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活络效灵丹对大鼠膝骨关节炎的修复作用及机制 被引量:3

Repair effect and mechanism of Huo-Luo-Xiao-Ling Dan on knee osteoarthritis in rats
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摘要 目的 探究活络效灵丹对大鼠膝骨关节炎的治疗作用及可能机制。方法 SD大鼠30只随机分成对照组(Control组)、模型组(KOA组)和活络效灵丹组(HLXL组),每组10只。HE染色观察软骨组织形态学变化;TUNEL法检测软骨组织细胞凋亡;免疫荧光检测软骨组织骨重塑介质表达;ELISA法检测关节液炎症因子水平;Western blot检测PI3K/AKT信号通路蛋白表达。结果 活络效灵丹能改善软骨组织形态;降低软骨组织细胞凋亡水平;降低RANKL表达;增加OPG表达;抑制关节液炎症因子TNF-α、IL-1β、IL-6和IL-18水平;激活PI3K/AKT信号通路。结论 活络效灵丹能改善大鼠膝骨关节炎,其机制可能与激活PI3K/AKT信号通路有关。 Objective To explore the therapeutic effect and possible mechanism of Huo-Luo-Xiao-Ling Dan on knee osteoarthritis in rats. Methods Thirty SD rats were randomly divided into control group, model group(KOA group)and Huo-Luo-Xiao-Ling Dan group(HLXL group), with 10 rats in each group. The histological changes of cartilage were detected by HE staining. Apoptosis of chondrocytes was detected by TUNEL assay. Immunofluorescence was used to detect the expression of bone remodeling mediators in cartilage. The levels of inflammatory factors in the joint fluid were detected by ELISA. The expression of PI3K/Akt signaling pathway related protein were detected by Western blot. Results HuoLuo-Xiao-Ling Dan improved the morphology of cartilage tissue, decreased the apoptosis level of cartilage tissue cells,decreased the expression of RANKL, increased the expression of OPG, inhibited the levels of TNF-α, IL-1β, IL-6 and IL-18 in the articular fluid, and activated the PI3K/Akt signaling pathway. Conclusion Huo-Luo-Xiao-Ling Dan can improve knee osteoarthritis in rats, and the mechanism may be related to PI3K/Akt signaling pathway.
作者 张奇先 丁爽 吴前 ZHANG Qi-xian;DING Shuang;WU Qian(Department of Orthopedics,Second Affiliated Hospital of Liaoning University of Traditional Chinese Medicine,Shenyang 110034;Department of Orthopedics,Affiliated Hospital of Liaoning University of Traditional Chinese Medicine,Shenyang 110033,China)
出处 《解剖科学进展》 CAS 2022年第3期319-322,共4页 Progress of Anatomical Sciences
基金 辽宁省自然科学基金(20180550528)。
关键词 活络效灵丹 膝骨关节炎 炎症因子 磷脂酰肌醇-3-激酶 蛋白激酶B Huo-Luo-Xiao-Ling Dan Knee osteoarthritis Inflammatory cytokines PI3K AKT
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