PLCE1 promotes myocardial ischemia-reperfusion injury in H/R H9c2 cells and I/R rats by promoting inflammation
PLCE1 promotes myocardial ischemia-reperfusion injury in H/R H9c2 cells and I/R rats by promoting inflammation
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DOI：
10.1042/bsr20181613
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发表时间：
2019-07-05
影响因子：
4
通讯作者：
Wang, Qiang
中科院分区：
文献类型：
--
作者：
Li, WenHua;Li, Yong;Wang, Qiang
心肌缺血再灌注损伤是冠心病发病率和死亡率的主要原因。如何在保证缺血心肌组织血供恢复的同时，避免或减轻缺血再灌注损伤，是临床上亟待解决的问题。本研究通过H9 c2 H/R（H/R，hypoxia-reoxygenation）模型和大鼠心肌I/R损伤模型，探讨磷脂酶C-1（PLCE 1）的功能。研究PLCE 1的表达及其在I/R损伤诱导的炎症反应中的作用及其可能的机制。结果表明，PLCE 1在H/R H9 c2和HL-1细胞中随缺氧时间的延长沿着增加。在心肌I/R大鼠中，PLCE 1在Sham组表达较低，而在I/R组表达明显升高。PLCE 1的过表达促进IL-6、TNF α和IL-1 α的表达，并降低IL-10的表达。PLCE 1的敲低降低了IL-6、TNF-α和IL-1 α的表达，并增加了IL-10的表达。此外，PLCE 1的过表达增加了p38、ERK 1/2和核因子-κ B（NF-κ B）P65的磷酸化，而PLCE 1的敲低抑制了它们的磷酸化。结论：PLCE 1在H/R H9 c2细胞和I/R大鼠中表达上调。PLCE 1过表达通过激活NF-α B信号通路促进炎症反应。
Myocardial ischemia-reperfusion (I/R) injury is a major contributor to the morbidity and mortality associated with coronary artery disease. How to ensure the recovery of blood supply to ischemic myocardial tissue while avoiding or reducing I/R injury remains a critical problem in clinical practice. In the present study, we examined the function of phospholipase C -1 (PLCE1) by an H9c2 H/R (H/R, hypoxia-reoxygenation) model and a rat myocardial I/R injury model. The expression of PLCE1 and its effect on I/R injury-induced inflammatory response as well as its possible underlying mechanism were investigated. Our results have shown that PLCE1 was progressively increased along with the increase in hypoxia time in the H/R H9c2 and HL-1 cells. In myocardial I/R rats, PLCE1 presented a low expression level in the sham group, however, it was increased sharply in the I/R group. Overexpression of PLCE1 promoted the expression of IL-6, TNF alpha, and IL-1 alpha, and decreased the expression of IL-10. Knockdown of PLCE1 decreased the expression of IL-6, TNF-alpha, and IL-1 alpha, and increased the expression of IL-10. Furthermore, overexpression of PLCE1 increased the phosphorylation of p38, ERK1/2, and nuclear factor-kappa B (NF-kappa B) P65 while knockdown of PLCE1 inhibited their phosphorylation. In conclusion, the present study provided evidence that PLCE1 was up-regulated in H/R H9c2 cell and I/R rat. Overexpression of PLCE1 promoted the inflammatoion via activation of the NF-alpha B signaling pathway.