电针对胶原诱导性关节炎大鼠血清中炎性细胞因子含量的影响

Effect of Electroacupuncture on Serum TNF-α,IL-1β and Intercellular adhesion molecule 1 Levels in Rheumatoid Arthritis Rats

目的:观察电针对胶原诱导性关节炎模型大鼠血清肿瘤坏死因子-α(TNF-α)、白介素-1β(IL-1β)和细胞间黏附分子-1(ICAM-1)含量的影响,探讨电针在治疗类风湿性关节炎(RA)中的作用机制。方法 :雄性Wistar大鼠60只,随机取8只做为正常组,其余大鼠采用鸡Ⅱ型胶原和弗氏不完全佐剂制备RA模型。造模成功后,选取其中24只随机分为模型组、泼尼松组和电针组,每组8只。电针组每日针刺大鼠双侧"足三里"和"昆仑"穴,30min/次,连续治疗10d。泼尼松组每日灌胃醋酸泼尼松龙0.1mL/10g。分别在造模前后和治疗结束后测量大鼠左踝关节直径,采用ELISA法检测大鼠血清的TNF-α、IL-1β和ICAM-1含量。结果:与正常组相比,模型组大鼠的踝直径和血清TNF-α、IL-1β和ICAM-1的含量均升高(P<0.05);与模型组比较,经电针和泼尼松治疗后的大鼠踝直径和血清TNF-α、IL-1β和ICAM-1的含量均降低(P<0.05);电针组与泼尼松组相比,差异无统计学意义(P>0.05)。结论:电针对RA大鼠具有治疗作用,有效减少血清TNF-α、IL-1β和ICAM-1的分泌可能是其作用机制之一。

Objective To observe the influence of electroacupuncture（EA）on serum TNF-α,IL-1βand Intercellular adhesion molecule 1（ICAM-1）levels in rheumatoid arthritis（RA）rats so as to explore its mechanism in relieving RA.MethodsEight Wistar rats were used as the normal control group in this study.The RA model was established by injecting mixture solution of incomplete Freund’s adjuvant and type Ⅱchicken collagen into the left paw.The 24 successful RA rats were randomly divided into model,medication（Prednisolone）and EA groups（n=8in each group）.EA（2Hz/100 Hz,1-2mA）was applied to＂Zusanli＂（ST 36）and ＂Kunlun＂（BL 60）for 30 min,once daily for 10 days.For rats of the medication group,Prednisolone acetate（0.1mL/10g）was intragastric infused daily.The rats’ left ankle diameter was measured before and after the treatment,and the contents of serum TNF-α,IL-1βand ICAM-1were assayed by ELISA.Results In comparison with the normal control group,the rats’ ankle diameter,serum TNF-α,IL-1βand ICAM-1contents were remarkably increased in the model group（P〈0.05）;while compared with the model group,the increased ankle diameter,and serum TNF-α,IL-1βand ICAM-1contents were obviously reversed in both medication and EA groups（P〈0.05）,without significant differences between the medication and EA groups（P〉0.05）.Conclusion EA intervention is effective in relieving RA rats’ inflammatory reactions by down-regulating the levels of serum TNF-α,IL-1βand ICAM-1.