摘要
目的:研究骨关节炎(OA)大鼠模型软骨组织中脂酰肌醇3激酶(phosphatidylinositol 3kinase,PI3K)/蛋白激酶B(protein kinase B,Akt)信号通路功能与细胞凋亡的相关性。方法:选择清洁级雄性Wistar大鼠作为实验动物,并随机分为OA模型组和对照组;采用木瓜蛋白酶溶液与L-半胱氨酸关节腔内注射的方式建立OA模型。造模后第4周和第8周时,测定关节软骨中PI3K/AKT信号分子、炎症介质、细胞凋亡标志分子、细胞自噬标志分子的表达量。结果:OA组大鼠关节软骨组织中p-PI3K、pAKT的表达量显著低于对照组;OA组大鼠关节软骨组织中白介素(IL)-1β、IL-6、IL-17、IL-18、eIF4E、Bax、Caspase-3、mTOR、Beclin1、Atg5、Atg7的表达量显著高于对照组,且与p-PI3K、p-AKT的表达量呈负相关,Bcl-2的表达量显著低于对照组且与p-PI3K、p-AKT的表达量呈正相关。结论:骨关节炎大鼠模型软骨组织中PI3K/AKT信号通路功能的抑制能够促进软骨细胞的凋亡和自噬。
Objective：To study the relationship between PI3K/AKT signaling pathway and apoptosis in cartilage tissue of rats with osteoarthritis（OA）.Methods：The clean male Wistar rats were selected as experimental animals and randomly divided into OA model group and control group.The OA model was established by intra-articular injection of papain solution and L-cysteine.Fourth weeks and eighth weeks after model establishment,the expression of PI3K/AKT signaling molecules,inflammatory mediators,apoptosis marker molecules and autophagy marker molecules in articular cartilage were determined.Results：p-PI3 Kand p-AKT expression in articular cartilage of OA group were significantly lower than those of control group;IL-1β,IL-6,IL-17,IL-18,eIF4 E,Bax,Caspase-3,mTOR,Beclin1,Atg5 and Atg7expression in articular cartilage of OA group were significantly higher than those of control group and negatively correlated with p-PI3 Kand p-AKT expression while Bcl-2expression in articular cartilage of OA group was significantly lower than that of control group and positively correlated with p-PI3 Kand p-AKT expression.Conclusions：The inhibition of PI3K/AKT signaling pathway in cartilage tissue of OA rat model can promote chondrocyte apoptosis and autophagy.
出处
《海南医学院学报》
CAS
2017年第11期1452-1455,共4页
Journal of Hainan Medical University
基金
陕西省自然科学基础研究计划项目(2016JQ8055)~~
