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目的:探讨硫酸多糖(DPS)抗增殖作用及其机制。方法:用MTT法评价DPS抗大鼠主动脉平滑肌细胞(VSMC)增殖作用。用流式细胞仪观察DPS对 VSMC胞浆内游离Ca~(2+)的含量、细胞周期和蛋白质含量的影响。结果:DPS在0.001-100mg/L浓度下,对Ang Ⅱ诱导的VSMC增殖均有明显抑制作用,最佳抑制浓度为1mg/L。流式细胞术分析结果表明,DPS在抗增殖的浓度(1mg/L)下能抑制VSMC从G_0/G_1到S期的转换,阻止VSMC进入G_2/M期;减少VSMC蛋白质的合成。DPS能明显抑制胞浆内游离Ca~(2+)浓度的升高,此作用可被一氧化氮合酶抑制剂(L-NAME)所阻断,提示一氧化氮可能介导了DPS降低胞浆内游离Ca~(2+)浓度的作用。结论:硫酸多糖DPS可拮抗Ang Ⅱ诱导的VSMC增殖,其作用机理可能与降低胞浆内游离Ca~(2+)浓度,抑制VSMC的DNA及蛋白质合成有关。
Objective: To investigate the antiproliferative effect of sulfate polysaccharide (DPS) and its mechanism. Methods: The proliferation of rat aortic smooth muscle cells (VSMCs) was evaluated by MTT assay. The effect of DPS on the content of free Ca 2+, the cell cycle and the content of protein in cytoplasm of VSMC were observed by flow cytometry. Results: DPS at a concentration of 0.001-100mg / L significantly inhibited the proliferation of VSMCs induced by Ang Ⅱ, with the optimal inhibitory concentration of 1mg / L. Flow cytometry analysis showed that DPS inhibited the VSMC from G_0 / G_1 to S phase at the antiproliferative concentration (1mg / L), prevented VSMC from entering G_2 / M phase and decreased VSMC protein synthesis. DPS can significantly inhibit the increase of intracellular free Ca 2+ concentration, which can be blocked by L-NAME, suggesting that nitric oxide may mediate the decline of DPS The role of intracellular free Ca ~ (2+) concentration. CONCLUSION: Sulfate polysaccharide DPS can antagonize the proliferation of VSMC induced by Ang Ⅱ, and its mechanism may be related to the decrease of intracellular free Ca 2+ concentration and the inhibition of VSMC DNA and protein synthesis.