Astragaloside IV (AS/IV) is one of the extracted components from the traditional Chinese medicine Astragalus which has been demonstrated to have potential capacity for anti-inflammation activity and for treating cardiovascular disease. Our purpose was to determine the function and underlying molecular mechanism of AS/IV in hypoxia/reoxygenation (H/R) injured in cardiomyocytes. Differentially expressed genes (DEGs) were screened using bioinformatic analysis, and the molecular targeting relationship was verified by the dual-luciferase report system. H/R injured cardiomyocytes were employed to explore the effect of AS/IV. QRT-PCR and Western blot analysis were applied to detect the expression of mRNA and proteins, respectively. Additionally, superoxide dismutase (SOD), lactic dehydrogenase (LDH) and MDA (malondialdehyde) levels were detected to determine the oxidative damage. Cell viability was assessed by CCK-8, and flow cytometry was used to evaluate cell apoptosis ratio. TGFBR1 and TLR2 were selected as DEGs. Additionally, AS/IV could enhance cell proliferation and upregulated miR-101a expression, which suppressed TGFBR1 and TLR2 expression in H/R injured cardiomyocytes. Moreover, the results of Western blot exhibited that the downstream genes (p-ERK and p-p38) in the MAPK signaling pathway were suppressed, which meant AS/IV could inhibit this pathway in H/R injured cardiomyocytes. Overall, this study demonstrated AS/IV could attenuate H/R injury in human cardiomyocytes via the miR-101a/TGFBR1/TLR2/MAPK signaling pathway axis, which means that it could serve as a possible alternate for H/R treatment.

中文翻译：

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黄芪甲苷IV通过调节miR-101a保护人心肌细胞免受缺氧/复氧损伤。

黄芪甲苷IV（AS / IV）是从中药黄芪中提取的成分之一，已被证明具有潜在的抗炎活性和治疗心血管疾病的能力。我们的目的是确定AS / IV在心肌细胞缺氧/复氧（H / R）中的功能和潜在的分子机制。使用生物信息学分析筛选差异表达基因（DEG），并通过双荧光素酶报告系统验证分子靶向关系。H / R损伤的心肌细胞被用来探讨AS / IV的作用。应用QRT-PCR和Western blot分析分别检测mRNA和蛋白质的表达。此外，超氧化物歧化酶（SOD）检测乳酸脱氢酶（LDH）和丙二醛（丙二醛）水平以确定氧化损伤。通过CCK-8评估细胞活力，并使用流式细胞术评估细胞凋亡率。选择TGFBR1和TLR2作为DEG。此外，AS / IV可以增强细胞增殖并上调miR-101a表达，从而抑制H / R损伤的心肌细胞中TGFBR1和TLR2的表达。此外，Western blot结果显示，MAPK信号通路中的下游基因（p-ERK和p-p38）被抑制，这意味着AS / IV可以抑制H / R损伤的心肌细胞中的该通路。总体而言，这项研究表明AS / IV可以通过miR-101a / TGFBR1 / TLR2 / MAPK信号传导途径轴减轻人心肌细胞的H / R损伤，这意味着它可以作为H / R治疗的替代方法。