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樱桃花青素对佐剂性关节炎大鼠自由基和炎症因子的影响
引用本文:何颖辉,肖诚,王跃生,赵林华,赵宏艳,仝燕,周静,贾宏伟,吕诚,李小明,吕爱平. 樱桃花青素对佐剂性关节炎大鼠自由基和炎症因子的影响[J]. 中国中药杂志, 2005, 30(20): 1602-1605
作者姓名:何颖辉  肖诚  王跃生  赵林华  赵宏艳  仝燕  周静  贾宏伟  吕诚  李小明  吕爱平
作者单位:1. 中国中医研究院,基础理论研究所,北京,100700;中药固体制剂制造技术国家工程研究中心,江西,南昌,330077
2. 中日友好医院,临床研究所,北京,100029
3. 中国中医研究院,中药研究所,北京,100700;中药固体制剂制造技术国家工程研究中心,江西,南昌,330077
4. 中国中医研究院,基础理论研究所,北京,100700
5. 中国中医研究院,中药研究所,北京,100700
基金项目:国家高技术研究发展计划(863计划)
摘    要:目的:观察樱桃花青素对佐剂性关节炎(AA)大鼠自由基和抗氧化功能以及炎症因子的影响.方法:将50只SD雄性大鼠随机分为5组即正常组、模型组、樱桃花青素高、中、低剂量组.对足爪肿胀进行测量,在光镜下观察各组组织形态学变化,用比色法检测了动物外周全血的谷胱甘肽过氧化物酶(GSH-PX)活性、血清超氧化物酶(SOD)活性、血清丙二醛(MDA)含量以及血清总抗氧化能力(T-AOC).用ELISA检测血清中TNF-α含量,用放射免疫法检测了足爪PGE2含量.结果:模型组和正常组相比GSH-PX,SOD活性和T-AOC能力下降,血清MDA含量升高,血清中TNF-α和足爪PGE2含量升高.樱桃花青素组能升高GSH-PX,SOD和T-AOC活力,降低血清MDA,TNF-α以及足爪PGE2含量.光镜下组织形态观察表明樱桃花青素各组能不同程度减轻滑膜增生,减少炎细胞浸润.结论:樱桃花青素能增强AA抗氧化能力,并能降低炎症细胞因子PGE2和TNF-α,从而减轻AA模型的关节炎损伤.

关 键 词:花青素  佐剂性关节炎  自由基  炎症因子
文章编号:1001-5302(2005)20-1602-04
收稿时间:2005-01-10
修稿时间:2005-01-10

Antioxidant and anti-inflammatory effects of cyanidin from cherries on rat adjuvant-induced arthritis
HE Ying-hui;XIAO Cheng;WANG Yue-sheng;ZHAO Lin-hua;ZHAO Hong-yan ;TONG Yan;ZHOU Jing;JIA Hong-wei;LU Cheng;LI Xiao-ming;LU Ai-ping. Antioxidant and anti-inflammatory effects of cyanidin from cherries on rat adjuvant-induced arthritis[J]. China Journal of Chinese Materia Medica, 2005, 30(20): 1602-1605
Authors:HE Ying-hui  XIAO Cheng  WANG Yue-sheng  ZHAO Lin-hua  ZHAO Hong-yan   TONG Yan  ZHOU Jing  JIA Hong-wei  LU Cheng  LI Xiao-ming  LU Ai-ping
Affiliation:1. Institute of Basic Theory, China Academy of Traditional Chinese Medicine, Beifing 100700, China ; 2. Institute of Meteria Medica, China Academy of Traditional Chinese Medicine, Beifing 100700, China ; 3. National Pharmaceutical Engineering Centre for Herbal Preparations, Nanchang 330077, China; 4. Institate of Clinical Research, China-Japan Friendship Hospital, Belting 100029, China
Abstract:OBJECTIVE: To assess the possible antioxidant and anti-inflammatory activity of cyanidin from cherries on adjuvant induced arthritis (AA) in SD rats. METHOD: Arthritis was induced by the complete Freud's adjuvant in male Sprague Dauley rats and assessed based on paw swelling. Rats were randomly divided into normal group (NM), adjuvant arthritis group (AA) and three cyanidin-treated groups in high dosage (HA), middle dosage (MA), and low dosage (LA). The morphological changes in the hind limbs were conducted under a light microscope. We detected glutathione (GSH) in whole blood and malonaldehyde (MDA), superoxide dismutase (SOD), total antioxidative capacity (T-AOC) activity in serum by special kits to assess the antioxidant effects of cyanidin on AA. Moreover, the prostaglandin E2 (PGE2) levels in paw tissues were determined by radioimmunoassay and TNF-alpha levels in serum were determined using ELISA kits specific for rat. RESULT: The cyanidin could protect against the paws swelling in AA rats. From the day 14 after AA induction, the swellings of the cyanidin treated groups at high dosage and low dosage were significantly reduced compared with the model group (P < 0.05, 0.01). Histological examination of sections through the hind limbs revealed alleviation of inflammatory reaction in the joint after the treatment. The cyanidin at high and low dosage could increase the GSH, SOD activity and T-AOC levels in whole blood or serums and decrease MDA in AA rats (P < 0.01). The cyanidin could decrease the PGE2 levels in paw tissues and the TNF-alpha levels in serum at high and low dosages (P < 0.01). CONCLUSION: The cyanidin could protect against the paws swelling in AA rats, and alleviate the inflammatory reaction in the joint, and the mechanism might be via the increase activity of GSH, SOD and T-AOC that improve the total antioxidative capacity and scavenge the free radicals, perhaps as a result of that the levels of the PGE2 in paw tissues and TNF-alpha contents in serum were decreased. The results suggest that the cyanidin from cherries could be one of the potential candidates for the alleviation of arthritis.
Keywords:cyanidin   adjuvant-induced arthritis   free-radical   inflammatory cytokines
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