摘要
目的观察阿魏酸对模拟缺血再灌注损伤兔窦房结细胞骨架蛋白F-actin和Vinculin的影响,探讨其保护窦房结细胞的机制。方法取新生乳兔窦房结细胞,以缺氧缺糖模拟缺血,以恢复氧和糖的供应模拟再灌注造成窦房结细胞损伤模型。正常对照组与模型组给予等体积培养基,阿魏酸高、中、低剂量组分别给予相应浓度药物(终浓度分别为100μmol/ml、20μmol/ml、10μmol/ml),运用酶标仪、激光共聚焦显微镜观察各组窦房结细胞活性、细胞骨架蛋白F-actin和Vinculin形态的变化。结果模型组活细胞量较正常对照组明显减少(P<0.01);细胞骨架蛋白F-actin和Vinculin裂解明显。阿魏酸高、中、低剂量组活细胞量明显高于模型组(P<0.01),F-actin和Vinculin结构较模型组明显完整,平均荧光强度明显高于模型组(P<0.01)。结论阿魏酸可抑制模拟缺血再灌注引起的窦房结细胞损伤;阿魏酸保护窦房结细胞的机制可能与保护细胞骨架蛋白F-actin和Vinculin从而维持细胞电生理稳定有关。
Objective To observe the impact of ferulic acid in F- actin and Vinculin of cytoskeleton in the rabbits with damaged atrionector of ischemic reperfusion and explore its protective mechanism on atrionector cells. Methods The atrionector cells of newly born rabbits were collected. The ischemia was simulated with deprivation of oxygen and glucose. The reperfusion was simulated with recovery of oxygen and glucose. The same volume medium was used in the normal control group and the model group. The medicine of corresponding concentrations was used in ferulic acid high dose group,middle dose group and low dose group( the final concentration was 100 μmol/ml,20 μmol/ml or 10 μmol/ml). ELIASA and laser scanning confocal microscope were used to observe the changes of atrionector cell activity and F- actin and Vinculin of cytoskeleton. Results The living cell amount in the model group was reduced apparently as compared with the normal control group( P < 0. 01). F- actin and Vinculin of cytoskeleton were split apparently. The living cell amount in ferulic acid high dose group,middle dose group and low dose group was higher apparently than that in the model group( P < 0. 01). The structure of F- actin and Vinculin was complete apparently as compared with the model group. The mean fluorescence intensity was higher apparently than that in the model group( P< 0. 01). Conclusion Ferulic acid inhibits the damaged atrionector of simulated ischemic reperfusion. The protective mechanism of ferulic acid is possibly related to the protection of F- actin and Vinculin of cytoskeleton so as to maintain the cellular electrophysiological stability.
出处
《世界中西医结合杂志》
2015年第1期110-113,共4页
World Journal of Integrated Traditional and Western Medicine
基金
国家自然科学基金项目(81173447)