血浆代谢物丙酮酸影响血管平滑肌细胞凋亡的研究

A Study on the Effect of Plasma Metabolite Pyruvate on Apoptosis of Vascular Smooth Muscle Cells

目的:旨在探索血浆代谢物丙酮酸对血管平滑肌细胞的凋亡作用。方法:选取人血管平滑肌细胞(vascular smooth muscle cell, VSMC),用血管紧张素II (Angiotensin II, Ang II)干预刺激细胞建立VSMC损伤模型,用不同浓度的特异性代谢物丙酮酸干预损伤细胞,再通过CCK8、TUNEL及流式等实验检测细胞凋亡情况。结果:VSMC细胞活力以Ang II浓度梯度依赖性降低。不同浓度的丙酮酸对VSMC细胞活力的影响不同,并在一定的浓度范围内丙酮酸对细胞活力的影响没有统计学差异。Ang II诱导的VSMC受损细胞模型中用丙酮酸干预之后呈现细胞活力恢复趋势。当丙酮酸(2 mmol/L)干预Ang II诱导的VSMC受损细胞模型时可以在一定程度上恢复细胞凋亡。结论:丙酮酸恢复Ang II干预损伤的血管平滑肌细胞活力。丙酮酸抑制Ang II干预的血管平滑肌细胞进一步凋亡。

Objective: To explore the apoptotic effect of plasma metabolite pyruvate on vascular smooth muscle cells. Method: Selecting human vascular smooth muscle cells (VSMCs), using angiotensin II (Ang II) intervention to stimulate cells to establish a VSMC injury model. Different concentrations of specific metabolite pyruvate were used to intervene in the damaged cells, and cell apoptosis was detected through CCK8, TUNEL, and flow cytometry experiments. Results: The viability of VSMC cells decreased in a gradient dependent manner with Ang II concentration. The effects of different concentrations of pyruvate on VSMC cell viability vary, and there is no statistically significant difference in the effect of pyruvate on cell viability within a certain concentration range. The Ang II induced VSMC damaged cell model showed a trend of cell viability recovery after intervention with pyruvate. When pyruvate (2 mmol/L) intervenes in Ang II induced VSMC damaged cell model, it can partially restore cell apoptosis. Conclusions: Acetate restores the vitality of vascular smooth muscle cells after Ang II intervention injury. Acetate inhibits further apoptosis of vascular smooth muscle cells intervened by Ang II.