摘要
目的:研究升清降糖合剂(SQ)对氧化损伤胰岛β细胞凋亡的保护作用,探讨其对凋亡蛋白Bcl-2和Bax、Akt蛋白表达的影响。方法:H2O2诱导胰岛细胞氧化损伤模型,流式细胞术测定胰岛细胞凋亡率,以荧光免疫法检测细胞凋亡蛋白Bcl-2和Bax的表达,免疫印迹测定细胞Akt磷酸化表达。结果:模型组细胞凋亡率增高,达(35.18±2.41)%,与正常组比较有差异(P<0.01),与SQ保护组比较有差异(P<0.01)。模型组细胞内Bax荧光表达较正常组增加(P<0.05);SQ保护组Bcl-2荧光表达上升,Bax荧光表达下降,与模型组比较,均有统计学差异(P<0.05)。对于胰岛细胞瘤株RINm5F,模型组磷酸化Akt蛋白表达减少,与正常组比较有统计学差异(P<0.05),与保护组比较有统计学差异(P<0.01);对于原代胰岛,模型组磷酸化Akt蛋白减少,与正常组比较有统计学差异(P<0.05),与保护组比较有统计学差异(P<0.05)。结论:升清降糖合剂可降低氧化损伤胰岛β细胞凋亡率,上调Bcl-2,抑制Bax蛋白表达,促进Akt磷酸化。升降糖合剂抗氧化和抗凋亡机制与调节凋亡蛋白Bcl-2和Bax及PI3K-Akt通路有关。
It is a study on protective mechanism of Shengqing Jiangtang decoction （SQ） on pancreatic beta - cells with oxidative damage. We made the oxidative damage of beta - cells by H2O2 and interfered with SQ, we assayed the cell apotosis rate, the expression levels of Bcl -2, Bax and phosphorylated Akt （pAkt） by flow cytometry, fluroimmuno - assay and Western Blot method, respectively. We found the apotosis rate of model group （35.18 ± 2.41 ）% had statistical defference compared with protection group （19.56 ± 1.08 ）% ,P 〈 0. 01. Bcl -2 expression increased and Bax expression decreased in protection group, which had a difference compared with model group（ P 〈 0.05 ） , respectively. We found pAkt protein expressed in both RINmSF and primary rat pancreatic islets. In each object, expression of pAkt declined in model group, which had a statistical difference compared with negative group; pAkt increased in protection group, which had a statistical difference compared with model group, respectively.
出处
《中华中医药学刊》
CAS
2011年第12期2692-2694,I0022,共4页
Chinese Archives of Traditional Chinese Medicine
基金
浙江省中医药科研基金资助项目(2008CA074)
