miR-138调控TrkA-TRPV1信号通路对KOA模型大鼠软骨损伤的影响  

Effect of miR-138 regulation of TrkA-TRPV1 signaling pathway on cartilage damage in KOA model rats

作　　者：杨砥 徐远坤 Yang Di;Xu Yuankun(Dept of Orthopedics and Traumatology, The First Affiliated Hospital of Guizhou University of Traditional Chinese Medicine, Guiyang 550002)

机构地区：[1]贵州中医药大学第一附属医院骨伤科,贵阳550002

出　　处：《安徽医科大学学报》2022年第5期786-790,共5页Acta Universitatis Medicinalis Anhui

基　　金：国家自然科学基金(编号:81860855);贵州卫生健康委科学技术基金(编号:gzwjkj2020-1-123)。

摘　　要：目的探究miR-138调控TrkA-TRPV1信号通路对膝骨性关节炎(KOA)模型大鼠软骨损伤的影响。方法选取40只健康SD大鼠,随机分为正常组、模型组、沉默组、过表达组,分别进行干预。对比各组大鼠行为学、软骨组织学评分,检测关节液中炎性因子[肿瘤坏死因子-α(TNF-α)、白介素(IL)-1、IL-6]及软骨组织中骨代谢标志物[基质金属蛋白酶(MMP-13)、Ⅱ型胶原(ColⅡ)]、TrkA、TRPV1、miR-138表达水平,分析miR-138对KOA大鼠软骨损伤的影响。结果与正常组相比,模型组、沉默组、过表达组大鼠行为学、软骨组织学评分升高(P<0.05);与过表达组相比,模型组、沉默组大鼠行为学、软骨组织学评分升高(P<0.05)。与正常组相比,模型组、沉默组、过表达组大鼠TNF-α、IL-1、IL-6水平及MMP-13、TrkA、TRPV1表达升高,ColⅡ、miR-138表达降低(P<0.05);与过表达组相比,模型组、沉默组大鼠TNF-α、IL-1、IL-6水平及MMP-13、TrkA、TRPV1表达升高,ColⅡ、miR-138表达降低(P<0.05)。结论miR-138可缓解KOA模型大鼠软骨损伤,其机制或与TrkA-TRPV1信号通路的抑制相关。Objective To analyze the effect of miR-138 regulating TrkA-TRPV1 signaling pathway on cartilage damage in knee osteoarthritis(KOA)model rats.Methods Forty healthy SD rats were selected and divided into normal group,model group,silent group and overexpression group with 10 rats in each.Behavioral and cartilage histological scores of rats in each group were compared.The expression levels of inflammatory factors[TUMOR necrosis factor-α(TNF-α),interleukin(IL)-1,IL-6]in articular fluid and bone metabolism markers[matrix metalloproteinase(MMP-13),typeⅡcollagen(ColⅡ)],TrkA,TRPV1 and Mir-138 in cartilage tissue were detected.The effect of Mir-138 on cartilage injury in KOA rats was analyzed.Results Compared with normal group,behavioral and cartilage histological scores of model group,silent group and overexpression group increased(P<0.05).Compared with overexpression group,behavioral and cartilage histological scores of model group and silent group increased(P<0.05).Compared with normal group,the levels of TNF-α,IL-1 and IL-6 and the expressions of MMP-13,TrkA and TRPV1 increased in model group,silent group and overexpression group,while the expressions of Col II and Mir-138 decreased(P<0.05).Compared with overexpression group,the levels of TNF-α,IL-1 and IL-6 and the expressions of MMP-13,TrkA and TRPV1 increased in model group and silent group,while the expressions of Col II and Mir-138 decreased(P<0.05).Conclusion miR-138 can alleviate cartilage injury in KOA model rats,and its mechanism may be related to the inhibition of TrkA-TRPV1 signaling pathway.

关 键 词：酪氨酸激酶A-顺势感受器电位香草受体1信号通路 miR-138 膝骨关节炎 软骨损伤 

分 类 号：R36[医药卫生—病理学]