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目的:研究极低密度脂蛋白(VLDL)对SD大鼠系膜细胞(MCs)的促增生作用以及VLDL对MCs P42 有丝分裂原活化的蛋白激酶(P42 MAPK)活性的影响。探讨P42 MAPK介导的细胞内信号转导途径在上述系膜细胞增生中的作用。 方法:采用XTT法测定不同时间、不同浓度VLDL对MCs的促增生作用,借助流式细胞术观察细胞凋亡情况以了解VLDL对MCs是否具有毒性作用;通过同位素标记法测定MCs P42 MAPK活性;观察P42 MAPK抑制剂PD98059抑制该激酶后MCs的增生情况以及激酶活性变化。 结果:①不同浓度VLDL(10~500 mg/ml)、不同时间(6~48h)与XTT光密度(AD)值呈线性关系[r分别为0.911(P<0.01、0.651 P<0.05)]。当VLDL浓度达1000mg/ml时,MCs出现凋亡;②VLDL可以以剂量关系(10 ~1000 mg/ml)促进MCs 的P42 MAPK活性(r=0.872, P<0.05);随VLDL刺激时间延长,P42 MAPK活性增加,但不呈线性关系,分别在30 min、6h、48 h出现波峰[分别为(118.67±6.43) cpm/k、(140.50±17.68) cpm/k与(128±5.66)cpm/k];③PD98059抑制了P42 MAPK后,P42 MAPK活性显著降低;不同浓度、不同时间VLDL刺激MCs后的XTT AD值也显著降低。 结论:①在一定浓度内(10 ~500mg/ml )VLDL可以以浓度、剂量依赖性的关系促进MCs的增生,但高浓度则可促进细胞凋亡,具有毒性作用;②VLDL
AIM: To investigate the effect of VLDL on the proliferation of rat mesangial cells (MCs) and the effect of VLDL on the activation of P42 MAPK in MCs P42 mitochondria. To investigate the role of P42 MAPK-mediated intracellular signal transduction pathway in mesangial cell proliferation. Methods: The effect of VLDL on promoting proliferation of MCs was observed by XTT method. The apoptosis of MCs was observed by flow cytometry to understand whether VLDL had a toxic effect on MCs. The activity of MCs P42 MAPK was measured by isotope labeling The P42 MAPK inhibitor PD98059 inhibited the proliferation of MCs and the change of kinase activity after this kinase. Results: ① The linear relationship between the concentration of VLDL (10 ~ 500 mg / ml) and the optical density (AD) of XTT at different times (r = 0.911, P <0.01 and 0.651 P <0.05, respectively) (2) VLDL can promote the P42 MAPK activity of MCs (r = 0.872, P <0.05) in dose-dependent manner (10 ~ 1000 mg / ml); with the prolongation of VLDL stimulation, P42 The MAPK activity increased but not linearly, with peaks at (118.67 ± 6.43) cpm / (140.50 ± 17.68) cpm and (128 ± 5.66) cpm / k ]; P98059 inhibited the P42 MAPK activity, P42 MAPK activity was significantly reduced; different concentrations and different time VLDL stimulated MCs XTT AD value was significantly reduced. Conclusion: (1) VLDL can promote the proliferation of MCs in a concentration-dependent and dose-dependent manner at a certain concentration (10-500mg / ml), but the apoptosis of MCs can be promoted by high concentration of VLDL. (2) VLDL