| 厉广洲.飞燕草素葡萄糖苷通过下调微小 RNA-106a保护缺氧复氧引起的心肌细胞损伤[J].安徽医药,2022,26(3):438-442. |
| 飞燕草素葡萄糖苷通过下调微小 RNA-106a保护缺氧复氧引起的心肌细胞损伤 |
| Delphinidin glucoside protects cardiomyocytes from hypoxia-reoxygenation-induced injury by downregulating miR-106a |
| |
| DOI：10.3969/j.issn.1009-6469.2022.03.004 |
| 中文关键词: 毛茛科 心肌再灌注损伤 飞燕草素葡萄糖苷 miR-106a 缺氧复氧 心肌细胞损伤 |
| 英文关键词: Ranunculaceae Myocardial reperfusion injury Delphinidin glucoside MiR-106a Hypoxia-reoxygenation Cardiomyocyte injury |
| 基金项目: |
|
| 摘要点击次数: 1293 |
| 全文下载次数: 409 |
| 中文摘要: |
| 目的探讨飞燕草素葡萄糖苷( DPg)对缺氧复氧( H/R)引起的心肌细胞损伤的影响及其机制。方法 2018年 4月至 2019年 10月，用 H9C2细胞建立心肌细胞 H/R损伤模型，用常规培养的细胞作为对照组；用终浓度为 50 μmol/L、100 μmol/L、1 000 μmol/L的 DPg培养液处理 H9C2细胞 24 h，而后进行 H/R处理，分别记为 H/R+50 μmol/L DPg组、 H/R+100 μmol/L DPg组、 H/R+1 000 μmol/L DPg组；抗微小 RNA-106a(anti-miR-106a)阴性对照( anti-miR-con)、 anti-miR-106a质粒转染至 H9C2细胞后进行 H/R处理记为 H/R+anti-miR-con组， H/R+anti-miR-106a组。 miR-106a阴性对照( miR-con)、 miR-106a分别转染至 H9C2细胞中同时用 100 μmol/L的 DPg处理 24 h，而后进行 H/R处理，记为 H/R+DPg+miR-con组， H/R+DPg+miR-106a组。 MTT法检测细胞活性；蛋白质印迹法( Western blotting)检测活化胱天蛋白酶 -3(cleaved-caspase-3)、细胞周期蛋白 D1(cyclin D1)蛋白表达水平；流式细胞术检测细胞凋亡；实时荧光定量逆转录聚合酶链反应( qRT-PCR)检测 miR-106a表达水平。结果与对照组相比， H/R组心肌细胞存活率显著降低，细胞凋亡率显著升高［(18.35±1.83)%比( 7.05±0.71)%］cleaved-caspase-3表达水平显著升高， miR-106a表达水平显著升高［( 3.56±0.36)比( 1.00±0.11)］(P<0.05)； DPg处理的心肌细胞存，活率显著升高；且 100 μmol/ LDPg组于 H/R组，细胞凋亡率显著降低［(10.25±1.03)%比( 18.35±1.83)%］，cleaved-caspase-3表达水平显著降低， miR-106a表达水平显著降低［( 1.53±0.15)比( 3.56±0.36)］(P<0.05)。 miR-106a低表达抑制 H/R引起的心肌细胞凋亡；高表达 miR-106a逆转了 DPg对 H9C2细胞增殖促进和凋亡抑制的作用。结论 DPg可促进细胞增殖、抑制细胞凋亡，保护 H/R引起的心肌细胞损伤；其机制可能与 miR-106a有关。 |
| 英文摘要: |
| Objective To investigate the effect and mechanism of delphinidin glucoside (DPg) on cardiomyocyte injury induced by hypoxia-reoxygenation (H/R).Methods From April 2018 to October 2019, H9C2 cells were used to establish a cardiomyocyte H/R injury model, and conventionally cultured cells were used as the control (NC) group; H9C2 cells were treated with DPg at concentrationsof 50 μmol/L, 100 μmol/L, and 1,000 μmol/L for 24 h and then treated with H/R, which were denoted as the H/R+50 μmol/L DPggroup, H/R+100 μmol/L DPg group, H/R+1,000 μmol/L DPg group; anti-microRNA-106a (anti-miR-106a) negative control (anti-miRcon), anti-miR-106a plasmid was transfected into H9C2 cells and then treated with H/R, which was recorded as the H/R+anti-miR-con group and H/R+anti-miR-106a group. MiR-106a negative control (miR-con) and miR-106a were transfected into H9C2 cells simultaneously with 100 μmol/L DPg for 24 h, followed by H/R treatment, which was recorded as the H/R+DPg+miR-con group and H/R+DPg+ miR-106a group. Cell viability was detected by MTT assay; cleaved caspase-3 and cyclin D1 protein expressions was detected by Western blotting; cell apoptosis was detected by flow cytometry; and qRT-PCR was used to detect the expression of miR-106a.Results Compared with the NC group, the survival rate of cardiomyocytes in the H/R group was significantly decreased, the apoptosis rate wassignificantly increased [(18.35±1.83)% vs. (7.05±0.71)%], the expression of cleaved caspase-3 was significantly increased, and the expression of miR-106a was significantly increased [(3.56±0.36) vs. (1.00±0.11)] (P<0.05); the survival rate of cardiomyocytes treatedwith DPg was significantly increased, while the apoptosis rate was significantly reduced in the 100 μmol/L DPg group compared withthe H/R group [(10.25±1.03)% vs. (18.35±1.83)%]; the expression level of cleaved-caspase-3 was significantly reduced, which was similar to the change in miR-106a [(1.53±0.15) vs. (3.56±0.36)] (P<0.05). Low expression of miR-106a inhibits H/R-induced cardiomyocyte apoptosis, while high expression of miR-106a reverses the effects of DPg on the proliferation promotion and apoptosis inhibition of H9C2 cells.Conclusion DPg can promote cell proliferation, inhibit cell apoptosis and protect cardiomyocytes from H/R-induced injury, and the mechanism may be related to miR-106a. |
|
查看全文
查看/发表评论 下载PDF阅读器 |
| 关闭 |
|
|
|
