摘要
目的:观察新痹痛灵对胶原诱导性关节炎大鼠及其滑膜组织中HMGB1 mRNA的影响。方法:新痹痛灵方中饮片经相关工艺提取后制为浸膏;将SD大鼠72只随机分出12只为正常组,其余进行胶原诱导性关节炎(CIA)造模,再将造模大鼠随机分为模型组,新痹痛灵高、中、低剂量组(3.2,1.6,0.8 g·kg-1·d-1)以及雷公藤多苷片组(0.008 g·kg-1·d-1),各组大鼠于二次免疫后当天开始ig给药,连续给药21 d。容积法测量大鼠关节体积,病理切片观察,RT-q PCR检测滑膜组织HMGB1mRNA的表达。结果:与正常组比较,模型组大鼠关节肿胀明显(P<0.01),滑膜组织HMGB1 mRNA的表达明显增加(P<0.01);与模型组比较,新痹痛灵高剂量组的关节肿胀于14,21 d明显减轻(P<0.05,P<0.01),且滑膜组织HMGB1 mRNA的表达明显降低(P<0.01)。关节病理切片显示新痹痛灵各剂量组及雷公藤多苷片组病变较模型组均有不同程度减轻。结论:新痹痛灵可减轻CIA大鼠关节肿胀、降低滑膜组织中HMGB1 mRNA的表达,通过抑制HMGB1而减少相关炎症通路的激活可能是新痹痛灵治疗类风湿关节炎的机制之一。
Objective： To observe the effect of New Bitongling （NBTL） on collagen-induced arthritis （CIA） rats and to investigate its influence on the expression of high mobility group box 1 （HMGB1） mRNA in the synovial tissues. Method： NBTL extractum was made by a series of processing technology. 12 of 72 SD rats were assigned to the normal group. The CIA models were induced in other rats, then they were divided into the model group, the low-, moderate-, high-dose NBTL groups （3.2, 1.6, 0. 8 g·kg^-1·d^-1 ） and tripterygium wilfordii Hook F （twHF） group （0. 008 g ·kg^-1·d^-1）. All rats received the corresponding drugs at the day of secondary immune and continuously dosed for 21 days by intragastric administration. The joint volumes were measured, the pathological tissues were observed and HMGB1 mRNA in the synovial tissues were detected by quantitative real time PCR （RTq-PCR）. Result： Compared with the normal group, the joints swelling was more obvious （P 〈 0.01 ） and the expression of HMGBlmRNA was higher in the model group （P 〈 0.01 ）. Compared with the model group, the joints swelling was improved at the 14th day （P 〈0.05） and the 21th day （P 〈0.01） and the expression of HMGBlmRNA in the synovial tissues decreased （P 〈 0.01 ） in the NBTL group at high dose. The pathological section of joints showed the lesions were improved in the all doses of NBTL and twHF groups as compared with the model group. Conclusion： NBTL could reduce joints swelling of CIA rats and inhibite the expression of HMGBlmRNA in the synovial tissues. The mechanism for therapy on rheumatoid arthritis of NBTL may be related to inhibiting the activation of inflammatory pathway through decreasing HMGB.
出处
《中国实验方剂学杂志》
CAS
CSCD
北大核心
2015年第5期159-162,共4页
Chinese Journal of Experimental Traditional Medical Formulae
基金
康缘中医药科技创新基金项目(HZ1003KY)
