MicroRNA-25对大鼠骨关节炎软骨细胞增殖和凋亡调节作用

摘要

To investigate miR-25 affects the cellular proliferation and apoptosis of osteoarthritis (OA) chondrocytes, osteoarthritis model of Male Sprague-Dawley rats (SD rats) was induced by injection of Papain and isolation of primary SD rat chondrocytes of OA.OA Chondrocytes were stimulated with interleukin-1β (IL-1β) 24 h in vitro.OA chondrocytes were transfected with miR-25 mimic and inhibitor, respectively.Cellular proliferation and apoptosis of OA chondrocytes were tested through the Annexin V-FITC/PI and CCK-8.Overexpression of miR-25 significantly suppressed apoptosis and downexpression of miR-25 promoted apoptosis of OA osteoarthritis.Meanwhile, overexpression of miR-25 induced cellular proliferation and downexpression of miR-25 inhibited proliferation of OA chondrocytes.miR-25, inhibited apoptosis and promoted proliferation of OA chondrocytes, had a significantly protective effect on pathogenesis of OA and may have a brand-new view of pathophysiological process of OA and provide potential therapeutic strategy in OA.%探讨miR-25对白细胞介素1β(IL-1β)促进OA软骨细胞凋亡和增殖的影响.以木瓜蛋白酶膝关节腔注射诱导骨性关节炎动物模型和SD大鼠骨性关节炎软骨细胞原代培养.IL-1β体外刺激OA软骨细胞,模拟骨性关节炎体外环境.MiR-25 mimic或inhibitor转染至OA软骨细胞.利用AnnexinV-FITC/PI和CCK-8法检测软骨细胞细胞凋亡和细胞增殖.miR-25过表达明显抑制软骨细胞凋亡而miR-25低表达促进软骨细胞凋亡(P<0.05);miR-25 mimic促进软骨细胞增殖,而miR-25 inhibitor 抑制软骨细胞增殖(P>0.05).miR-25介导OA发病发生,进展中发挥着保护性调节作用,抑制OA软骨细胞凋亡和促进其增殖作用,可能对OA发病机制有新的认识和提示OA新治疗策略.