麻黄碱调控AMPK/NF-κB信号通路改善大鼠膝骨关节炎的实验研究
Experimental study on ephedrine ameliorates knee osteoarthritis in rats by regulating AMPK/NF-κB signaling pathway
  
DOI:10.3969/j.issn.1006-7108.2023.10.003
中文关键词:  麻黄碱  膝骨关节炎  AMPK/NF-κB信号通路
英文关键词:ephedrine  knee osteoarthritis  AMPK/NF-κB signal pathway
基金项目:河南省中医药科学研究专项课题(2023ZY2097);2021年河南省中医药拔尖人才培养项目资助[豫卫中医函(2021)15号]
作者单位
王俊杰1 郭中华1* 史栋梁1 丁琳琳2 1. 河南省中医院骨病一科河南 郑州 450053 2. 金水区总医院中医科河南 郑州 450008 
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中文摘要:
      目的 探讨麻黄碱(Ephedrine)调控腺苷酸活化蛋白激酶(AMPK)/核转录因子-κB(NF-κB)信号通路对大鼠膝骨关节炎(KOA)的影响。方法 建立KOA大鼠模型,将大鼠分为Sham组、KOA组、Ephedrine组(40.0 mg/kg)、Ephedrine(40.0 mg/kg)+Compound C组(0.2 mg/kg),药物分组干预后,分别检测大鼠膝关节宽度与疼痛阈值,番红O-固绿染色观察软骨组织病理变化并进行Mankin评分,ELISA法检测关节液TNF-α、IL-1β、COX-2水平,免疫组化检测软骨组织IL-1β、MMP-13蛋白表达,Western blot检测AMPK/NF-κB通路相关蛋白水平。结果 与Sham组比较,KOA组软骨组织损伤严重,膝关节宽度、Mankin评分、关节液TNF-α、IL-1β、COX-2水平及软骨组织IL-1β、MMP-13、p-NF-κB p65/NF-κB p65水平显著升高,疼痛阈值及软骨组织p-AMPK/AMPK水平显著降低(P<0.05);与KOA组比较,Ephedrine组软骨组织病理损伤减轻,膝关节宽度、Mankin评分、关节液TNF-α、IL-1β、COX-2水平及软骨组织IL-1β、MMP-13、p-NF-κB p65/NF-κB p65水平显著降低,疼痛阈值及软骨组织p-AMPK/AMPK水平显著升高(P<0.05);与Ephedrine组比较,Ephedrine+ Compound C组大鼠软骨组织损伤加重,膝关节宽度、Mankin评分、关节液TNF-α、IL-1β、COX-2水平及软骨组织IL-1β、MMP-13、p-NF-κB p65/NF-κB p65水平显著升高,疼痛阈值及软骨组织p-AMPK/AMPK水平显著降低(P<0.05)。结论 麻黄碱通过激活AMPK通路抑制NF-κB信号通路,抑制炎症反应,改善KOA大鼠软骨损伤。
英文摘要:
      Objective To investigate the impact of ephedrine on knee osteoarthritis (KOA) in rats by regulating AMPK/NF-κB signaling pathway. Methods KOA rat models were established and grouped into Sham group, KOA group, Ephedrine group (40.0mg/kg), and Ephedrine group (40.0mg/kg)+Compound C group (0.2mg/kg). After drug grouping intervention, the knee joint width and pain threshold of rats were measured respectively,the pathological changes of cartilage tissue were observed with safranine O-solid green staining and Mankin score was performed,the levels of TNF-α, IL-1β and COX-2 in synovial fluid were detected by ELISA,the expression of IL-1β and MMP-13 proteins in cartilage tissue was detected by immunohistochemistry,Western blot was applied to detect the level of AMPK/NF-κB pathway related proteins. Results Compared with Sham group, the cartilage tissue of KOA group was seriously damaged,the knee joint width, Mankin score, levels of TNF-α, IL-1β, COX-2 in joint fluid, and levels of IL-1β, MMP-13, and p-NF-κB p65/NF-κB p65 in cartilage tissue were significantly higher, and the pain threshold and the level of p-AMPK/AMPK in cartilage tissue were significantly lower (P<0.05);compared with KOA group, the pathological damage of cartilage tissue in Ephedrine group was reduced,the knee joint width, Mankin score, levels of TNF-α, IL-1β, COX-2 in joint fluid, and levels of IL-1β, MMP-13, and p-NF-κB p65/NF-κB p65 in cartilage tissue were significantly lower, and the pain threshold and the level of p-AMPK/AMPK in cartilage tissue were significantly higher (P<0.05); compared with the Ephedrine group, the injury of cartilage tissue in the Ephedrine+Compound C group was aggravated,the knee joint width, Mankin score, levels of TNF-α, IL-1β, COX-2 in joint fluid, and levels of IL-1β, MMP-13, and p-NF-κB p65/NF-κB p65 in cartilage tissue were significantly higher, and the pain threshold and the level of p-AMPK/AMPK in cartilage tissue were significantly lower (P<0.05). Conclusion Ephedrine can inhibit NF-κB signal pathway, inhibit inflammatory reaction and improve cartilage injury in KOA rats by activating AMPK pathway.
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