摘要
目的:研究吲哚-2,3-二酮对肿瘤坏死因子α(TNF-α)所致大鼠主动脉平滑肌A7r5细胞增殖的影响。方法:取指数生长期A7r5细胞,分为空白对照(20%高糖改良马丁琼脂培养基)组、模型(TNF-α5 ng/ml)组和10-8、10-7、10-6、10-5mg/ml吲哚-2,3-二酮(相应质量浓度的吲哚-2,3-二酮+TNF-α5 ng/ml)组,采用MTT法检测各组A7r5细胞的光密度以评价其增殖作用,采用流式细胞术碘化丙啶染色法检测各组细胞的增殖周期变化。结果:与空白对照组比较,模型组细胞的光密度明显增加,S期与G2/M期细胞明显增加,G0/G1期细胞明显减少,差异具有统计学意义(P<0.05)。与模型组比较,10-7、10-6、10-5mg/ml吲哚-2,3-二酮组细胞的光密度明显减小,10-8mg/ml吲哚-2,3-二酮组G2/M期细胞明显减少,10-7、10-6mg/ml吲哚-2,3-二酮组S期细胞均明显减少,差异具有统计学意义(P<0.01或P<0.05),其余差异无统计学意义(P>0.05)。结论:吲哚-2,3-二酮对TNF-α所致的平滑肌细胞增殖具有抑制作用。
OBJECTIVE: The investigate the effects of indol-2, 3-dione on the proliferation of rat thoracic aortic vascular smooth muscle A7r5 cells induced by TNF-α. METHODS: A7r5 cells at exponential phase were collected and divided into blank control group (20% DMEM medium), model group (TNF-α 5 ng/ml) and 10^-8, 10^-7, 10^-6, 10^-5 mg/ml indol-2, 3-dione groups (relevant concentration of indol-2, 3-dione+TNF-α 5 ng/ml). The optical density of A7r5 cells was detected by MTT method to evaluate proliferation effects, and the cell cycle of A7r5 cells proliferation was monitored by flow cytometry propidium iodide stain- ing. RESULTS: Compared with blank control group, optical density of A7r5 cells was increased significantly in model group; the proportion of A7r5 cells at S phase and G2/M phase increased significantly, and that of A7r5 cells at G0/G1 phase decreased signifi- cantly; there was statistical significance (P〈0.05). Compared with model group, optical density of A7r5 cells in 10 7, 10^-6 and 10^-5 mg/ml indol-2, 3-dione groups decreased significantly; the proportion of A7r5 cells at G2/M phase decreased significantly in 10^-8 mg/ml indol-2, 3-dione group, and that of A7r5 cells at S phase decreased significantly in 10^-7 and 10^-6 mg/ml indol-2, 3-di- one groups; there was statistical significance (P〈0.01 or P〈0.05). Other difference had no statistical significance (P〉0.05). CONCLUSIONS: Indol-2, 3-dione can inhibit the proliferation of A7r5 cells induced by TNF-α.
出处
《中国药房》
CAS
北大核心
2015年第4期467-469,共3页
China Pharmacy
基金
山东省自然科学基金资助项目(No.ZR2010HM129)