目的 探索黄芪多糖（APS）对过氧化氢（H2O2）诱发的大鼠心肌细胞H9C2的保护作用及可能机制。方法 实验分为①对照组；②对照＋APS组；③H2O2损伤组；④H2O2损伤+APS修复组，采用乳酸脱氢酶（LDH）漏出量测定、3-（4，5-二甲基噻唑-2）-2，5-二苯基四氮唑溴盐[3-（4，5-dimethyl-2-thiazolyl）-2，5-diphenyl-2-H-tetrazolium bromide，MTT]检测、免疫荧光染色、原位末端标记法（TUNEL）、逆转录-聚合酶链反应（RT-PCR）以及蛋白质印迹（WB）等实验方法，观察APS对H2O2引起的心肌细胞损伤、死亡的影响以及过氧化物酶体增殖物激活受体γ共激活因子1（PGC-1）/肌肉因子（irisin）信号通路在其中的参与情况。结果 与对照组相比，H2O2损伤组，细胞死亡率显著提高[（23.3±1.14）% vs.（12.81±0.71）%，P＜0.001]；与H2O2组相比，H2O2损伤+APS修复组黄芪多糖组能够显著降低过氧化氢引起的细胞死亡[（16.93±0.64）% vs. （23.3±1.14）%，P＜0.001]、提高细胞生存率[（65.77±5.08）% vs. （39.95±4.90）%，P＜0.05）]、减轻细胞凋亡[（18.90±1.14）% vs. （4.80±0.39）%，P＜0.001]。黄芪多糖处理后，irisin及其上游调控因子PGC-1α的信使核糖核酸（mRNA）转录水平和蛋白表达量均明显提高，差异具有统计学意义（P＜0.05）。结论 黄芪多糖对心肌细胞的保护作用至少部分是通过PGC-1α/irisin信号通路实现。

Objective This study explores the effect and mechanism of Astragalus polysaccharide in hydrogen peroxide-induced cardiomyocyte injury. Methods H9C2 cells were divided into four groups: ①control, ②control+APS group, ③H2O2 injury, ④H2O2+APS group. LDH leakage assay, MTT assay, immunofluorescence staining, TUNEL, RT-PCR, and western blot were employed to evaluate the effects of astragalus polysaccharides on cardiomyocyte apoptosis and death caused by hydrogen peroxide. PCR and western blot also examined PGC-1 α and irisin expression. Results Compared with the control group, the cell death rate after H2O2 admission increased from [(12.81±0.71)% vs. (23.3±1.14)%, P<0.001]. Astragalus polysaccharides could significantly reduce cell death caused by hydrogen peroxide [(16.93±0.64)% vs. (23.3±1.14)%, P<0.001], improve cell survival rate [(65.77 ±5.08)% vs. (39.95 ± 4.90)%, P<0.05], and inhibit cell apoptosis [(18.90±1.14)% vs. (4.80±0.39)%, P<0.001]. In addition, the mRNA and expression of irisin and its upstream regulator PGC-1α increased remarkably after astragalus polysaccharide treatment (P<0.05). Conclusion The protective effect of astragalus polysaccharides on cardiomyocytes is at least partly mediated by PGC-1 α/ Irisin signal path activation.

河南省医学科技攻关计划(联合共建项目) (LHGJ20191207)