damage of lung tissues and inhibited inflammatory response in lung tissues and BALF. Furthermore, CVF pretreatment had the function of ameliorating pulmonary permeability and preserving integrity of tight junctions in IR condition. In conclusion, our results indicated that complement depletion induced by CVF could inhibit I/R-induced inflammatory response and alleviate lung I/R injury. The mechanisms of its protective effects might be ameliorated blood-air barrier damage.
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影响因子：
3.2
作者：
Glasgow, SC;Kanakasabai, S;Chapman, WC
通讯作者：
Chapman, WC
影响因子：
4.4
作者：
Kambas, Konstantinos;Markiewski, Maciej M.;Ritis, Konstantinos D.
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Ritis, Konstantinos D.
影响因子：
--
作者：
Bosmann, Markus;Ward, Peter A.
通讯作者：
Ward, Peter A.
影响因子：
4.8
作者：
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通讯作者：
Vogel, CW
影响因子：
4.6
作者：
Fiser, SM;Tribble, CG;Kron, IL
通讯作者：
Kron, IL