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作 者:梁卫[1] 周群[2] 沈家敏 吴艮艮 张丽玲[1] 陈晔[1] 姚亮宇 LIANG Wei;ZHOU Qun;SHEN Jia-min;WU Gen-gen;ZHANG Li-ling;CHEN Ye;YAO Liang-yu(No.454 Hospital of PLA, Nanjing 210002, China;Nanjing University of Chinese Medicine, Nanjing 210023, China;Xuzhou Medical University, Xuzhou 221004 China)
机构地区:[1]解放军第四五四医院,江苏南京210002 [2]南京中医药大学,江苏南京210023 [3]徐州医科大学,江苏徐州221004
出 处:《中国中医药信息杂志》2017年第12期52-55,共4页Chinese Journal of Information on Traditional Chinese Medicine
摘 要:目的观察风湿痹痛方对胶原诱导型关节炎(CIA)大鼠血清细胞因子及滑膜组织Fas/Fas L m RNA表达的影响,探讨其相关的作用机制。方法采用大鼠足部皮内注射牛Ⅱ型胶原乳化剂方法建立CIA模型。实验大鼠随机分为空白组、模型组、雷公藤多苷组和风湿痹痛方低、中、高各剂量组,各给药组给予相应药物灌胃,连续14 d。观察各组大鼠体质量和关节炎评分;ELISA检测血清白细胞介素(IL)-1β、IL-15、转化生长因子(TGF)-β1含量;RT-PCR检测滑膜组织Fas、Fas L的m RNA表达。结果与模型组比较,风湿痹痛方中、高剂量组大鼠足部关节炎评分和血清IL-15含量显著降低,TGF-β1含量显著升高(P<0.01),风湿痹痛方高剂量组Fas m RNA表达显著降低,Fas L m RNA表达显著升高(P<0.05)。结论风湿痹痛方对CIA有一定的免疫调节作用,其机制可能是通过调控Fas/Fas L凋亡系统,诱导滑膜组织细胞凋亡,抑制滑膜增生。Objective To observe the effects of Fengshi Bitong Prescription(FSBT)on cytokines in serum and Fas/FasL mRNA expression system in synovium;To discuss relevant mechanism of action.Methods Rats were given foot intradermal injection of bovine typeⅡcollagen emulsion to establish collagen-induced arthritis(CIA)model.After successful modeling,they were randomly divided into6groups:normal control group,CIA model group,tripterygium glycosides group,FSBT high-,medium-,and low-dose groups.Each medication group was given relevant medicine for gavage for14d.The weight and arthritis scores of CIA rats were observed.Serum levels of IL-1β,IL-15,and TGF-β1were detected by ELISA.Expressions of Fas and FasL mRNA in synovium of CIA rats were detected by real-time PCR.Results Compared with model group,the foot arthritis score and serum levels of IL-15in FSBT high-and medium-dose groups significantly decreased(P<0.01),and the serum level of TGF-β1significantly increased(P<0.05).Expression of Fas significantly decreased and FasL significantly increased in FSBT high-dose group(P<0.05).Conclusion FSBT may have certain immune regulation effects on rheumatoid arthritis.Its mechanism may be in regulating Fas/FasL apoptosis system,thereby inducing apoptosis of synovial cells and inhibiting synovial hyperplasia.
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