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壮药龙钻通痹方对胶原诱导型关节炎大鼠血清及滑膜Fas/FasL系统的影响 被引量:14

Effects of Longzuan Tongbi Recipe on Fas/FasL Systems in Serum and Synovium of Collagen-induced Arthritis Rats
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摘要 目的观察壮药龙钻通痹方对胶原诱导型关节炎(collagen-induced arthritis,CIA)大鼠血清及滑膜Fas/FasL系统的影响。方法 60只雄性Wistar大鼠随机选取10只作为正常对照组,其余50只采用牛Ⅱ胶原蛋白与弗氏不完全佐剂混合液诱导制作CIA模型,造模后分为模型组,甲氨蝶呤组(MTX组),壮药龙钻通痹方高、中、低剂量组(简称壮药高、中、低剂量组),每组10只。模型组灌服生理盐水,MTX组按0.27mg/100g大鼠体重灌胃MTX溶液,每周1次,灌胃4周;壮药高、中、低剂量组分别予以壮药龙钻通痹方汤剂(4.32、2.16、1.08g/mL)灌胃,每日2次,灌胃30日。HE染色观察滑膜形态变化;ELISA法定量检测干预后大鼠血清、滑膜组织匀浆液Fas/FasL的表达。结果正常组中为正常滑膜细胞,模型组中滑膜细胞增殖明显,下层脂肪细胞减少或变形,成纤维细胞增多,伴有淋巴细胞及单核细胞浸润;MTX组及壮药低、中、高剂量组较模型组明显改善。与正常组比较,模型组血清及滑膜组织Fas表达升高,血清FasL表达降低(P<0.05,P<0.01);与模型组比较,MTX组、壮药中、高剂量组血清及滑膜组织Fas表达降低,MTX组、壮药低、中、高剂量组血清及MTX组、壮药中、高剂量组滑膜组织FasL表达升高(P<0.05,P<0.01);与MTX组比较,壮药低剂量组血清及壮药低、中剂量组滑膜组织Fas表达升高,壮药高剂量组血清及滑膜组织Fas表达降低,壮药低、中剂量组血清及滑膜组织FasL表达降低,壮药高剂量组血清及滑膜组织FasL表达升高(P<0.05,P<0.01)。结论调节Fas/FasL系统介导的细胞凋亡机制,减缓类风湿关节炎的病理反应可能是壮药龙钻通痹方控制与治疗类风湿关节炎的作用机制之一。 Objective To observe the effect of Longzuan Tongbi Recipe (LTR) on Fas/FasL systems in serum and synovium of collagen-induced arthritis (CIA) rats. Methods Ten rats were randomly selected from 60 male Wistar rats as a normal control group. CIA model was prepared by injecting type Ⅱ bovine collagen and incomplete Freund's adjuvant mixture in the rest 50 rats. After modeling rats were divided into the model group, the methotrexate (MTX) group, high, middle, and low dose LTR groups, 10 in each group. Normal saline was administered to rats in the model group by gastrogavage. MTX solution (0.27 mg/100 g) was administered to rats in the MTX group by gastrogavage, once per week for 4 successive weeks. LI-R (4.32, 2. 16, 1.08 g/mL) was administered to rats in the 3 LTR groups by gastrogavage, twice per day for 30 successive days. Morphological changes of synovium were observed by HE staining. Expression levels of Fas/FasL in rat serum and synovium were quantitatively detected by ELISA. Results Normal synovium cells could be seen in the normal group. But they were obviously proliferated, fat cells in the lower synovium were reduced or deformed, fibroblasts were increased in the model group, accompanied with infiltration of lymphocytes and monocytes. All these changes were more obviously alleviated in the MTX group, and the 3 LTR groups. Compared with the normal control group, Fas expression level in-creased in rat serum and synovium, serum FasL expression level decreased in the model group (P 〈0.05, P 〈0.01 ). Compared with the model group, Fas expression level decreased in rat serum and synovium in the MTX group, high and middle dose LTR groups ; Fas expression level in rat serum increased in the MTX group and 3 LTR groups; Fas expression level in synovium increased in the MTX group, high and middle dose LTR groups (P 〈0.05, P 〈0.01 ). Compared with the MTX group, Fas expression level in serum of the low dose LTR group, and Fas expression level in synovium of low and middle dose LTR groups was elevat- ed; Fas expression level in serum and synovium of the high dose LTR group was reduced; FasL expres- sion level in serum and synovium of low and middle dose LTR groups was reduced; FasL expression level in serum and synovium increased of the high dose LTR group (P 〈0.05, P 〈0.01 ). Conclusion LTR could control and treat rheumatoid arthritis, and its mechanism might lie in regulating Fas/FasL systems mediated cell apoptosis, and relieving pathological reaction of rheumatoid arthritis.
出处 《中国中西医结合杂志》 CAS CSCD 北大核心 2016年第8期981-985,共5页 Chinese Journal of Integrated Traditional and Western Medicine
基金 国家自然科学基金资助项目(No.81460765) 广西自然科学基金资助项目(No.2013GXNSFAA019141)
关键词 壮药 龙钻通痹方 胶原诱导型关节炎 FAS/FASL 凋亡 Guangxi Zhuang medicine Longzuan Tongbi Recipe collagen-induced arthritis Fas/ FasL apoptosis
作者简介 通讯作者:庞宇舟,Tel:0771-3103626,E-mall:Pangyz422@sina.com
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  • 1Scott DL, Wolfe F, Huizinga TW. Rheumatoid ar- thritis [ J ]. Lancet, 2010, 376 (9746): 1094 - 1108.
  • 2Hong S, Kim E J, Lee E J, et al. TNF-alpha con- fers resistance to Fas-mediated apoptosis in rheumatoid arthritis through the induction of solu- ble Fas[J]. Life Sci, 2015, 122(1 -2): 37 -41.
  • 3Mor A, Abramson SB, Pillinger MH. The fibro- blast-like synovial cell in rheumatoid arthritis, a key player in inflammation and joint destruction [J]. Clin Immunol, 2005, 115(2): 118-128.
  • 4Pope RM. Apoptosis as a therapeutic tool in rheu- matoid arthritis[J]. Nat Rev Immunol, 2002, 2 (7) : 527 - 535.
  • 5Li X, Zhang Z, Peng A, et al. Effect of CD95 on inflammatory response in rheumatoid arthritis fi- broblast-like synoviocytes [ J ]. Cell Immunol, 2014, 290(2) :209 -216.
  • 6Peng SL. Fas (CD95)-related apoptosis and rheu- matoid arthritis [ J ]. Rheumatology (Oxford), 2006, 45(1) ; 26 -30.
  • 7Ogawa Y, Kuwahara H, Kimura T, et al. Thera- peutic effect of anti-Fas antibody on a collagen in- duced arthritis model[J]. J Rheumatol, 2001, 28 (5) : 950 -955.
  • 8Cha HS, Bae EK, Ahn JK, et al. Slug suppres- sion induces apoptosis via Puma transactivation in rheumatoid arthritis fibroblast-like synoviocytes treated with hydrogen peroxide[ J ]. Exp Mol Med, 2010,42(6) : 428 -436.
  • 9Garcia S, Liz M, Gomez-Reino J J, et al. Akt ac- tivity protects rheumatoid synovial fibroblasts from Fas-induced apoptosis by inhibition of Bid cleavage [ J ]. Arthritis Res Ther, 2010, 12 (1): R33.
  • 10王振亮,姚乃礼.石藤胶囊对佐剂性关节炎大鼠TNF-α,IL-1β的影响[J].中国实验方剂学杂志,2012,18(8):195-198. 被引量:7

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