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目的:探讨冠心舒通胶囊含药血清对晚期糖基化终产物(AGEs)诱导血管平滑肌细胞(VSMCs)增殖的影响及其可能机制。方法:分别以0.5g/kg、1g/kg、2g/kg剂量冠心舒通胶囊内容物对大鼠灌胃给药28d制备冠心舒通胶囊含药血清;以各剂量含药血清单独或联合体外制备的AGE-牛血清白蛋白(AGE-BSA)处理原代培养大鼠VSMCs,MTT法检测各处理组细胞增殖水平、RT-PCR检测细胞血小板源性生长因子-B(PDGF-B)mRNA表达水平、酶联免疫吸附法(ELISA)检测培养上清PDGF-B浓度。结果:40mg/L终浓度AGE-BSA显著增强VSMCs增殖水平(P<0.05),0.5g/kg、1g/kg、2g/kg剂量冠心舒通胶囊含药血清对正常VSMCs生长未见显著影响(P>0.05),但显著抑制AGE-BSA诱导的VSMCs增殖(P<0.05),作用具有明显的剂量依赖性。AGE-BSA诱导VSMCs PDGF-B表达与分泌显著增强(P<0.05),1g/kg、2g/kg剂量冠心舒通胶囊含药血清可有效抑制AGE-BSA这一作用(P<0.05),0.5g/kg剂量血清对AGE-BSA这一作用则未见明显影响(P>0.05)。结论:冠心舒通胶囊可剂量依赖性抑制AGEs诱导的VSMCs增殖,作用机制与抑制AGE诱导的PDGF-B表达与分泌有关。
Objective: To investigate the effect of Guanxin Shutong capsule containing serum on the proliferation of vascular smooth muscle cells (VSMCs) induced by advanced glycation end products (AGEs) and its possible mechanism. Methods: The contents of Guanxin Shutong capsule were given intragastrically to rats at doses of 0.5g / kg, 1g / kg and 2g / kg for 28 days to prepare the serum containing Guanxintushutong capsule. Primary cultured rat VSMCs were treated with AGE-BSA (AGE-BSA) in vitro. The proliferation of VSMCs was detected by MTT assay. The expression of platelet-derived growth factor-B (PDGF- mRNA expression level, and the concentration of PDGF-B in culture supernatant was detected by enzyme-linked immunosorbent assay (ELISA). Results: AGE-BSA at a final concentration of 40 mg / L significantly enhanced the proliferation of VSMCs (P <0.05). No significant effect of the serum containing Guanxin Shutong Capsule at 0.5g / kg, 1g / kg and 2g / kg on the growth of normal VSMCs was observed (P> 0.05), but significantly inhibited AGE-BSA-induced proliferation of VSMCs (P <0.05). The effect was dose-dependent. The effect of AGE-BSA on the expression and secretion of PDGF-B in VSMCs was significantly enhanced (P <0.05). The effect of AGE-BSA at 1g / kg and 2g / Serum of 0.5g / kg AGE-BSA serum had no significant effect (P> 0.05). CONCLUSION: Guanxinshutong capsule can inhibit AGEs-induced proliferation of VSMCs in a dose-dependent manner. The mechanism is related to inhibition of AGE-induced PDGF-B expression and secretion.