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李然, 王振裕, 王燕丽, 等. 三参通脉合剂通过上调microRNA-146a改善大鼠心肌细胞H9C2的氧化损伤[J]. koko体育app 学报(医学版), 2024, 55(3): 630-634. DOI:
引用本文: 李然, 王振裕, 王燕丽, 等. 三参通脉合剂通过上调microRNA-146a改善大鼠心肌细胞H9C2的氧化损伤[J]. koko体育app 学报(医学版), 2024, 55(3): 630-634. DOI:
LI Ran, WANG Zhenyu, WANG Yanli, et al. Sanshentongmai Mixture Improves Oxidative Damage in Rat Cardiomyocytes H9C2 via Upregulation of microRNA-146a[J]. Journal of Sichuan University (Medical Sciences), 2024, 55(3): 630-634. DOI:
Citation: LI Ran, WANG Zhenyu, WANG Yanli, et al. Sanshentongmai Mixture Improves Oxidative Damage in Rat Card🐻iomyocytes H9C2 via Upregulation of microRNA-146a[J]. Journal of Sichuan University (Medical Sciences), 2024, 55(3): 630-634. DOI:

三参通脉合剂通过上调microRNA-146a改善大鼠心肌细胞H9C2的氧化损伤

Sanshentongmai Mixture Improves Oxidative Damage in Rat Cardiomyocytes H9C2 via Upregulation of microRNA-146a

  • 摘要:
    目的 探讨三参通脉(Sanshentongmai, SSTM)合剂调节微小RNA-146a(microRNA-146a)对大鼠心肌细胞H9C2氧化损伤的影响及作用机制。
    方法 体外培养大鼠心肌细胞H9C2,过氧化氢(H2O2)作为氧化剂制作H9C2氧化应激模型。通过三参通脉干预,观察H2O2诱导的H9C2细胞氧化损伤的变化以及microRNA-146a的表达,探讨三参通脉对H9C2的保护作用及其作用机制。将体外培养的H9C2分为空白组、H2O2氧化损伤模型组(简称模型组)、H2O2模型+三参通脉药物(500 μg/mL,处理72 h)组(简称模型加药组)。通过细胞计数试剂盒CCK8检测细胞活力,酶联免疫吸附试验(enzyme-linked immunosorbent assay, ELISA)检测血清N端脑钠肽前体(N-terminal pro-brain natriuretic peptide, Nt-proBNP)、一氧化氮(nitric oxide, NO)、超敏C反应蛋白(high-sensitivity C-reactive protein, Hs-CRP)和血管紧张素Ⅱ(angiotensin Ⅱ)水平,实时荧光定量PCR(RT-PCR)检测系统检测microRNA-146a表达水平。
    结果 通过CCK8法检测细胞活力,发现在药物质量浓度为500 μg/mL时,细胞增殖改善达到顶峰,故选用此浓度为干预浓度。ELISA检测的心衰相关指标:Nt-proBNP、NO、Hs-CRP、angiotensin Ⅱ水平中,与空白组比较,模型加药物组中Nt-proBNP、angiotensin Ⅱ表达上调(P<0.05),NO表达下调(P<0.05),Hs-CRP与空白组比较表达差异无统计学意义,说明三参通脉可以有效改善大鼠心肌细胞H9C2氧化损伤。最后,RT-PCR法检测microRNA-146a在各组的表达可以看出,15 μmol/L H2O2处理可以明显降低microRNA-146a表达,而模型加药组中microRNA-146a表达较模型组升高(P<0.05),与空白组对比差异无统计学意义。
    结论 三参通脉可以明显抵抗H2O2诱导的H9C2细胞氧化损伤,可能是通过上调microRNA-146a从而发挥心肌保护作用。
     
    Abstract:
    Objective To investigate the effect of Sanshentongmai (SSTM) mixture on the regulation of oxidative damage to rat cardiomyocytes (H9C2) through microRNA-146a and its mechanism.
    Methods H9C2 were cultured in vitro, H2O2 was used as an oxidant to create an oxidative damage model in H9C2 cells. SSTM intervention was administered to the H9C2 cells. Then, the changes in H2O2-induced oxidative damage in H9C2 cells and the expression of microRNA-146a were observed to explore the protective effect of SSTM on H9C2 and its mechanism. H9C2 cells cultured in vitro were divided into 3 groups, including a control group, a model group of H2O2-induced oxidative damage (referred to hereafter as the model group), and a group given H2O2 modeling plus SSTM intervention at 500 μg/L for 72 h (referred to hereafter as the treatment group). The cell viability was measured by CCK8 assay. In addition, the levels of N-terminal pro-brain natriuretic peptide (Nt-proBNP), nitric oxide (NO), high-sensitivity C-reactive protein (Hs-CRP), and angiotensin were determined by enzyme-linked immunosorbent assay (ELISA). The expression level of microRNA-146a was determined by real-time PCR (RT-PCR).
    Result H9C2 cells were pretreated with SSTM at mass concentrations ranging from 200 to 1500 μg/L. Then, CCK8 assay was performed to measure cell viability and the findings showed that the improvement in cell proliferation reached its peak when the mass concentration of SSTM was 500 μg/L, which was subsequently used as the intervention concentration. ELISA was performed to measure the indicators related to heart failure, including Nt-proBNP, NO, Hs-CRP, and angiotensin Ⅱ. Compared with those of the control group, the expressions of Nt-proBNP and angiotensin Ⅱ in the treatment group were up-regulated (P<0.05), while the expression of NO was down-regulated (P<0.05). There was no significant difference in the expression of Hs-CRP between the treatment group and the control group. These findings indicate that SSTM could effectively ameliorate oxidative damage in H9C2 rat cardiomyocytes. Finally, according to the RT-PCR findings for the expression of microRNA-146a in each group, H2O2 treatment at 15 μmol/L could significantly reduce the expression of microRNA-146a, and the expression of microRNA-146a in the treatment group was nearly doubled compared with that in the model group. There was no significant difference between the treatment group and the control group.
    Conclusion SSTM can significantly resist the H2O2-induced oxidative damage of H9C2 cells and may play a myocardial protective role by upregulating microRNA-146a.
     

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