摘要
目的研究骨炎消巴布剂对膝关节骨关节炎(KOA)PI3K/AKT信号通路相关蛋白表达水平的影响。方法正常组不作处理,其余组采用膝关节注射碘乙酸钠建立KOA家兔模型,造模成功后随机分为模型组、巴布剂基质组、奇正消痛贴组、骨炎消巴布剂组。模型组不给药,其余组分别给予巴布剂基质、奇正消痛贴、骨炎消巴布剂外敷,连续给药6周。HE染色观察各组家兔膝关节滑膜组织病理变化,免疫组化检测关节滑膜Bcl-2、Bax、Caspase-3的表达,ELISA法检测血清中IL-1β、IL-17、TNF-α水平,RT-PCR及Western blot检测软骨组织中PI3K、AKT、Caspase-3 mRNA表达及蛋白水平。结果与模型组比较,骨炎消巴布剂干预的关节滑膜炎性细胞浸润减少,Bcl-2表达显著上升(P<0.01),Bax、Caspase-3表达显著降低(P<0.01),IL-1β、IL-17、TNF-α显著降低(P<0.01),软骨组织中PI3K、AKTmRNA及蛋白水平显著上升(P<0.01),Caspase-3 mRNA表达及蛋白水平显著降低(P<0.01)。结论骨炎消巴布剂通过激活PI3K/AKT信号通路,抑制炎症因子的分泌,促进Bcl-2的表达,降低Bax、Caspase-3水平,抑制软骨细胞凋亡的发生,保护软骨细胞,进而延缓KOA的病情进展。
Objective To study the effect of Guyanxiao cataplasm on knee osteoarthritis(KOA)effect of PI3K/Akt signal pathway related protein expression.Methods The normal group was not treated,and the other groups were injected with sodium iodoacetate into the knee to establish koa rabbit model.After successful modeling,they were randomly divided into model group,cataplasm matrix group,Qizheng Xiaotong Plaster group and Guyanxiao plaster group.The model group was not treated,and the other groups were treated with cataplasm matrix,Qizheng Xiaotong Plaster and bone Guyanxiao cataplasm was applied externally for 6 weeks.The histopathological changes of rabbit knee synovium were observed by HE staining,the expressions of Bcl-2,Bax and Caspase-3 in synovium were detected by immunohistochemistry,and in serum was detected by ELISA IL-1β、IL-17、TNF-α.Results compared with the model group,the infiltration of synovitis cells decreased,the expression of Bcl-2 increased significantly(P<0.01),the expression of Bax and Caspase-3 decreased significantly(P<0.01),and the expression of IL-1β、IL-17、TNF-αThe levels of PI3K,Akt mRNA and protein in cartilage increased significantly(P<0.01),and the expression of caspase-3 mRNA and protein decreased(P<0.01).Conclusion Guyanxiao cataplasm can inhibit the secretion of inflammatory factors,promote the expression of Bcl-2,reduce the levels of Bax and caspase-3,inhibit the occurrence of chondrocyte apoptosis,protect chondrocytes and delay the progress of KOA by activating PI3K/Akt signal pathway.
作者
李田洋
高小凤
王宝娟
郑曙光
LI Tian-yang;GAO Xiao-feng;WANG Bao-juan;ZHENG Shu-guang(Guizhou University of Traditional Chinese Medicine,Guiyang,Guizhou 550025,China;First Affiliated Hospital of Guizhou University of Traditional Chinese Medicine,Guiyang Guizhou 550002,China)
出处
《时珍国医国药》
CAS
CSCD
北大核心
2022年第10期2330-2334,共5页
Lishizhen Medicine and Materia Medica Research
基金
国家自然科学基金(81960914)。
