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目的探讨果糖制备的糖基化终末产物(AGEs)对大鼠脑基底动脉血管平滑肌细胞(BASMC)的增殖以及氯沙坦对增殖的影响和机制。方法培养大鼠脑基底动脉血管平滑肌细胞,用CCK8法测定不同浓度(1,5,10μmol/L)氯沙坦对果糖制备的AGEs(200mg/L)预处理48h诱导血管平滑肌细胞增殖的影响。用western blotting检测AGEs以及氯沙坦处理后对ERK蛋白表达影响。结果 AGEs刺激血管平滑肌细胞增殖(0.827±0.069比0.364±0.052,P<0.01)。给予氯沙坦(5,10μmol/L)后,细胞增殖明显下降(0.658±0.064和0.381±0.058比0.827±0.069,P<0.01)。AGEs还使平滑肌细胞内活性氧簇(ROS)生成增多,并显著增加ERK1/2蛋白表达,氯沙坦则明显抑制ROS和ERK1/2蛋白水平。结论果糖制备的AGEs诱导脑基底动脉血管平滑肌细胞增殖,氯沙坦可能通过阻断AT1受体而抑制ROS和ERK1/2表达,减少平滑肌细胞的异常增殖。
Objective To investigate the effects of glycosylation end products (AGEs) produced by fructose on the proliferation of rat basilar artery vascular smooth muscle cells (BASMC) and the effects of losartan on proliferation. Methods The basilar artery smooth muscle cells of rat were cultured and the effects of losartan at different concentrations (1,5 and 10 μmol / L) on the proliferation of vascular smooth muscle cells induced by fructose (AGEs) (200 mg / L) for 48 h were determined by CCK8 assay. The effects of AGEs and losartan on ERK protein expression were detected by western blotting. Results AGEs stimulated the proliferation of vascular smooth muscle cells (0.827 ± 0.069 vs 0.364 ± 0.052, P <0.01). Cell proliferation was significantly decreased after losartan (5 and 10 μmol / L) administration (0.658 ± 0.064 vs 0.381 ± 0.058 vs. 0.827 ± 0.069, P <0.01). AGEs also increased the production of reactive oxygen species (ROS) in smooth muscle cells and significantly increased the expression of ERK1 / 2. Losartan significantly inhibited the expression of ROS and ERK1 / 2. CONCLUSION: AGEs derived from fructose can induce the proliferation of vascular smooth muscle cells in basilar artery. Losartan may inhibit the expression of ROS and ERK1 / 2 and block the abnormal proliferation of smooth muscle cells by blocking AT1 receptor.