白介素-35对脂多糖所致内皮祖细胞损伤的保护作用研究

The study of protective effect of IL-35 on the injury of endothelial progenitor cells induced by lipopolysaccharide

目的探究白介素-35(IL-35)对脂多糖(LPS)所致内皮祖细胞(EPC)损伤的保护作用及机制。方法选取购自南昌大学实验动物科学中心的健康雄性SD大鼠6只,分离培养EPC细胞,随机分为Control组、LPS组(给予LPS)、IL-35组(给予IL-35+LPS)及Wortmannin组(IL-35+LPS+Wortmannin)。分析EPC细胞分组处理后增殖情况,利用流式细胞术检测细胞凋亡情况,检测并比较PI3K/Akt通路相关蛋白及活性表达情况。结果LPS组细胞增殖能力明显低于Control组(P<0.05);IL-35组细胞增殖能力明显高于LPS组(P<0.05);Wortmannin组细胞增殖能力明显低于IL-35组(P<0.05)。LPS组细胞凋亡率明显高于Control组(P<0.05),IL-35组细胞凋亡率明显低于LPS组(P<0.05),Wortmannin组细胞凋亡率明显高于IL-35组(P<0.05)。LPS组P-PI3K和P-Akt相对表达量均明显低于Control组(P<0.05);IL-35组PPI3K和P-Akt相对表达量高于LPS组(P<0.05);Wortmannin组P-PI3K和P-Akt相对表达量明显低于LPS组(P<0.05)。结论IL-35预处理能有效逆转LPS引起的EPC细胞增殖和凋亡变化,且这种保护是通过激活PI3K/Akt信号机制发挥作用。

Objective To investigate the protective effect and mechanism of interleukin-35(IL-35)on lipopolysaccharide(LPS)induced endothelial progenitor cell(EPC)injury.Methods 6 healthy male SD rats purchased from the Laboratory Animal Science Center of Nanchang University were selected.EPC were isolated and cultured and randomly divided into Control group,LPS group(LPS),IL-35 group(IL-35+LPS),and Wortmannin group(IL-35+LPS+Wortmannin).After group treatment,the proliferation of EPC cells were detected.The apoptosis was detected by flow cytometry,and PI3K/Akt pathway related proteins and active expression were detected and compared.Results The cell proliferative capacity in the LPS group was significantly lower than that in the Control group(P<0.05).The cell proliferative capacity in the IL-35 group was significantly higher than that in the LPS group(P<0.05).The cell proliferative capacity in the Wortmannin group was significantly lower than that in the IL-35 group(P<0.05).The apoptosis rate in LPS group was significantly higher than that in Control group(P<0.05),the apoptosis rate in IL-35 group was significantly lower than that in LPS group(P<0.05),and the apoptosis rate in Wortmannin group was significantly higher than that in IL-35 group(P<0.05).Relative expression of P-PI3K and P-Akt in LPS group were significantly lower than Control group(P<0.05).Relative expression of P-PI3K and P-Akt in IL-35 group were significantly higher than LPS group(P<0.05).Relative expression of P-PI3K and P-Akt in Wortmannin group was significantly lower than that of LPS group(P<0.05).Conclusion IL-35 pretreatment could effectively reverse the LPS induced changes of EPC cell proliferation and apoptosis,and this protection was activated by PI3K/Akt signaling.