摘要
目的观察藤莓汤对胶原诱导性关节炎(collagen-induced arthritis,CIA)大鼠滑膜过氧化物酶体增殖物激活受体-γ(peroxisome proliferator activated receptor gamma,PPARγ)、核转录因子-κB(nuclear factor kappa B,NF-κB)、IL-17表达的影响,探讨该方抑制类风湿关节炎(rheumatoid arthritis,RA)滑膜免疫炎性病理损伤的分子机制。方法建立SD大鼠CIA模型,将成模大鼠随机分为模型组、西药组、中药高剂量组、中药低剂量组,并设正常组,每组6只。正常组与模型组予去离子水10 m L/(kg·d)灌胃,西药组予来氟米特1.87mg/(kg·d)灌胃,中药高、低剂量组分别以藤莓汤生药量31.8、15.9 g/(kg·d)灌胃,连续干预12周。干预结束后检测PPARγ、P65、IL-17蛋白及mRNA表达。结果与正常组比较,模型组PPARγ、P65、IL-17 mRNA及蛋白表达上调(P<0.01)。与模型组比较,中药高剂量组PPARγ蛋白表达上调,P65、IL-17 mRNA及蛋白表达下调,差异有统计学意义(P<0.01);西药组及中药低剂量组PPARγmRNA及蛋白表达上调,P65、IL-17 mRNA及蛋白表达下调,差异有统计学意义(P<0.01)。结论藤莓汤可改善CIA大鼠关节滑膜病理损伤,抑制免疫炎性因子表达。
Objective To observe the effects of Tengmei Decoction （TMD） on the expressions of peroxisome proliferator activated receptor gamma （ PPARγ）, nuclear factor kappa B （ NF-κB ）, and IL- 17 in synovium of collagen-induced arthritis （CIA） rats, and to study its molecular mechanism of inhibi- ting synovial immune inflammatory injuries. Methods CIA model was established in Sprague-Dawley rats. Successfully modeled rats were randomly divided into the model group, the positive drug group, high and low dose TMD groups, 6 in each group. Besides, a normal group was set up （n =6）. Deionized water （10 mL · kg-1 · d-1） was administrated to rats in the normal group and the model group by gastro-gavage. Leflunomide （1.87 mg · kg -1 ·d -1 ） was administrated to rats in the positive drug group by gastro-gavage. TMD （31.8 g crude drugs · kg-1 · d -1 and 15.9 g crude drugs · kg-1· d -1） was administrated torats in high and low dose TMD groups respectively by gastrogavage. The intervention lasted for 12 suc- cessive weeks. Protein and mRNA levels of PPARγ, P65, and IL-17 were detected at the end of intervention. Results Compared with the normal group, mRNA and protein expression levels of PPARγ, P65, and IL-17 were up-regulated in the model group （P 〈0.01 ）. Compared with the model group, PPARγ, pro- tein expression level was up-regulated, mRNA and protein expression levels of P65 and IL-17 were down- regulated in high dose TMD group （P 〈0.01 ）. mRNA and protein expression levels of PPARγ were up- regulated, mRNA and protein expression levels of P65 and IL-17 were down-regulated in the positive drug group and low dose TMD group （P 〈0.01 ）. Conclusions TMD could ameliorate pathological damage of joint synovium, and inhibit expressions of immune inflammatory factors.
出处
《中国中西医结合杂志》
CAS
CSCD
北大核心
2017年第4期458-463,共6页
Chinese Journal of Integrated Traditional and Western Medicine
基金
教育部高等学校博士学科专项科研基金(No.20120013110006)
