基于NF-κB/NLRP3信号轴探讨大血藤对CIA大鼠的治疗作用及机制

Research on the Therapeutic Mechanism of Sargentgloryvine Stem on CIA Rats Based on NF-κB/NLRP3 Pathway

  • 摘要: 目的  考察大血藤对胶原诱导型关节炎(CIA)大鼠的症状改善作用和机制。 方法   建立大鼠CIA模型,持续观察大鼠体质量、关节肿胀度、关节炎指数,ELISA检测血清TNF-α、IL-1β、IL-6、IL-18水平;Western blot法检测大鼠关节滑膜RANKL、p-IκB-α、NF-κB/p65、p-NF-κB/p65、NLRP3、Caspase-1表达。 结果   模型组大鼠自第2周出现体质量增长的趋势明显减缓(P < 0.01),而关节炎指数和关节肿胀度均显著增加(P < 0.05),大鼠关节有红肿进而不能负重状态,而大血藤能显著改善CIA大鼠相关症状,表现为降低足肿胀、关节炎指数评分以及改善体质量数据。与正常组比较,模型组大鼠血清TNF-α、IL-1β、IL-6、IL-18水平以及关节滑膜RANKL、p-IκB-α、NF-κB/p65、p-NF-κB/p65、NLRP3、Caspase-1表达显著升高(P < 0.01), 而大血藤中、高剂量组上述指标较模型组显著降低(P < 0.05, P < 0.01)。 结论   大血藤能改善CIA大鼠的炎症反应,延缓病理进展,其机制可能与降低促炎因子的释放及抑制NF-κB/NLRP3信号通路有关。

     

    Abstract: OBJECTIVE   To investigate the symptom improvement and mechanism of sargentgloryvine stem on collagen-induced arthritis (CIA) in rats. METHODS  The CIA model in rats was established, and the body weight, joint swelling degree and arthritis index were observed continuously. The levels of TNF-α, IL-1β, IL-6 and IL-18 in serum were detected by ELISA. The expressions of RANKL, p-IκB-α, NF-κB/p65, p-NF-κB/p65, NLRP3 and Caspase-1 in synovial joint of rats were detected by Western blot. RESULTS  The weight growth of rats in the model group slowed down significantly from the second week, while the arthritis index and joint swelling degree increased significantly. The joints of rats were red and swollen and could not bear weight, while sargentgloryvine stem could significantly improve the related symptoms of CIA rats, such as reducing foot swelling, arthritis index score and improving body weight data. The levels of TNF-α, IL-1β, IL-6 and IL-18 in serum and the expressions of RANKL, p-IκB-α, NF-κB/p65, NF-κB/p65, NLRP3 and Caspase-1 in synovial joint of model group were significantly higher than those in normal group (P < 0.01), while the above indexes in sargentgloryvine stem middle and high dose groups were significantly lower than those in model group (P < 0.05, P < 0.01). CONCLUSION  Sargentgloryvine stem can improve the inflammatory response and delay the pathological progress of CIA rats, and the mechanism may be related to the reduction of pro-inflammatory cytokines release and the inhibition of NF-κB/NLRP3 signal pathway.

     

/

返回文章
返回