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目的 观察牛磺酸 (Tau)对溶血磷脂酸 (LPA)诱导的大鼠血管平滑肌细胞 (VSMC)增殖作用的影响。方法 在培养的大鼠血管平滑肌细胞上 ,测定3 H 胸腺嘧啶核苷(3 H TdR)参入和丝裂素活化蛋白激酶 (MAPK)活性 ;硫代巴比妥酸盐 (TBA)法测脂质过氧化终产物丙二醛 (MDA)含量。结果 LPA (1× 10 -9~ 1× 10 -7mol·L-1)呈浓度依赖性增加VSMC 3 H TdR参入 ,5、10和 2 0mmol·L-1Tau及MAPK抑制剂PD0 980 59预孵育后分别使LPA (1× 10 -7mol·L-1)诱导的3 H TdR参入较单独LPA组减少 15 %、34%、4 8%和 5 4 % (P <0 0 5或P <0 0 1)。LPA增加VSMCMAPK活性 ,5、10和 2 0mmol·L-1Tau预孵育降低LPA(1× 10 -7mol·L-1)刺激的MAPK活性 ,较单纯LPA孵育低14 %、35 %和 4 4 % (P <0 0 5或P <0 0 1)。随着加入LPA的浓度增加 ,细胞MDA含量增加。与 1× 10 -7mol·L-1LPA组比较 ,5、10和 2 0mmol·L-1Tau预处理的细胞较LPA单独孵育组细胞MDA含量分别低 18%、2 7%、4 5 % (P<0 0 5或P <0 0 1) ,LPA诱导细胞MDA生成的作用不受PD0 980 59预孵育的影响 (P >0 0 5 )。结论 LPA呈浓度依赖性促进VSMC增殖和脂质过氧化 ,前者与其细胞内信号传导MAPK途径有关 ,Tau可有效拮抗LPA诱导的VSMC增殖、MAPK激活和脂质过氧化损伤 ,Tau
Objective To observe the effect of taurine on the proliferation of vascular smooth muscle cells (VSMC) induced by lysophosphatidic acid (LPA) in rats. Methods 3H-thymidine incorporation and mitogen-activated protein kinase (MAPK) activity were measured in cultured rat vascular smooth muscle cells. Lipid levels were measured by thiobarbituronate (TBA) Peroxidation final product malondialdehyde (MDA) content. Results LPA (1 × 10 -9 ~ 1 × 10 -7 mol·L-1) increased VSMC 3 H TdR incorporation in a dose-dependent manner. After pretreatment with 5, 10 and 20 mmol·L-1 Tau and MAPK inhibitor PD0 980 59, 3 H TdR induced by LPA (1 × 10 -7 mol·L-1) decreased by 15%, 34%, 48% and 54% (P <0 05 or P 0 01, respectively, compared with LPA alone ). LPA increased the activity of VSMCMAPK. Preincubation with 5, 10 and 20 mmol·L -1 Tau reduced the MAPK activity stimulated by LPA (1 × 10 -7 mol·L -1), which was 14%, 35% and 44% lower than LPA alone P <0 0 5 or P <0 0 1). As the concentration of LPA was added, the cell MDA content increased. Compared with 1 × 10 -7 mol·L-1 LPA group, the MDA content of cells pretreated with 5, 10 and 20 mmol·L-1 Tau was 18%, 27% and 45% lower than those incubated with LPA alone (P < 0 05 or P 0 01). The effect of LPA on cell MDA production was not affected by the preincubation of PD0 98059 (P> 0.05). Conclusion LPA can promote VSMC proliferation and lipid peroxidation in a concentration-dependent manner. The former is related to its intracellular signaling MAPK pathway. Tau can effectively antagonize LPA-induced VSMC proliferation, MAPK activation and lipid peroxidation injury, Tau