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目的:研究人参果提取物对过氧化氢(H2O2)诱导人脐静脉内皮细胞(ECV304细胞)损伤的保护作用。方法:体外培养的ECV304细胞随机均分为正常对照(常规培养液)组、模型(常规培养液)组与人参果提取物1、2、3、4(10、20、40、80μg/ml)组,给予相应药物培养ECV304细胞24 h后,用H2O2(0.3 mmol/L)培养ECV304细胞4 h以复制细胞氧化损伤模型;采用MTT法检测细胞活力以筛选最适质量浓度。体外培养的ECV304细胞随机均分为正常对照(常规培养液)组、模型(常规培养液)组与人参果提取物(80μg/ml)组,给予相应药物培养ECV304细胞24 h后同上复制细胞氧化损伤模型。采用HE染色观察细胞形态;采用流式细胞仪测定细胞周期;检测丙二醛(MDA)含量和乳酸脱氢酶(LDH)、超氧化物歧化酶(SOD)活性。结果:人参果提取物最适给药质量浓度为80μg/ml。与正常对照组比较,模型组细胞部分皱缩,边缘模糊,细胞有融合现象;细胞活力减弱;G1期细胞比例升高,S期和G2期细胞比例降低;SOD活性减弱,MDA含量增加,LDH活性增强,差异有统计学意义(P<0.01)。与模型组比较,人参果提取物组细胞损伤程度减轻;G1期细胞进入S期和G2期的细胞比例升高,G1期细胞比例降低,S期细胞比例升高;SOD活性增强,MDA含量减少,LDH活性减弱,差异有统计学意义(P<0.01)。结论:人参果提取物对H2O2损伤的ECV304细胞具有保护作用,其机制可能与加快细胞周期进程、抗氧化作用有关。
Objective: To study the protective effect of extract from ginseng fruit on the injury of human umbilical vein endothelial cells (ECV304) induced by hydrogen peroxide (H2O2). Methods: ECV304 cells cultured in vitro were randomly divided into normal control (conventional culture) group, model (conventional culture) group and ginseng fruit extract 1,2,3,4 (10,20,40,80μg / ml) group After ECV304 cells were cultured for 24 h, the ECV304 cells were cultured with H2O2 (0.3 mmol / L) for 4 h to replicate the cell model of oxidative damage. Cell viability was measured by MTT assay to select the optimal concentration. ECV304 cells cultured in vitro were randomly divided into normal control group (conventional culture) group, model (conventional culture medium) group and ginseng fruit extract (80μg / ml) group, ECV304 cells were cultured with corresponding drugs for 24 h, model. Cell morphology was observed by HE staining. Cell cycle was measured by flow cytometry. Malondialdehyde (MDA) content, lactate dehydrogenase (LDH) and superoxide dismutase (SOD) activity were measured. Results: The optimum concentration of ginseng fruit extract was 80μg / ml. Compared with the normal control group, the cells in the model group were partially shrunk, the edges were fuzzy and the cells had the phenomenon of confluence; the cell viability was weakened; the proportion of cells in G1 phase was increased; the proportion of cells in S and G2 phases was decreased; the activity of SOD was decreased; the content of MDA Activity increased, the difference was statistically significant (P <0.01). Compared with the model group, the degree of cell damage in the ginseng fruit extract group was alleviated; the proportion of cells entering the S phase and the G2 phase in G1 phase increased, the proportion of cells in the G1 phase decreased, the proportion of the S phase cells increased, the activity of SOD increased, the MDA content decreased, LDH activity decreased, the difference was statistically significant (P <0.01). CONCLUSION: Ginseng fruit extract has a protective effect on ECV304 cells injured by H2O2. Its mechanism may be related to accelerating cell cycle progression and antioxidation.