目的 探讨乌头汤对白细胞介素-1β(IL-1β)诱导的退变软骨细胞外基质稳态的影响,为乌头汤的临床应用提供理论依据.方法 选取4周龄SPF级雄性SD大鼠10只,5%异氟醚吸入麻醉后剔取大鼠双膝关节软骨,使用机械-酶消化法分离后培养软骨细胞,并将软骨细胞随机分为空白组、模型组和乌头汤组.空白组使用含10%FBS 的DMEM培养基进行培养;模型组采用10 ng/mL IL-1β溶液干预24 h复制退变软骨细胞模型;乌头汤组采用10 ng/mL IL-1β干预24 h后使用150 μg/mL乌头汤水提物干预24 h.采用qPCR和Western blot检测3组软骨细胞中基质金属蛋白酶(MMP)-3、MMP-13、含Ⅰ型血小板结合蛋白基序的解聚蛋白样金属蛋白酶(AD-AMTS)-4和ADAMTS-5的mRNA相对表达水平和蛋白表达量.结果 与空白组比较,模型组中MMP-3、MMP-13、ADAMTS-4、ADAMTS-5 mRNA相对表达水平和蛋白表达量均明显提高(P均＜0.05);与模型组比较,乌头汤组MMP-3、MMP-13、ADAMTS-4、ADAMTS-5 mRNA相对表达水平和蛋白表达量均明显降低(P均＜0.05).结论 乌头汤通过抑制软骨细胞中MMP-3、MMP-13、ADAMTS-4和ADAMTS-5的表达,来维持软骨细胞外基质稳态,延缓骨关节炎软骨退变.

目的:观察膝骨关节炎患者易筋经干预前后,疼痛、焦虑以及脑区局部一致性(ReHo)的变化情况,探讨易筋经调控情绪缓解膝骨关节炎慢性疼痛的脑机制.方法:将38例膝骨关节炎(KOA)慢性疼痛患者随机分配到易筋经组、静蹲组各19例,最终易筋经组18例,静蹲组16例完成试验.两组分别进行易筋经训练、静蹲训练,干预周期均为每周3次,每次30min,连续12周.所有受试者干预期间均未服用止痛药物.干预前后分别进行疼痛视觉模拟评分法(VAS)、汉密尔顿焦虑量表(HAMA)评分,并进行静息态fMRI扫描,分析组间、组内差异.结果:12周干预后,两组患者VAS评分均有改善(P＜0.05),易筋经组效果优于静蹲组(P＜0.05);易筋经组干预前后HAMA评分显著下降(P＜0.05).易筋经组干预后右侧颞极:颞中回、右侧颞下回、右侧颞中回、右侧枕中回、右侧中央沟盖、右侧脑岛、右侧距状裂周围皮层、右侧颞上回、右侧缘上回、右内侧和旁扣带脑回、左内侧和旁扣带脑回、左侧补充运动区、右侧中央后回、右侧中央前回等脑区ReHo值较干预前增强(P＜0.05);静蹲组干预后右侧梭状回Re-Ho值较干预前增加(P＜0.05);组间比较发现,易筋经组较静蹲组右内侧和旁扣带脑回、右侧角回、右侧顶上回等脑区ReHo值变化明显(P＜0.05).相关性分析发现,KOA慢性疼痛患者疼痛与焦虑呈正相关(P＜0.05);右侧角回、右内侧和旁扣带脑回激活峰值与疼痛程度呈负相关,与焦虑程度呈正相关(P＜0.05).结论:易筋经能够缓解KOA慢性疼痛、焦虑症;KOA慢性疼痛严重程度与焦虑症相关;易筋经调节情绪相关脑区激活程度,从而缓解KOA慢性疼痛.

Endoplasmic reticulum stress (ERS) has been identified to be an important factor leading to chondrocyte apoptosis in osteoarthritis (OA). Previous studies have confirmed that Achyranthes bidentata polysaccharides (ABPS) can inhibit chondrocyte apoptosis; however, the mechanism of action of ABPS on chondrocyte ERS remains unclear. Thus in this study, we aim to investigate whether ABPS could inhibit OA-associated chondrocyte apoptosis by regulating ERS, especially by observing the relationship between the lncRNA NEAT1 and miR-377-3p, to explore further the protective mechanism of ABPS in OA. In vitro and in vivo experiments showed that ABPS inhibited chondrocyte ERS by regulating the expression of lncRNA NEAT1 and miR-377-3p. Moreover, both lncRNA NEAT1 silencing and miR-377-3p inhibition could attenuate the therapeutic effect of ABPS on ERS. Dual-luciferase results indicated that miR-377-3p targets the lncRNA NEAT1 gene in mouse chondrocytes. Therefore, we concluded that ABPS could inhibit thapsigargin (TG)-induced chondrocyte ERS through the lncRNA NEAT1/miR-377-3p axis.

中药复方以及中药单体可调控类风湿关节炎相关长链非编码RNA(LncRNA)分子的表达水平,进而延缓类风湿关节炎疾病进程.基于中医药辨证论治,从祛风通络、温经散寒、健脾除湿、补益肝肾角度,探讨中药复方以及中药单体调节关联LncRNA治疗类风湿关节炎的分子作用机制,为中医药防治类风湿关节炎提供新的途径与方法.

Achyranthes bidentata polysaccharides (ABPS) is an active ingredient of the flowering plant Achyranthes bidentata that has been previously reported to be effective for the treatment of osteoarthritis (OA). However, the underlying molecular mechanism remain to be fully clarified. Emerging studies have shown that the long non-coding RNA (lncRNA) growth arrest-specific transcript 5 (GAS5) is involved in the pathogenesis of OA. Therefore, the present study aimed to investigate the potential mechanism of ABPS by focusing on its effects on the regulation of chondrocyte extracellular matrix (ECM) homeostasis, with particular emphasis on lncRNA GAS5. In the present study, the modified Hulth method was used to construct OA rats, which were gavaged with 400 mg/kg ABPS for 8 weeks. Histopathological changes in cartilage and subchondral bone were evaluated by hematoxylin-eosin staining and Safranin O-fast green staining. In in vitro experiments, IL-1β-treated chondrocytes were infected with Lenti-lncRNA GAS5. Fluorescence in situ hybridization assay was performed to measure the expression of the lncRNA GAS5 in chondrocytes. Moreover, the relative expression level of lncRNA GAS5 in cartilage tissue and chondrocytes was detected using reverse transcription-quantitative PCR. Western blot analysis was used to detect protein expression levels of MMP-9, MMP-13, TIMP-1, TIMP-3 and type II collagen in cartilage tissue and chondrocytes. The results indicated that ABPS delayed the degradation of the ECM by chondrocytes in addition to reducing lncRNA GAS5 expression both in vivo and in vitro. Furthermore, silencing of lncRNA GAS5 expression in IL-1β-treated chondrocytes downregulated the protein expression of MMP-9 and MMP-13 whilst upregulating the expression of tissue inhibitor matrix metalloproteinase (TIMP)-1, TIMP-3 and type II collagen. To conclude, the present study provides evidence that ABPS can inhibit the expression of lncRNA GAS5 in chondrocytes to regulate the homeostasis of ECM, which in turn may delay the occurrence of cartilage degeneration during OA.

Objective To evaluate the effect of Rongjin Niantong Recipe on knee osteoarthritis model rats, and to explore the mechanism of delaying cartilage degeneration in knee osteoarthritis based on long noncoding RNA (lncRNA) NEAT1 and Nrf2/ARE pathway. Methods After adaptive feeding for one week, a total of 45 SPF SD rats aged two months were randomly divided into blank group and sodium iodoacetate group, with 15,30 cases in each group. Under anesthesia, 0.05 mL sodium iodoacetate at a concentration of 20 mg/mL was injected into the right knee joint to establish the knee osteoarthritis model, and the blank group was injected with the same amount of normal saline. After modeling was assessed to be successful, the sodium iodoacetate group were randomly divided into model group and Rongjin Niantong Recipe group, with 15 cases in each group. The Rongjin Niantong Recipe group were given 1.9 g/(kg·d) the medicine by gavage, and the blank group and the model group were given the same amount of normal saline by gavage for eight weeks. After the intervention, all groups were sacrificed under anesthesia, and the right knee tissues were separated and collected; HE staining was used to observe the pathological changes; Western blot was used to detect the expression levels of Nrf2, heme oxygenase-1 (HO-1), NAD (P) H quinone oxidoreductase-1 (NQO-1), kelch like ECH-associated protein 1 (Keap1) and inducible nitric oxide synthase (iNOS) in cartilage; Real-time PCR was used to detect the expression of lncRNA NEAT1 in cartilage tissue. Results 1) Pathological changes of cartilage tissue: the cartilage matrix was light red and uniform, with complete tissue structure and clear tissue margins of each layer in the blank group; in the model group, the chondrocytes grew in clusters with thinner tangent layer. The surface layer was destroyed and the transitional layer and the radiation layer became disordered and partial calcified. There were obvious calcifications in the calcified layer. In addition, the adhesion line between the calcified layer and the subchondral bone fluctuated greatly and was discontinuous. The tangents of the superficial layer in the Rongjin Niantong Recipe group were completed and basically paralleled to the articular surface, and the transitional layer, radiation layer, calcification layer and other layers were relatively clear. 2) Expressions of Nrf2/ARE pathway related proteins in the cartilage: compared with the blank group, the protein expression levels of Keap1 and iNOS of the model group significantly increased (P<0.05) and the protein expression levels of Nrf2, HO-1 and NQO-1 significantly decreased (P<0.05). Compared with the model group, the protein expression levels of Keap1 and iNOS in the Rongjin Niantong Recipe group significantly decreased (P<0.05), while the protein expression levels of Nrf2, HO-1 and NQO-1 significantly increased (P<0.05). 3) Expressions of lncRNA NEAT1 in cartilage: compared with the blank group, the expression level of lncRNA NEAT1 in the model group was significantly higher (P<0.05); compared with the model group, the expression level of lncRNA NEAT1 in the Rongjin Niantong Recipe group significantly decreased (P<0.05). Conclusion Rongjin Niantong Recipe can delay cartilage degeneration in rats with osteoarthritis. The mechanism may be related to the down-regulation of lncRNA NEAT1 level, up-regulation of Nrf2 signal and antioxidant signal molecules expressions, and down-regulation of pro-oxidation signal molecules and inhibition of oxidative stress level.

目的:探讨易筋经功法对膝骨关节炎(KOA)患者下肢肌群协调激活能力的影响.方法:将2018年9月至2019年9月在福建中医药大学附属康复医院门诊和社区招募58例KOA患者随机分为试验组30例和对照组28例,分别进行易筋经功法训练与本体感觉训练.通过采集两组受试者骨关节炎指数和坐-站、上/下楼梯任务中下肢肌群的肌电值,分析比较膝关节屈肌共激活比(CR)变化差异,同时检测两组干预前后关节液中白细胞介素(IL)-1、IL-6、肿瘤坏死因子α(TNF-α)变化.结果:试验组总有效率显著优于对照组,WOMAC疼痛评分低于对照组(P＜0.05).坐-站任务中,干预后试验组膝关节屈肌CR较干预前减小(P＜0.05),且小于同期对照组(P＜0.05);治疗组在降低IL-l、IL-6含量方面优于对照组(P＜0.05).结论:易筋经功法锻炼可以提高下肢肌群的协调激活能力,降低膝关节屈肌共激活比,改善膝关节稳定性,并能抗炎止痛.

目的:采用静息态功能磁共振成像、任务态功能磁共振成像观察易筋经对膝骨关节炎慢性疼痛患者脑功能的影响.方法:选取KOA慢性疼痛患者38例,按照1∶1的比例随机分为试验组与对照组,每组各19例,试验组进行易筋经功法训练,对照组进行静蹲训练,连续12周,每周3次.训练前后采用西部安大略省和麦克马斯特大学骨关节炎指数(WOMAC)评分进行评估,并观察静息态低频振幅率(fALFF)以及任务态脑功能激活程度.结果:试验组脱落1例,对照组脱落3例.经12周干预后,两组WOMAC总分、WOMAC疼痛评分、WOMAC功能障碍评分均显著降低(P＜0.05);试验组干预后WOMAC僵硬评分显著降低(P＜0.05),试验组干预后WOMAC疼痛评分、WOMAC功能障碍评分低于对照组(P＜0.05).干预后,静息态功能磁共振成像检测发现,试验组KOA慢性疼痛患者右侧颞中回、双侧楔叶、右侧颞上回、右侧楔前叶、左内侧和旁扣带脑回、左侧补充运动区、右侧中央前回fALFF值增加;对照组右侧背外侧额上回、右侧顶上回fALFF值下降;组间比较发现,试验组左侧楔叶、右侧楔前叶fALFF值改变优于对照组.干预后,任务态功能磁共振成像检测发现,试验组双侧补充运动区、左侧小脑上部、左侧楔叶、左侧楔前叶激活增加;对照组右侧楔叶激活减弱.且试验组WOMAC疼痛评分与右侧楔前叶fALFF差值呈正相关,与左侧楔叶、左侧楔前叶任务态激活差值呈负相关.结论:相比一般运动疗法,身心疗法易筋经改善KOA慢性疼痛的作用效果更好;易筋经缓解KOA慢性疼痛患者静息痛、诱发痛的作用机制与默认网络相关,易筋经可能通过同时调控感觉运动网络,从而缓解KOA慢性疼痛.

类风湿关节炎是涉及炎症、骨破坏、滑膜增生的慢性自身免疫性疾病，熊果酸治疗类风湿关节炎效果显著，可通过抑制炎症因子的表达、调节免疫反应、骨保护、诱导滑膜成纤维细胞凋亡等多种途径发挥作用。通过分析熊果酸治疗类风湿关节炎的可能作用途径，为部分阐述熊果酸的科学内涵提供理论依据。

目的 基于PERK通路探讨荣筋拈痛方(RJNTD)对毒胡萝卜素(TG)诱导的软骨细胞内质网应激反应的抑制作用.方法 将30只4周龄SPF级雄性C57BL/6小鼠处死后,体外分离双膝软骨细胞置于低糖DMEM培养基培养,经Ⅱ型胶原免疫细胞化学染色法鉴定后将软骨细胞分成空白组、对照组、模型组和中药组.空白组常规培养4 h,对照组常规培养4 h后更换300μg/mL RJNTD培养液培养12 h,模型组用25μmol/L TG培养液培养4 h后改为常规培养,中药组用25μmol/L TG培养液培养4 h后更换300μg/mL RJNTD培养液培养12 h.干预后采用Real-time PCR检测各组软骨细胞中miRNA-377-3p相对表达水平;Western blot检测各组软骨细胞中内质网降解增强子(EDEM1)、蛋白激酶R样内质网激酶(PERK)、转录激活子4(ATF4)、免疫球蛋白重链结合蛋白(BIP)与DNA损伤诱导基因153(GADD153)蛋白表达水平.结果 对照组各指标与空白组比较均无统计学意义(P均>0.05);与空白组比较,模型组及中药组miRNA-377-3p相对表达水平显著降低(P<0.05),且中药组较模型组降低更不明显(P<0.05);与空白组比较,模型组及中药组EDEM1、PERK、ATF4、BIP、GADD153蛋白表达水平均升高(P均<0.05),且中药组上述各指标较模型组升高更不明显(P均<0.05).结论 RJNTD可通过PERK通路抑制内质网应激反应,进而发挥延缓TG诱导的软骨细胞退变作用,其潜在作用机制可能与调节miRNA-377-3p相关.

目前,治疗类风湿关节炎的优选策略是控制炎症与其他病理反应,缓解其疼痛不适等临床症状.槲皮素具有抑制炎症介质的表达和分泌、抗氧化、免疫调节、抑制基质金属蛋白酶的生成,以及抑制滑膜细胞增生等多种生物活性,可抑制类风湿关节炎的病理进程.槲皮素在预防和治疗类风湿关节炎上具有广阔的应用和发展前景.

目的:探讨膝骨关节炎患者中医体质的分布特点及其与体质量指数、年龄、性别的相关性.方法:收集84例膝骨关节炎患者的基本信息,判断体质类型,分析其与相关指标的相关性.结果:阳虚质、血瘀质、阴虚质患者最多;兼夹体质占总数的50.0％;百分比＞2％的体质有9种;痰湿质的超重和肥胖患者多于偏瘦和正常体重者,气虚、血瘀质肥胖患者多于偏瘦者;偏颇质大龄患者多于年轻者;女性阳虚患者多于男性;平和质与年龄呈负相关(P＜0.05),阳虚质与性别呈正相关(P＜0.05),痰湿质与体质量指数呈正相关(P＜0.05).结论:膝骨关节炎患者的主要体质为阳虚、血瘀、阴虚质;随着年龄增加,患者逐渐倾向于兼夹体质;女性患者阳虚质比例多于男性患者;体质量增加,痰湿质的比例也增加.

类风湿关节炎的治疗方法颇多,但以改善病情、缓解临床症状为主.山柰酚是从姜科植物山柰的根茎提取的黄酮醇类化合物,具有抗氧化、抗炎及免疫调节等作用,尤其在干预类风湿关节炎的病理进程方面已成为研究热点之一.探讨山柰酚治疗类风湿关节炎的作用机制,以期为山柰酚对类风湿关节炎治疗的进一步研究提供思路.

膝骨关节炎的治疗以改善临床症状、延缓疾病进展为主要策略.升麻素苷具有抗炎、镇痛、解热,以及抗血小板聚集等多种药理活性作用,可以通过抑制炎症反应,抗氧化作用,抑制基质金属蛋白酶的表达等,缓解膝骨关节炎的炎性症状,干预其病理进程.升麻素苷对细胞周期的调节作用,对核转录因子-κB信号通路和丝裂原活化蛋白激酶信号通路调控机制,尚有待进一步研究.

随着全社会人口老龄化的加剧,绝经后女性罹患骨质疏松性骨关节炎的风险亦呈现高发趋势,严重危害中老年人的健康.研究证实血管形成及功能异常是加剧骨质疏松、骨关节炎病理退变的重要事件.H型血管(内皮细胞)在骨与软骨损伤修复中兼具成骨和成血管偶联功能,其形态与功能异常将影响骨质疏松、骨关节炎的损伤修复.铁死亡作为近年来发现的一种新型细胞死亡模式,其主要由铁依赖性脂质过氧化和活性氧诱导损伤引起细胞膜断裂,线粒体变小等改变.而H型血管铁死亡对骨质疏松性骨关节炎病程的影响途径及调节机制尚需进一步探讨,旨在为今后以H型血管铁死亡为切入点进而防治骨质疏松性骨关节炎开辟新方向.

目的:基于生物信息学和网络药理学方法,筛选荣筋拈痛方君药牛膝相关活性成分,通过动物体内体外实验观察其对骨关节炎相关治疗靶点的影响.方法:通过中药系统药理学数据库与分析平台(TCMSP)数据库筛选中药牛膝主要活性成分和治疗靶点;通过GEO数据库获得与疾病的差异表达基因,并进行交叉分析;采用实时荧光定量聚合酶链式反应(Real-time PCR),蛋白免疫印迹法(Westemblot)检测牛膝主要活性成分对骨关节炎大鼠体内体外富集治疗靶点的影响.结果:牛膝作用骨关节炎相关活性成分共20种,槲皮素为其中重要成分之一;靶基因共3个,其中骨桥蛋白(OPN),纤维蛋白溶解抑制剂-1(PAI-1)等为该网络中的关键基因;基因本体(GO)分析共获得相关条目227条,涉及到的功能包括创伤生理反应调节(GO:1903034),创伤反应负调节(GO:1903035)等.京都基因与基因组百科全书(KEGG)通路分析获得相关通路12条,涉及细胞外基质受体相互作用(hsa04512)等.动物实验中,与正常组比较,模型组OPN,PAI-1 mRNA和蛋白表达量增加与模型组比较,槲皮素组OPN,PAI-1 mRNA和蛋白表达量降低(P＜0.05).细胞实验中,与正常组比较,模型组OPN,PAI-1蛋白表达量增加,Ⅱ型胶原(CollagenⅡ)蛋白表达量降低;与模型组比较,槲皮素组和抑制剂组OPN,PAI-1蛋白表达量降低,CollagenⅡ蛋白表达量明显增加(P＜0.05).结论:牛膝可能主要通过其活性成分(槲皮素)下调软骨细胞OPN,PAI-1靶mRNA表达,上调CollagenⅡ蛋白表达,实现抑制软骨退变,防治骨关节炎.

H型血管作为一种高表达血小板-内皮细胞粘附分子-1(CD31)与内皮黏蛋白(Emcn)的特殊血管类型,常分布于成骨活跃的部位,因其周围聚集大量骨祖细胞,具有成血管与成骨偶联作用,与骨质疏松症病程预后转归关系密切.探讨H型血管与骨形成之间的偶联作用对骨质疏松症病理进程的影响机制,以期为骨质疏松症的防治提供新思路.

Objective:To construct the active component target of Hindu datura and the disease target of rheumatoid arthritis by using network pharmacology, to predict the specific molecular signal and pathway of hindu datura in the treatment of rheumatoid arthritis, and to analyze its potential therapeutic target and molecular mechanism.Methods:All the chemical components of hindu datura were summarized and screened through Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform(TCMSP)database, retrieval was performed with the preset oral bioavailability(OB)≥30%and drug like(DL)≥0.18.Uniprot database was used to screen the entire correlation basis of the effective chemical compound.After screening the disease target with"rheumatoid arthritis"as the retrieval word using GeneCards and OMIM database, the superimposed target area between the drug target of hindu datura and the disease target of rheumatoid arthritis was summarized and analyzed, and it could be used as the prediction target gene of hindu datura for treating rheumatoid arthritis.Network targets were constructed and analyzed for the exported data based on Cytoscape 3.7.1 software and STRING 7.8 database.Finally, GO functional enrichment analysis and KEGG signal pathway analysis were performed to further screen the main targets and signal pathways.Results:①Through screening and analysis, 27 effective compounds, 318 corresponding target genes and 125 predicted target genes were obtained for the treatment of rheumatoid arthritis.②The core genes in PPI network mainly included JUN, AKT1, RELA, MAPK1, etc.③GO functional enrichment analysis showed that the biological process(BP)for the treatment of rheumatoid arthritis by hindu datura mainly involves response to lipopolysaccharide, response to lipopolysaccharide, response to molecule of bacterial origin, response to metalion, response to oxidative stress, response to steroid hormone, cellular response to oxidative stress, reactive oxygen species metabolic process, response to oxygen levels, etc..The cell component(CC)consisted of membrane raft, membrane region, plasma membrane raft and presynaptic membrane; molecular functions(MF)mainly involved the nuclear receptor activity, transcription factor activity(direct ligand regulated sequence-specific DNA binding), steroid hormone receptor activity, cytokine receptors, cytokine activity, DNA-binding transcription activator activity, RNA polymeraseⅡtranscription factor binding, kinase regulator activity, receptor ligand activity, etc.The analysis of KEGG signaling pathway showed that the obvious pathway of hindu datura in the treatment of rheumatoid arthritis may involve IL-17 signaling pathway, TNF signal pathway, HIF-1signalpathway, Toll-like receptor signal pathway, etc.Conclusion:The potential mechanism of hindu datura for the treatment of rheumatoid arthritis is to exert anti-inflammatory, analgesic and antioxidant effects, which involve a number of interactive signal pathways.

目的:基于核转录因子-κB(NF-κB)炎症相关信号通路,观察乌头汤水提物对脂多糖(LPS)诱导体外培养软骨细胞炎症模型的影响.方法:①制备乌头汤水提物;②分离、培养软骨细胞;③噻唑蓝(MTT)法检测乌头汤对LPS诱导软骨细胞活性的影响;采用Western Blot法检测NF-κB p65、IκB激酶复合物(IKK)、磷酸化核因子 κB抑制蛋白(pIκB)含量表达.结果:①MTT实验结果显示,乌头汤水提物对LPS诱导软骨细胞的最佳干预时间和浓度分别为24 h和150μg?mL-1;②Western Blot检测结果显示,乌头汤水提物100μg?mL-1组、150μg?mL-1组、200μg?mL-1组对LPS诱导的软骨细胞干预24 h后,可调节与炎症相关的NF-κB p65、IKK、pIκB含量表达,尤其以乌头汤水提物150μg?mL-1组变化显著(P<0.01).结论:乌头汤通过降低LPS诱导的软骨细胞中与炎症相关的NF-κB途径调节因子含量表达,发挥抗炎作用.

目的:利用生物信息学方法分析肿瘤坏死因子-α(TNF-α)和白细胞介素-17A(IL-17A)对骨关节炎患者成纤维样滑膜细胞的作用机制.方法:从GEO数据库中下载GSE93720基因芯片数据集,利用GEO2R筛选出差异表达基因.用DAVID 6.8在线数据库对差异表达基因进行GO分析和KEGG信号通路分析,String数据库构建蛋白质间相互网络,导入Cytoscape 3.7.1软件进行可视化编辑,筛选出网络中的核心基因,然后用MCODE插件进行子网络模块分析.结果:共筛选出差异表达基因256个,其中上调基因213个,下调基因43个.差异最显著的5个基因是C15orf48、CXCL8、CCL20、CXCL3、CXCR4.上调的差异基因GO分析主要涉及免疫反应、炎症反应、信号转导、细胞因子活性、趋化因子活性等.上调的差异基因KEGG信号通路分析主要涉及细胞因子-细胞因子受体相互作用、肿瘤坏死因子信号通路、趋化因子信号通路等.结论:利用生物信息学方法分析TNF-α 和IL-17A诱导的骨关节炎成纤维样滑膜细胞的基因表达谱变化,为探究骨关节炎的发病机制提供指导.