Liu Jun, He Xiaole, Zhen Ping, Zhou Shenghu, Li Xusheng
Department of Orthopaedics Center, Lanzhou General Hospital of PLA, Lanzhou 730050, China.
Department of Gerontology, Xijing Hospital, the Fourth Military Medical University, Xi'an 710032, China.
Zhejiang Da Xue Xue Bao Yi Xue Ban. 2016 May 25;45(5):453-460. doi: 10.3785/j.issn.1008-9292.2016.09.02.
To investigate the effect of diosgenin (Dgn) on chondrocytes and its relation to JAK2/STAT3 signaling pathway in mice with osteoarthritis (OA). Fifteen male C57BL/6 mice were randomly divided into three groups:control group, OA group and OA+Dgn group. After 4 weeks of treatment, the histopathological changes of cartilage tissue were observed by toluidine blue staining under light microscopy and the ultrastructure of chondrocytes was observed under electron microscopy. The primarily cultured chondrocytes of OA mice were randomly divided into 4 groups:(1) OA group, (2) Dgn group, (3) Dgn+AG490 group, (4) AG490 group. The expression of p-JAK2, p-STAT3, Bax, succinate dehydrogenase (SDH) and cytochrome c oxidase (COX) were detected by Western blotting, and superoxide dismutase (SOD) was detected using colorimetric method. The morphological observation showed that the chondrocytes of OA group presented considerable pathological changes, while the chondrocytes in OA+Dgn group maintained intact membrane. Electron microscopy observation found obvious injury in cartilage tissues of OA group, while that in OA+Dgn group remained smooth. Compared with OA group, the expressions of p-JAK2 and p-STAT3 in chondrocytes of Dgn group were increased (all <0.05), and the expressions of Bax protein, SDH, COX and SOD were decreased (all <0.05). While compared with Dgn group, the expressions of p-JAK2, p-STAT3, SDH, COX and SOD in chondrocytes of Dgn+AG490 group were decreased (all <0.05), and the expression of Bax protein was increased (<0.05). Diosgenin can inhibit apoptosis and increase mitochondrial oxidative stress capacity of chondrocytes in mice with osteoarthritis, which is closely related to the activation of JAK2/STAT3 signaling pathway.
探讨薯蓣皂苷元（Dgn）对骨关节炎（OA）小鼠软骨细胞的影响及其与JAK2/STAT3信号通路的关系。将15只雄性C57BL/6小鼠随机分为三组：对照组、OA组和OA+Dgn组。治疗4周后，光镜下用甲苯胺蓝染色观察软骨组织的组织病理学变化，电镜下观察软骨细胞的超微结构。将OA小鼠原代培养的软骨细胞随机分为4组：（1）OA组，（2）Dgn组，（3）Dgn+AG490组，（4）AG490组。采用蛋白质免疫印迹法检测p-JAK2、p-STAT3、Bax、琥珀酸脱氢酶（SDH）和细胞色素c氧化酶（COX）的表达，采用比色法检测超氧化物歧化酶（SOD）。形态学观察显示，OA组软骨细胞呈现明显的病理变化，而OA+Dgn组软骨细胞膜保持完整。电镜观察发现OA组软骨组织有明显损伤，而OA+Dgn组软骨组织表面仍光滑。与OA组比较，Dgn组软骨细胞中p-JAK2和p-STAT3的表达升高（均P<0.05），Bax蛋白及SDH、COX、SOD的表达降低（均P<0.05）。与Dgn组比较，Dgn+AG490组软骨细胞中p-JAK2、p-STAT3、SDH、COX及SOD的表达降低（均P<0.05），Bax蛋白表达升高（P<0.05）。薯蓣皂苷元可抑制骨关节炎小鼠软骨细胞凋亡并提高其线粒体氧化应激能力，这与JAK2/STAT3信号通路的激活密切相关。
