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作 者:丰瑞兵 陈利锋[2] 王华松[2] 陈芳[2] 王俊伟[1] 王庆伟[1] 邓超[1] FENG Rui-bing CHEN Li-feng WANG Hua-song CHEN Fang WANG Jun-wei WANG Qing-wei DENG Chao(Hubei University of Traditional Chinese Medicine, Wuhan Hubei 430061,China Wuhan General Hospital of PLA, Wuhan Hubei 430070, China)
机构地区:[1]湖北中医药大学,湖北武汉430061 [2]中国人民解放军武汉总医院,湖北武汉430070
出 处:《中医药导报》2017年第17期25-27,31,共4页Guiding Journal of Traditional Chinese Medicine and Pharmacy
基 金:中国博士后科学基金(2015M582905);湖北省卫计委中医药科研项目(2013Z-Y37)
摘 要:目的:探索益气活血方对佐剂型关节炎大鼠TLR2、TLR9的影响。方法:将60只Wistar大鼠随机分成空白组、模型组、益气活血方高剂量组(高剂量组)、益气活血方中剂量组(中剂量组)、益气活血方低剂量组(低剂量组)、雷公藤组。除空白组外其余大鼠通过弗氏完全佐剂诱导建立佐剂型关节炎模型。造模2周后,进行给药。空白组和模型组每日给予蒸馏水10 mL/kg,高、中、低剂量组分别给予2 g/mL,1 g/mL,0.5 g/mL益气活血方汤剂、雷公藤组给予0.94 mg/mL雷公藤多苷片水溶液,持续3周。检测大鼠关节炎症指数、大鼠TLR2、TLR9的蛋白表达水平。结果:造模大鼠均表现出足爪肿胀,关节炎症指数、TLR2、TLR9蛋白表达均高于空白组(P<0.01)。高、中、低剂量组、雷公藤组AI、TLR2、TLR9蛋白的表达水平均低于模型组(P<0.05)。高、中剂量组AI均低于低剂量与雷公藤组(P<0.05)。高剂量组TLR2、TLR9蛋白表达低于雷公藤组(P<0.05)。结论:益气活血方能抑制佐剂型关节炎大鼠的关节炎症表现,其作用机制可能与抑制TLR2、TLR9的过度表达有关。Objective: To explore the effect of YQHXP on TLR2 and TLR9 of adjuvant arthritis rats. Method: The 60 Wistar rats were randomly divided into control group, model group, YQHXP high dose group (YQHXP-H), YQHXP middle dose group (YQHXP-M), YQHXP low dose group (YQHXP-L) and Tripterygium Glycosides tablets group (TGT). Except the control group, rats of other groups were induced by Complete Freund's Adjuvant (CFA) to establish adjuvant arthritis (AA) rat model. Two weeks after first modeling, each drug groups were given medicines accordingly by gastric perfusion for 3 weeks. The blank group and the model group were given distilled water 10 mL/kg daily. The YQHXP-H, YQHXP-M, and YQHXP-L were given YQHXP at 2 g/mL, 1 g/mL and 0.5 g/mL respectively. Tripterygium Glycosides tablets group was given tripterygium glycosides aqueous solution at 0.94 mg/mL. Arthritis index and the protein expression levels of TLR2 and TLR9 were main outcome measures. Results: All model rats showed paw swelling, and the inflammatory index and the expression of TLR2 and TLR9 were higher than those in the blank group (P〈0.01). The YQHXP-H, YQHXP-M, YQHXP-L and Tripterygium Glycosides tablets group showed lower AI and protein expression levels of TLR2 and TLR9 than the model group (P〈0.05). The YQHXP-H and YQHXP-M showed lower AI than the model group (P〈0.05); The YQHXP-H showed lower protein expression levels of TLR2 and TLR9 than the model group (P〈0.05). Conclusion: The YQHXP can inhibit joint inflammation of the AA rat model, and its therapeutic mechanism may be associated with its inhibition the excessive expression of TLR2 and TLR9.
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