摘要
目的防治血运重建后组织的缺血-再灌注损伤是当前血管微创领域的研究热点,文中在细胞水平进一步探讨红景天苷对心肌细胞缺血-再灌注损伤的保护作用及其部分机制。方法将H9C2细胞株培养后取对数期细胞,分为4组:1正常对照组:正常培养24 h后进行相关指标检测;2缺氧/复氧组:用缺氧培养液培养16 h后换为正常培养液培养8 h,进行相关指标检测;3缺氧/复氧+红景天苷组:在换缺氧培养液的同时加入20μL(200μg/m L)红景天组苷,余步骤同缺氧/复氧组;4缺氧/复氧+红景天苷+LY294002组:在加入红景天苷前30 min加入磷脂酰肌醇-3-激酶通道阻滞剂LY294002,余步骤同缺氧/复氧组。经上述处理后,用MTT法检测药物对细胞增殖的影响;检测培养液中活性氧水平。结果与缺氧/复氧+红景天苷组H9C2细胞抑制率[(27.95±4.41)%]比较,缺氧/复氧组、缺氧/复氧+红景天苷组+LY294002[(37.40±2.56)%、(35.63±2.16)%]均增加(P<0.05)。而缺氧/复氧组、缺氧/复氧+红景天苷组+LY294002抑制率差异无统计学意义(P>0.05)。与正常对照组活性氧水平(11.62±0.71)比较,缺氧/复氧组、缺氧/复氧+红景天苷组、缺氧/复氧+红景天苷组+LY294002(36.55±2.08、30.44±1.07、36.46±2.02)均增加(P<0.05);与缺氧/复氧组比较,缺氧/复氧+红景天苷组活性氧水平减少(P<0.05),而缺氧/复氧+红景天苷组+LY294002差异无统计学意义(P>0.05)。结论红景天苷可通过抑制细胞凋亡、降低活性氧水平发挥对H9C2细胞缺血-再灌注损伤的保护作用。该作用可以被磷脂酰肌醇-3-激酶通道阻滞剂LY294002抑制,提示红景天苷的抗MIRI作用可能与PI3K信号通路有关。
Objective Tissue reperfusion injury is one of the main factors affecting the result of revascularization which is a research hotspot about prevention and treatment of myocardial isehemia-reperfusion injury （ MIRI ） in current field of cardiology. The aim of the study was to discuss the protective effects of salidroside on H9C2 cell with MIRI and explore its mechanism in order to provide a scientific and objective basis for MIRI by using Chinese medicine. Methods H9C2 cell line was inoculated to cell culture bottle, followed by the detection of related indexed on logarithmic phase cells. There were 4 groups： ①normal control group, H9C2 cells being cultivated in cell incubator for 24 h; ②I/R group, cells being cultivated in hypoxia culture medium for 16 h followed by 8 h＇s cultivation in normal culture medium; ③I/R ± S group, the addition of 20 μL（200μg/mL） salidroside solution at the time of replacing hypoxia liquid time followed by the same steps as I/R group; ④I/R ± S ±LY294002 group, adding PI3K LY294002 30 minutes before the addition of 20 μL（200 μg/mL） salidroside followed by the same steps as I/R group. Then MTT method was applied to detect the effects of medicine on cell proliferation and ROS level in culture medium. Results ①Effects on cell proliferation： Significant decrease of inhibition rate was found in I/R ± S group compared with I/R group （27.95 ±4.41 vs 37.40 ± 2.56, P 〈 0. 001 ）. Inhibition rate was significantly upregulated in I/R ＋ S ＋ LY294002 group （ 35.63 ± 2.16 vs 27.95 ± 4.41, P = 0. 003 ）. There was no statistical differences between control group and I/R ＋ S ± LY294002 group （ 35.63 ± 2.16 vs 37.40 ± 2.56, P 〉 0.05 ）.②ROS level ： ROS levels in I/R group, I/R ＋ S group, I/R ＋ S ＋ LY294002 group were increased compared to control group （36.55 ± 2.08, 30.44 ± 1.07, 36.46 ± 2.02 vs 11.62 ± 0.71, P 〈 0. 001 ） respectively. ROS level in IfR ± S group was significantly downregulated compared with that in I/R gro
出处
《医学研究生学报》
CAS
北大核心
2016年第6期593-597,共5页
Journal of Medical Postgraduates
基金
江苏省中医药局科技项目(LZ11177)
