摘要
目的:探索甜茶素对棕榈酸诱导INS-1细胞损伤的保护机制。方法:MTT法检测正常对照组、棕榈酸模型组、不同浓度甜茶素组细胞存活率,透射电镜观察各组细胞超微结构,免疫电镜观察各组细胞色素C的易位表达。结果:不同浓度甜茶素对棕榈酸诱导的INS-1细胞具有保护作用,超微结构保存较好;模型组细胞凋亡增多且超微结构损伤严重,Cyt C蛋白从线粒体释放入细胞质。结论:甜茶素可以提高棕榈酸诱导INS-1损伤的细胞存活率,抑制细胞凋亡的发生,其机制可能与抑制棕榈酸引起的氧化应激和阻碍Cyt C从线粒体转位入细胞质,激活细胞凋亡蛋白酶级联反应有关。
ObjectiveTo investigate the protective mechanism of Rubusoside treating on the palmitic acid - induced INS - 1 cells. Methods MTI" assay was used to detect the cell viability rate of control group, palmitic acid group and different concentrations of Rubusoside group. Transmission electron microscope (TEM) was used to observe the uhrastructur of every group and the immune electron microscopy was used to detect cytochrome C translocationexpression. Results As evidenced by M33" assay, the cell viabihty signifi- cantly was enhanced by different concentrations Rubusoside pretreatment. TEM revealed degenerative changes in the ultramicroscopic structure of palmitic acid - induced INS - 1 cells whereas various concentrationpretreatment with Rubusoside could significantly attenuated the deterioration of the damage. Immune electron microscopy showed that different concentrations Rubusoside could prevent the cy- tochrome C releasing from mitochondria to cytoplasm with palmitic acid induced. Conclusion Rubusoside can improve the survival rate of palmitic acid - induced INS - 1 cells and inhibit the occurrence of apoptosis. It is suggested that the mechanism may be associated with the inhibition of the oxidative stress induced by palmitic acid and prevent the cytochrome C releasing from mitochondrial to cytoplasm, which can activate caspase cascade and a downstream signaling to apopotosis.
出处
《中国民族民间医药》
2015年第24期16-18,26,共4页
Chinese Journal of Ethnomedicine and Ethnopharmacy
基金
广西自然科学基金(2012GXNSFBA053108)
广西医科大学"未来学术之星"大学生课外创新科研课题(WLXSZX16022)
广西医科大学青年基金(GXMUYSF18)