类风湿关节炎病人滑膜细胞增生与fas和bcl-2基因的表达

目的探讨类风湿关节炎（ＲＡ）病人滑膜细胞增生是否与细胞凋亡有关。方法通过体外转录合成,并标记ｆａｓ及其配体（ｆａｓＬ）和ｂｃｌ－２ＲＮＡ探针,应用原位杂交方法检测１９例滑膜组织的基因表达。用免疫组织化学方法检测蛋白表达。用ＤＮＡ电泳和流式细胞分析仪检测细胞凋亡。结果７例ＲＡ病人滑膜衬里层细胞明显增生,其中６例有ｆａｓｍＲＮＡ表达,５例表达ｂｃｌ－２,而ｆａｓＬｍＲ－ＮＡ在所有病例均不表达。在ＲＡ滑膜衬里层中,ｂｃｌ－２ｍＲＮＡ总是伴随ｆａｓ而表达,且ｆａｓ和ｂｃｌ－２的表达率较骨性关节炎（ＯＡ）及正常对照者（ＮＣ）明显增高（Ｐ＜０．０５）。免疫组织化学结果表明,ｆａｓ和ｂｃｌ－２蛋白在滑膜衬里层有表达。从６例ＲＡ、４例ＯＡ病人及３例正常对照者滑膜组织中提取ＤＮＡ,仅１例ＯＡ病人可见典型的ＤＮＡ梯形图形。培养的ＲＡ和ＯＡ病人滑膜细胞经流式细胞分析仪检测,表明自发凋亡的细胞很少（＜５％）。结论ＲＡ病人滑膜细胞内不存在明显的细胞凋亡现象,ｂｃｌ－２过量表达可能抑制了ＲＡ滑膜细胞凋亡,是ＲＡ滑膜细胞增生的原因之一。     

Immunohistochemical study of Fas antigen expression in synovial tissues from patients with rheumatoid arthritis

ＩｍｍｕｎｏｈｉｓｔｏｃｈｅｍｉｃａｌｓｔｕｄｙｏｆＦａｓａｎｔｉｇｅｎｅｘｐｒｅｓｉｏｎｉｎｓｙｎｏｖｉａｌｔｉｓｕｅｓｆｒｏｍｐａｔｉｅｎｔｓｗｉｔｈｒｈｅｕｍａｔｏｉｄａｒｔｈｒｉｔｉｓＹｕＱｉｎｇｈｏｎｇ于清宏,ＬｉｕＸｉａｎｇｙｕａｎ刘湘源...     

滑膜成纤维细胞的原代培养及生物特性

目的研究滑膜成纤维细胞的原代培养方法及生物特性。方法收集行关节腔镜术或关节置换术的患者的膝关节滑膜标本,其中类风湿关节炎、骨关节炎、关节创伤病例各6例,分别采用酶消化法、组织块法进行滑膜成纤维细胞的原代培养并进行生物特性的观察及鉴定。结果总共有6例类风湿关节炎、4例骨关节炎、4例关节创伤患者关节滑膜成功培养出成纤维样滑膜细胞,其中9例应用酶消化法,5例应用组织块法,经鉴定成纤维样滑膜细胞的纯度99%。结论本课题成功应用酶消化法和组织块法进行滑膜成纤维细胞的原代培养,所培养细胞适用于进行滑膜成纤维细胞相关的研究。     

Programmed cell death 5 correlates with disease activity and interleukin-17 in serum and synovial fluid of rheumatoid arthritis patients

Background Programmed cell death 5 (PDCD5) is a novel apoptotic regulatory gene that promotes apoptosis in various tumor cells.Studies have shown that PDCD5 accelerates the apoptosis of synoviocytes in...     

雷公藤多甙诱导类风湿关节炎滑膜细胞凋亡的研究

目的:评估抗风湿中药雷公藤多甙(TripterygiumGlycosides,TG)诱导滑膜细胞凋亡(Apo)在类风湿关节炎(RA)治疗中的作用,探讨其药理机制。方法:用光镜、电镜、共聚焦显微镜、流式细胞仪(FCM)及DNA凝胶电泳检测不同浓度TG诱导RA滑膜细胞凋亡情况。结果:TG组凋亡细胞百分率显著高于骨性关节炎(OA)组(P<0.01)和正常人组(P<0.01),TG组凋亡细胞百分率为(55±11.2)%。结论:TG可以诱导滑膜细胞凋亡,并且这可能是其治疗RA的机制之一。     

关节炎患者血清肿瘤坏死因子α的检测及意义

目的探讨类风湿关节炎(RA)、强直性脊柱炎(AS)和骨关节炎(OA)患者血清肿瘤坏死因子α(TNF-α)的水平及临床意义.方法应用双抗体夹心ELISA法测定RA、AS、OA和正常对照者的血清TNF-α并与炎性指标血沉(ESR)和C反应蛋白(CRP)作相关分析.结果RA病人血清TNF-α水平明显高于正常对照组(P＜0.001),血清TNF-α水平与炎性指标(ESR和CRP)及类风湿因子滴度呈正相关.AS组和正常对照组血清TNF-α比较有显著性差异(P＜0.005),但与炎性指标无相关性.OA组中有5例血清TNF-α水平高于正常对照组,但是两组差异无统计学意义,OA组ESR和CRP正常.结论TNF-α是关节疾病发生、发展的重要因素,在RA炎症反应中处于中心地位.     

长春新碱对类风湿关节炎滑膜细胞作用的研究

目的 :评价长春新碱 (VCR)诱导滑膜细胞凋亡作用在治疗类风湿关节炎 (RA)中的意义。方法 :采用光镜、电镜、流式细胞仪及 DNA凝胶电泳等方法对不同浓度的 VCR诱导 9例体外培养的 RA病人及对照组 5例骨关节炎 (OA)与 4例正常人(NC)关节滑膜细胞凋亡情况进行了研究。结果 :加药前 RA、OA及 NC组凋亡细胞百分率分别为 3.8%± 0 .6 %、0 .8%± 0 .3%及0。加药后均显著升高 ,RA组可高达 6 7.5 %± 15 .1% (P<0 .0 1) ,OA组为 38.4%± 6 .8% (P<0 .0 1) ,NC组为 15 .7%± 1.5 % (P<0 .0 1)。 RA组凋亡细胞百分率显著高于 OA组 (P<0 .0 1)和 NC组 (P<0 .0 1)。结论 :诱导滑膜细胞凋亡可能是 VCR治疗 RA的机制之一 ,同时可为临床选择合理药物及药量提供依据     

丹参诱导成纤维样滑膜细胞caspase-1基因表达研究

目的探讨丹参对类风湿关节炎患者和骨关节炎患者的成纤维样滑膜细胞（FLSs）caspase-1 mRNA表达的影响。方法类风湿关节炎（RA）患者关节滑液和骨关节炎（OA）患者关节滑液中游离滑膜样细胞经原代培养,分别用终浓度为0、0.2、0.4、0.8、1.6和3.2mg/ml的丹参作用24h后,观察形态;提取总RNA并逆转录成cDNA,采用SYBR green适时荧光定量PCR方法检测caspase-1的表达。结果无论RA还是OA,在丹参浓度为0.2mg/ml时,FLSs形态变化不明显;当丹参浓度为0.4mg/ml及以上时,FLSs发生凋亡样改变。caspase-1的基础表达量（未加丹参刺激）在RA FLSs与OA FLSs中为差异无统计学意义（P〉0.05）;以丹参浓度为0作为对照组,无论是在RAFLSs,还是在OA FLSs中,Caspase-1的表达量均随丹参浓度增加而增加,并且在丹参浓度为0.4mg/ml时开始差异有统计学意义（P〈0.001）。结论 caspase-1在RAFLSs和OA FLSs中的表达无明显变化可能表明两种细胞的炎性性质的一致性;丹参可诱导FLSs caspase-1在mRNA水平的表达增加,且呈剂量关系,这可能与丹参抗炎和（或）诱导FLSs凋亡有关。     

透痹转气法对类风湿关节炎关节滑膜AQP1表达的影响

目的:观察透痹转气法(TBZQ)对类风湿关节炎(RA)疗效及对水通道蛋白1(AQP1)的影响。方法:研究对象25例,RA组10例为活动期RA有膝关节肿痛者,OA组15例为膝关节骨性关节炎患者。RA组应用透痹转气法治疗1疗程(3月),治疗2疗程后观察临床疗效及CRP、RF等指标变化。检测RA组治疗前、后及OA组治疗前关节滑膜AQP1基因表达。结果:RA组临床症状明显改善,炎症指标明显降低(P<0.05);AQP1在膝关节滑膜细胞有表达,治疗前RA组较OA组表达增强,治疗后RA组增强的表达下调(P<0.05)。结论:透痹转气法明显改善RA患者的症状,降低炎症指标;AQP1高表达可能是RA关节肿痛机制之一。     

程序化细胞死亡因子5过表达促进雷公藤内醇酯诱导的类风湿关节炎成纤维样滑膜细胞凋亡

目的:探讨程序化细胞死亡因子5(progrmmed cell death 5,PDCD5)过表达对雷公藤内醇酯(triptolide)诱导类风湿关节炎成纤维样滑膜细胞(rheumatiod arthritis fibroblast-likes synoviocytes,RA FLS)凋亡的作用.方法:体外分离培养RA FLS进行腺病毒Ad-PDCD5(含有PDCD5基因的腺病毒载体)的转染,分别用免疫印迹法和流式细胞术检测Ad-PDCD5转染后的RA FLS中PDCD5蛋白表达及经雷公藤内醇酯处理后的PDCD5蛋白过表达的RAFLS的凋亡率.结果:用感染复数(multiplicity of infection,MOI)分别为50、100、200和300的Ad-PDCD5感染RAFLS 36 h后,PDCD5蛋白表达水平呈现剂量依赖性增加.未经雷公藤内醇酯处理的非感染组、Ad-null组(不含目的基因的空载体)和Ad-PDCD5组RA FLS的凋亡之间差异无统计学意义,经雷公藤内醇酯处理后,其RA FLS的凋亡率分别为(22.51±3.87)%,(28.77±12.97)%和(48.87±12.69)%.表明此腺病毒体系能够有效地使PDCD5蛋白过表达,在RA FLS中,单独使用雷公藤内醇酯或者单独转染PDCD5都不能明显地诱导细胞凋亡,但过表达PDCD5再进行雷公藤内醇酯处理可以诱导细胞凋亡.结论:腺病毒Ad-PDCD5转染使PDCD5过表达,从而能够促进雷公藤内醇酯诱导的RA FLS凋亡,为类风湿关节炎的临床治疗提供了一个可能的干预靶点.     

PDCD5 Correlates with Disease Activity and IL-17 in Rheumatoid Arthritis

Background Programmed cell death 5 (PDCD5) is a novel apoptotic regulatory gene, which has a promoting effect on apoptosis of various tumor cells. Studies showed that PDCD5 accelerates the apoptosis of synoviocytes in vitro, implying its potential role in the pathogenesis of rheumatoid arthritis (RA). The objective of this study was to examine the expression of PDCD5 in serum and synovial fluid of RA and to determine its effect on the expression of inflammatory cytokine, interleukin-17 (IL-17), as well as the assessment of disease activity in RA. Methods PDCD5 and IL-17 levels in serum and synovial fluid from 18 RA patients and 22 Osteoarthritis (OA) patients were detected by ELISA. The concentrations of serum PDCD5 in 40 healthy people were also detected as control. As disease activity indices, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), rheumatoid factor (RF), and X-ray grading scale were also evaluated. Results The serum and synovial fluid PDCD5 levels in RA patients were significantly higher than those in OA and healthy controls. The serum PDCD5 level was inversely correlated with CRP and ESR. Further, serum PDCD5 level in RF negative group was significantly higher than that in positive group. In addition, PDCD5 level had a negative correlation with IL-17 level both in serum and synovial fluid of RA patients. However, the differences of synovial fluid PDCD5 level in RA patients with different Larsen stages were not detectable. Conclusions These results suggest that PDCD5 might play a role in the pathogenesis of RA. Insufficient apoptosis of FLS and inflammatory cells in RA could possibly cause the increased expression of PDCD5 protein. Meanwhile, PDCD5 level correlated negatively with disease activity indices and IL-17 level, implying it as a potential target in the diagnosis and treatment of RA.     

5-羟色胺受体与调节性T 细胞在抑郁症免疫功能紊乱中的关联作用

目的 观测抑郁症患者免疫失衡的特征,从5-羟色胺受体(5-HT1aR)和调节性T 细胞表达变化的关系,探讨抑郁症免疫失衡的可能机制.方法 采集27例抑郁症患者外周血,利用ELISA方法测定血清细胞因子IL-2,IL-10,TGF-β1浓度,逆转录-聚合酶链反应(RT-PCR)方法检测患者5-HT1aR和FoxP3的mRNA水平,免疫磁珠分离调节性T细胞,共聚焦显微镜观察调节性T细胞5-HT1aR受体和FoxP3的共表达,并与正常对照组进行对照.结果 与正常对照组标本相比,抑郁症患者血清IL-2表达水平上调[(184.681±8.472)pg/ml,(82.845±12.292)pg/ml],IL-10[(6.765±0.611)pg/ml,(9.593±0.921)pg/ml],TGF-β1[(14.042±2.170)ng/ml,(20.981±3.98)ng/ml]的表达水平降低(均P <0.01);外周血中调节性T细胞数量减少[(13.139±4.587)107个,(20.583±3.484)107个],单个核细胞5-HT1aR和FoxP3的mRNA表达水平降低(均P <0.01);同时通过共聚焦显微镜观察到调节T细胞上的5-HT1aR及FoxP3表达减弱.结论 抑郁症患者中存在免疫失衡现象,5-HT1aR通过影响调节性T细胞在抑郁症患者免疫失衡的病理生理机制发挥着重要的作用.     

CXCL16/CXCR6在类风湿关节炎成纤维样滑膜细胞中的表达及其在滑膜细胞增殖中的作用

目的：探讨趋化因子CXCL16及其受体CXCR6在类风湿关节炎（rheumatoid arthritis,RA）患者成纤维样滑膜细胞（fibroblast-like synoviocytes,FLS）中的表达及其对FLS增殖的作用。方法:纳入RA 8例、骨关节炎（osteoarthritis,OA）7例、健康对照3例,采用组织块贴壁方法体外分离培养人膝关节FLS,第3~5代细胞用于后续研究。Western blot方法检测CXCL16及其受体CXCR6在3组FLS的表达水平;不同浓度的重组人CXCL16(0、10、50、100、200 μg/L)刺激3组FLS后,细胞活性检测试剂盒-8（cell counting kit,CCK-8）检测FLS增殖水平;Western blot方法检测重组人CXCL16刺激后RA-FLS中pAKT/AKT水平;ELISA法检测重组人CXCL16刺激后RA-FLS培养上清中TNF-ɑ、IL-6、MMP-3、RANKL水平。结果: RA-FLS中CXCL16、CXCR6蛋白表达水平均明显高于OA组和对照组（P<0.05）,OA组和对照组间差异无统计学意义;重组人CXCL16（50、100、200 μg/L）刺激后RA-FLS增殖能力明显高于非刺激组（P均<0.05）,OA组和对照组FLS经CXCL16刺激后细胞增殖水平无明显变化（P>0.05）;200 μg/L CXCL16刺激后,RA-FLS表达pAKT/AKT明显增高;CXCL16（50、100、200 μg/L）刺激后,RA-FLS培养上清中IL-6和RANKL表达明显增加（P < 0.05）,而MMP-3、TNF-ɑ水平无明显变化。结论:CXCL16及其受体在RA-FLS中表达增高,重组人CXCL16可促进RA-FLS增殖活化、分泌炎性因子增加,提示CXCL16参与了RA的滑膜炎症。     

补阳还五汤对TNFa诱导血管内皮细胞释放vWF及表达组织？…

OBJECTIVE: To study the effects of Buyang huanwu decoction (BHD) on the release of von Willebrand factor(vWF) and the expression of tissue factor(TF) activity induced by tumor necrosis factor alpha (TNF alpha) in cultured bovine aortic endothelial cells (BAECs). METHODS: BAECs from neonatal cox were cultured and 4-8 passages were used. Cells were incubated for 8 hours after addition of different treatments. The supernatant was used to measure vWF and BAECs lysate to determine TF activity. RESULTS: 1. Compared with the control, TNF alpha enhanced the expression of TF activity(12.79 +/- 2.59 vs. 4.69 +/- 0.83, P < 0.01) and the effects were in dose-dependent manner(r = 0.9712, P < 0.01); BHD inhibited the effects of TNF alpha(P < 0.01). 2. Compared with the control, TNF alpha promoted the release of vWF from endothelial cells (13.28 +/- 4.76 vs. 6.42 +/- 2.84, P < 0.01) and BHD inhibited the effect of TNF alpha(P < 0.01). CONCLUSION: BHD can inhibit the expression of TF and the release of vWF induced by TNF alpha.     

Effect of anaphylatoxin C3a, C5a on the tubular epithelial-myofibroblast transdifferentiation in vitro

Background  Tubulointerstitial renal fibrosis is the common end point of progressive kidney diseases, and tubular epithelial-myofibroblast transdifferentiation (TEMT) plays a key role in the progress of tubulointerstitial renal fibrosis. Anaphylatoxin C3a and C5a are identified as novel profibrotic factors in renal disease and as potential new therapeutic targets. The aim of this study was to investigate whether C3a, C5a can regulate TEMT by transforming growth factor-β1 (TGF-β1)/connective tissue growth factor (CTGF) signaling pathway and the effects of C3a and C5a receptor antagonists (C3aRA and C5aRA) on C3a- and C5a-induced TEMT.

Methods  HK-2 cells were divided into C3a and C5a groups which were subdivided into four subgroups: control group, 10 ng/ml TGF-β1 group, 50 nmol/L C3a group, 50 nmol/L C3a plus 1 μmol/L C3aRA group; control group, 10 ng/ml TGF-β1 group, 50 nmol/L C5a group, 50 nmol/L C5a plus 2.5 μmol/L C5aRA group. TGF-β1 receptor antagonist (TGF-β1RA) 10 μg/ml was used to investigate the mechanism of C3a- and C5a-induced TEMT. Electron microscopy was used to observe the morphological changes. Immunocytochemistry staining, real-time PCR and Western blotting were used to detect the expressions of α smooth muscle actin (α-SMA), E-cadherin, Col-I, C3a receptor (C3aR), C5aR, CTGF and TGF-β1.

Results  HK-2 cells cultured with C3a and C5a for 72 hours exhibited strong staining of α-SMA, lost the positive staining of E-cadherin, and showed a slightly spindle-like shape and loss of microvilli on the cell surface. The expressions of α-SMA, E-cadherin, Col-I, C3aR, C5aR, TGF-β1 and CTGF in C3a- and C5a-treated groups were higher than normal control group (P <0.05). C3aRA and C5aRA inhibited the expressions of α-SMA, Col-I, C3aR, C5aR, and up-regulated the expression of E-cadherin (P <0.05). TGF-β1 and CTGF mRNA expressions induced by C3a and C5a were partly blocked by TGF-β1RA (P <0.05).

Conclusion  C3a and C5a can induce TEMT via the up-regulations of C3aR and C5aR mRNA and the activation of TGF-β1/CTGF signaling pathway in vitro.

     

类风湿关节炎和骨关节炎患者膝关节置换术后并发症的临床对照研究

目的 :对比骨性关节炎(osteoarthritis,OA)和类风湿关节炎(rheumatoid arthritis,RA)患者膝关节置换术后并发症发生情况.方法 :选取67例RA和78例OA患者,均行膝关节置换术治疗,观察并记录患者的术前,术后3d和5d的VAS评分、ROM评分,随访2年期间并发症发生情况,对比OA和RA患者膝关节置换术后并发症发生情况.结果 :与术前相比,RA组术后5d的VAS评分明显降低,OA组术后3d,5d的VAS明显降低,OA组术后3d,5d的VAS评分明显低于RA组.术前两组ROM评分无统计学差异,与术前相比,RA组术后3 d的ROM评分明显降低,OA组术后5d的ROM评分明显增加,OA组术后3d,5d的ROM评分明显高于RA组,随访2个年期间,RA组2年内翻修率和伤口并发症发生率均明显高于OA组,关节失稳,假体松动,下肢深静脉血栓发生率比较,无统计学差异.两组主要伤口并发症为伤口渗液,发生率相比无统计学差异.其他3种并发症发生率相比,也没有统计学差异.结论 :骨关节炎患者经人工膝关节置换术治疗后,并发症发生较少,膝关节活动较术前改善明显,疼痛度减轻.     

miR-let-7d-HMGA2通路调控缺氧诱导的类风湿关节炎滑膜成纤维样细胞增殖

目的 研究缺氧在类风湿关节炎（rheumatoid arthritis, RA）滑膜成纤维样细胞（fibroblast-like synoviocytes, FLS）增殖中的作用及机制。 方法 采用HE染色法检测RA和对照骨关节炎（osteoarthritis, OA）滑膜组织FLS增生情况。分离原代RA-FLS并采用流式细胞术鉴定;将RA-FLS置于常氧（21%O2）或缺氧环境（3%O2）中培养,CCK-8法检测细胞增殖水平的变化,RT-PCR检测miR-let-7d表达的变化。通过类似物或抑制物改变miR-let-7d的表达,观察其对RA-FLS增殖、凋亡的影响;探究miR-let-7d靶基因在缺氧诱导的RA-FLS增殖中的作用。 结果 FLS在RA滑膜中增生明显,在缺氧环境下RA-FLS增殖加快,miR-let-7d表达水平降低;过表达miR-let-7d抑制RA-FLS增殖,但对细胞凋亡水平无明显影响;进一步的研究证实miR-let-7d靶基因HMGA2参与缺氧诱导的RA-FLS增殖。 结论 miR-let-7d-HMGA2通路调控缺氧诱导的RA-FLS增殖。     

MRI结合血清、关节液中NO、MMP3水平在膝关节类风湿与骨性关节炎的诊断价值

目的探讨磁共振成像(magnetic resonanceimaging,MRI)联合血清及关节液中一氧化氮(Nitric Oxide,NO)、基质金属蛋白酶-3(matrix metalloproteinase-3,MMP-3)水平鉴别诊断膝类风湿性关节炎(rheumatoid arthritis,RA)、骨关节炎(osteoarthritis,OA)的价值及影像特点分析。方法选取2017年10月-2018年10月本院收治的40例RA患者作为RA组,同期收治的44例OA患者作为OA组。比较两组MRI影像特点,血清及关节液中NO、MMP3水平,分析MRI、血清及关节液中NO、MMP3水平单独诊断及联合诊断的效能。结果 RA组内侧胫骨关节骨髓水肿率与OA组无明显差异(P>0.05),RA组内侧胫骨关节囊性坏死率显著高于OA组(P<0.05),RA组外侧胫骨骨关节骨髓水肿、囊性坏死率均显著高于OA组(P<0.05),RA组内侧、外侧II^III级半月板损伤率均显著高于OA组(P<0.05),RA组滑膜增生率显著高于OA组(P<0.05);RA组血清和关节液NO、MMP-3水平均显著高于OA组(P<0.05);经受试者工作特征曲线(receiver operating characteristic curve,ROC)分析,MRI联合血清和关节液中NO、MMP3诊断价值高于各单项检查指标。结论 RA和OA的MRI影像学图像存在一定差异,MRI联合血清和关节液NO、MMP-3指标诊断,可进一步提高两者鉴别诊断价值。     

Fcα受体在类风湿性关节炎人成纤维样滑膜细胞的表达与功能研究

目的探讨Fcα受体在类风湿性关节炎人成纤维样滑膜细胞的表达特征及其功能。方法采用RT-PCR和免疫荧光技术,从基因和蛋白水平检测Fcα受体在类风湿性关节炎人成纤维样滑膜细胞(RA FLS)的表达;采用ELISA方法,检测IgA对RA FLS分泌IL-6的影响。结果采用RT-PCR和免疫荧光染色方法,均检测到Fcα受体在RA FLS的表达。sIgA与RAFLS孵育12h后,细胞分泌IL-6的水平明显增高,差异具有显著性(P<0.01)。mIgA与RA FLS孵育12h后,细胞分泌IL-6的量无明显改变(P>0.05)。sIgA+TNF-α同时与RA FLS孵育12h后,细胞分泌IL-6含量明显高于sIgA或TNF-α单一组(P<0.01)。结论 Fcα受体在类风湿性关节炎人成纤维样滑膜细胞存在表达,sIgA增高RA FLS分泌IL-6的水平,并与TNF-α产生协同作用。     

Expression of CC Chemokine Ligand 5 in Patients with Rheumatoid Arthritis and Its Correlation with Disease Activity and Medication

Objective To determine the levels of CC chemokine ligand 5 （CCL5） in serum and synovial fluid （SF） from patients with rheumatoid arthritis （RA） and their relations with disease activity and medication. Methods CCL5 in serum and SF was quantified by enzyme-linked immunosorbent assay （ELISA） in 28 RA patients and 21 osteoarthritis （OA） patients. In RA patients, the correlations of CCL5 levels in serum and SF with disease activity were analyzed. Meanwhile, the serum CCL5 levels among RA patients treated with disease-modifying antirheumatic drugs （DMARDs）, Tripterygium Glucosides, and other Chinese herbs without disease-modifying effects were also compared. Results CCL5 levels in both serum and SF of RA patients were significantly higher than those of OA patients （P 〈 0.05）. Moreover, the level of CCL5 was higher in SF than that in serum of RA patients （P 〈 0.01）. Serum CCL5 level was correlated significantly with the number of swollen joints （r = 0.3329, P 〈 0.05）, erythrocyte sedimentation rate （r = 0.4001, P 〈 0.05）, and C reactive protein （r = 0.3735, P 〈 0.01） In addition, the level of CCL5 had a trend of lower in patients treated with DMARDs or Tripterygium Glucosides than those treated with other Chinese herbs, although the difference was not significant among those patients due to the small number of patients in each group. Conclusions In RA patients, the expression of CCL5 increases and correlates with some clinical and laboratory parameters of RA, which indicate that CCL5 plays an important role in RA and may serve as a useful marker of disease activity. DMARDs and Tripterygium Glucosides might exert their clinical effects through reducing CCL5 production in RA.