目的 基于胃饥饿素(Ghrelin)/核转录因子κB(nuclear factor kappa-B,NF-κB)信号通路探讨银莱汤治疗胃肠积热合并肺炎幼龄大鼠的作用机制.方法 36只SPF级4周龄雄性大鼠随机分为6组,分别为正常组、模型组、银莱汤组、胃饥饿素组、胃饥饿素受体拮抗剂组、胃饥饿素受体拮抗剂合银莱汤组,每组6只.除正常组外,其余各组均采用高热量饮食联合脂多糖(lipopolysaccharide,LPS)雾化的方式制备胃肠积热合并肺炎模型,并分别给予银莱汤、胃饥饿素或胃饥饿素受体拮抗剂处理.每日监测大鼠进食量、体质量、肛温等指标;采用苏木精—伊红(hematoxylin-eosin,HE)染色观察肺组织病理学改变;酶联免疫吸附法(enzyme-linked immuno sorbent assay,ELISA)检测各组大鼠血清中白细胞介素-1β(interleukin-1β,IL-1β)、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、白细胞介素-6(interleukin-6,IL-6)炎症因子及Ghrelin水平,分析Ghrelin与各炎症因子水平的相关性;蛋白免疫印迹法(Western blot,WB)检测肺组织中细胞核因子-κB p65(nuclear factor-κB p65,NF-κB p65)、κBα磷酸化抑制剂(phosphorylated inhibitor ofκBα,p-IκBα)、κBα抑制剂(inhibitor ofκBα,IκBα)蛋白的表达.结果 与正常组相比,模型组大鼠血清中炎症因子IL-1β、TNF-α、IL-6水平显著升高,Ghrelin水平显著降低(P<0.01),肺组织中NF-κB p65、p-IκBα相对表达显著升高,IκBα相对表达显著降低(P<0.01).与模型组相比,银莱汤组、胃饥饿素组大鼠血清中炎症因子水平显著降低,Ghrelin水平显著升高(P<0.01),肺组织中NF-κB p65、p-IκBα相对表达显著降低,IκBα相对表达显著升高(P<0.01);胃饥饿素受体拮抗剂组大鼠血清中炎症因子水平显著升高,Ghrelin水平显著降低(P<0.01),肺组织中NF-κB p65相对表达明显升高(P<0.05),p-IκBα相对表达有升高趋势(P>0.05),IκBα相对表达显著降低(P<0.01).与银莱汤组相比,胃饥饿素受体拮抗剂合银莱汤组大鼠血清中炎症因子水平显著升高,Ghrelin水平显著降低(P<0.01),肺组织中NF-κB p65、p-IκBα 相对表达显著升高,IκBα 相对表达显著降低(P<0.01).血清中Ghrelin与IL-1β水平呈负相关(r=-0.958,P<0.01);Ghrelin与TNF-α水平呈负相关(r=-0.975,P<0.01);Ghrelin与IL-6水平呈负相关(r=-0.962,P<0.01).结论 银莱汤可通过提高胃肠积热合并肺炎幼龄大鼠体内Ghrelin水平,进而抑制NF-κB炎症信号通路激活,从而起到治疗作用.

目的 探究胃肠积热合并肺炎小鼠肠系膜淋巴结与肺组织中CD80+CD86+MHC-II+的树突细胞(dendritic cell,DC)细胞的比例以及Th1、Th2、Th17、Treg细胞的比例的变化关系,探讨银莱汤对DC调控的T细胞分化的影响.方法 将24只SPF级C57/BL6J小鼠随机分为正常组、模型组、银莱汤治疗组,每组8只.采用高热量饮食饲喂合并脂多糖(lipopolysaccharide,LPS)雾化吸入的方式制备胃肠积热合并肺炎的模型组,治疗组予银莱汤(每100 g体质量予0.5 g/mL)进行灌胃治疗.隔日监测小鼠体重、活动状态等一般状况;采用HE染色观察肺组织与结肠组织病理变化;采用ELISA法检测小鼠血清及结肠组织中LPS含量;用流式细胞术分析小鼠肠系膜淋巴结及肺组织中CD80+CD86+MHC-II+的DC细胞的比例,以及Th1、Th2、Th17、Treg的比例.结果 模型组与正常组相比,肺组织炎症损伤严重,经银莱汤治疗后明显缓解,血清及结肠组织中LPS水平降低;肺组织中模型组CD80+CD86+MHC-II+的DC细胞比例显著升高(P<0.0001),经银莱汤治疗后比例下降至正常水平.结论 银莱汤可以有效缓解胃肠积热合并肺炎小鼠的肺部炎症,其作用机制可能与降低血清中LPS浓度,调节Th1、Th2、Th17、Treg细胞平衡有关.

目的 探究银莱汤对胃肠积热合并肺炎大鼠5-羟色胺(5-hydroxytryptamine,5-HT)水平,以及辅助性T细胞17(T helper cell 17,Th17)与调节性T细胞(regulatory T cell,Treg)细胞平衡的影响,阐明银莱汤治疗胃肠积热合并肺炎的相关机制.方法 将30只4周龄SPF级大鼠随机分为正常组、胃肠积热组、肺炎组、胃肠积热合并肺炎组、银莱汤组治疗组,每组6只.正常组给予大鼠维持饲料、纯水灌胃、纯水雾化;胃肠积热组给予高热量饲料配合牛奶灌胃制备胃肠积热模型;肺炎组采用脂多糖(lipopolysaccharide,LPS)(0.5 mg/mL)雾化吸入制备肺炎模型;胃肠积热合并肺炎组以特制高热量饲料联合LPS雾化制备胃肠积热合并肺炎模型;银莱汤治疗组在胃肠积热合并肺炎模型的基础上给予银莱汤(每100g体重按照0.56 g/mL)灌胃.每日监测大鼠进食量、体质量、肛温等指标.采用HE染色观察肺组织病理学改变;酶联免疫吸附法(enzyme-linked immunosorbent assay,ELISA)检测各组大鼠血清中5-HT及白细胞介素(interleukin,IL)-6、IL-1β、IL-17A、IL-10、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)等细胞因子水平;蛋白免疫印迹法(Western blot,WB)检测肠系膜淋巴结(mesenteric lymph nodes,MLNs)中Th17细胞、Treg细胞特异性转录因子Rorγt和Foxp3的表达水平;RT-PCR和WB检测结肠组织色氨酸羟化酶(tryptophan hydroxylase,Tph)1的表达.结果 与肺炎组相比,胃肠积热合并肺炎组大鼠肺部炎性损伤明显;血清5-HT、IL-10水平降低,IL-17A水平升高,TNF-α、IL-1β、IL-6等促炎因子水平升高;结肠Tph1的mRNA及蛋白表达水平降低;MLNs中Rorγt蛋白表达升高、Foxp3蛋白表达降低.与胃肠积热合并肺炎组相比,银莱汤治疗组大鼠肺部炎性损伤减轻,血清5-HT水平、IL-10水平升高,IL-17A水平降低,TNF-α、IL-1β、IL-6等促炎因子水平降低;结肠Tph1 mRNA及蛋白表达水平升高;MLNs中Rorγt蛋白表达降低、Foxp3蛋白表达升高.结论 胃肠积热合并肺炎可导致大鼠机体炎性因子水平升高、5-HT水平降低以及Th17/Treg细胞失衡;银莱汤可以通过调节胃肠积热合并肺炎大鼠5-HT水平,调节Th17/Treg细胞平衡,进而起到治疗作用.

中医药防治疫病历史悠久,积累了丰富的经验,形成了独特的辨证论治体系.疫病常用的辨证体系包括卫气营血辨证、三焦辨证、六经辨证、表里辨证,各体系能够从不同角度对于疫病病机进行辨证.在疫病的诊疗中,要注重辨证与辨病相结合,在辨证思维的指导下,辨别疫病的病性、病所、病期、病势、病理,则可确定相应的治则治法,从而确定方剂、配伍选药.文章对疫病的辨证与辨病进行了梳理和总结,有利于提高疫病的临床辨治水平.

目的:探究银莱汤对胃肠积热合并肺炎大鼠Th17/Treg细胞平衡的影响,探讨银莱汤治疗胃肠积热合并肺炎的机制.方法:将30只SPF级大鼠随机分为正常组、模型组、银莱汤治疗组,每组10只.模型组与银莱汤治疗组采用高热量饮食联合LPS雾化的方式制备胃肠积热合并肺炎模型,银莱汤治疗组给予银莱汤(0.5g·mL-1·100 g-1)灌胃治疗.每日监测大鼠进食量、体质量、肛温等指标;采用HE染色观察肺组织炎性损伤情况;ELISA法检测各组大鼠血清中TNF-α、IL-1β、IL-6、IL-17A、TGF-β、IL-10等细胞因子水平;流式细胞术分析外周血及肠系膜淋巴结(MLNs)中Th17、Treg细胞比例;RT-PCR检测肺组织ROR γ t、Foxp3 mRNA表达.结果:与模型组比较,银莱汤治疗组肺部炎性损伤明显缓解,血清TNF-α、IL-1 β、IL-6水平显著降低(P＜0.05,P＜0.01);外周血及MLNs中Th17细胞比例显著下降,Treg细胞比例显著升高(P＜0.01,P＜0.05);同时,银莱汤治疗组外周血IL-17A表达显著降低(P＜0.05),TGF-β、IL-10表达显著升高(P＜0.05);肺组织ROR γ t mRNA表达显著降低(P＜0.01),Foxp3 mRNA表达显著升高(P＜0.01).结论:银莱汤可有效缓解胃肠积热合并肺炎大鼠肺组织炎性损伤,其作用机制可能与调节Th17/Treg细胞平衡有关.

目的 基于中医传承辅助平台V2.5软件,探讨活血化瘀法治疗膝骨关节炎的组方用药规律.方法检索中国期刊全文数据库(CNKI)、万方数据库(Wanfang)、维普数据库(VIP),收集活血化瘀法治疗膝骨关节炎的相关文献,录入中医传承辅助平台建立数据库,采用关联规则、复杂系统熵聚类等方法进行相关数据挖掘.结果共筛选出155个中药处方,涉及164味中药,对其进行分析,方剂中应用频次在前3位的活血药分别是牛膝、当归、鸡血藤,频次最高的药性为温,药味为甘,药物归经为肝.通过关联规则分析,挖掘出16个核心组合和8个新处方.结论活血化瘀法治疗膝骨关节炎,药物的配伍以牛膝为核心,和血药与活血药相须为用,最常配伍补益肝肾药,次为益气补血药.

目的:探究汉黄芩素对巨噬细胞炎症反应中氧化应激的抑制作用.方法:将巨噬细胞RAW264.7分为对照组(正常培养不予刺激),模型组(LPS和ATP联合刺激,LPS刺激4 h后加入ATP刺激30 min),汉黄芩素干预组(同样予以LPS和ATP联合刺激,LPS刺激的同时加入汉黄芩素).检测试剂盒检测SOD、NO、MDA分泌水平,免疫荧光检测各组细胞Nrf2的核转位情况,RT-qPCR检测Nrf2和抗氧化酶mRNA转录水平.结果:与模型组相比,汉黄芩素可减少LPS-ATP联合刺激的巨噬细胞MDA、NO分泌水平,上调Nrf2 mRNA的表达并促进胞浆内Nrf2的核转位,上调胞内抗氧化酶HO-1、SOD、GPx、CAT及NQO-1 mRNA的转录,增加SOD的活性.结论:汉黄芩素对LPS-ATP诱导的巨噬细胞氧化应激具有抑制作用,可能是通过抑制氧化应激来下调ROS水平,起到减轻炎症反应的作用.

目的 通过观察藤莓汤(Tengmei Decoction,TMD)对胶原诱导性(collagen-induced arthritis,CIA)大鼠滑膜中突变型P53 (Mutant P53,mt-p53)、增殖诱导配体(a proliferation-inducing ligand,APRIL),白细胞介素2 (Lnterleukin 2,IL-2)表达的影响,探讨藤莓汤抑制类风湿关节炎(rheumatoid arthritis,RA)滑膜免疫炎性损伤的分子机制.方法 建立CIA大鼠模型,中药给药组分为TMD高剂量组、TMD低剂量组,分别以TMD生药量31.8、15.9g/(kg·d-1)灌胃;模型组、阳性对照组分别予去离子水10 mL/(kg·d-1)、来氟米特1.87mg/(kg-1·d-1)灌胃;另设正常对照组,予去离子水10 mL/(kg·d-1),各组连续干预12周.干预结束后检测mt-P53、APRIL、IL-2蛋白及mRNA表达.结果 与正常组比较,模型组APRIL、mt-P53、IL-2 mRNA转录水平上调(P＜0.01);mt-P53、IL-2蛋白表达上调(P＜ 0.01,P＜0.05).与模型组比较,各治疗组APRIL mRNA转录水平,mt-P53、IL-2mRNA转录水平及蛋白表达水平下调,(P＜ 0.01,P＜0.05);结论TMD能够降低大鼠关节滑膜、血清中mt-P53、IL-2、APRIL表达水平,改善关节炎模型大鼠关节滑膜免疫炎性损伤,可能与TMD抑制关节滑膜过度增殖,降低炎症因子的表达有关.

目的 观察秦苓液对尿酸性肾病大鼠过氧化物酶体增殖物激活受体 γ 辅助激活因子-1α(peroxi-some proliferator activated receptor coactivator-1 alpha,PGC-1α)、白介素-1β(interleukin beta,IL-1β)、受激活调节正常T细胞表达和分泌因子(regulated upon activation normal T cell expressed and secreted factor,RANTES)的影响.方法采用腺嘌呤灌胃伴酵母饲料喂养大鼠的方法进行造模,成模后随机分为模型组,阳性药物组,秦苓液大、中、小剂量组,每组12只大鼠.选6只正常大鼠作为正常对照组.各组分别用药连续干预6周和8周后采用实时荧光定量逆转录聚合酶链反应(real time reverse transcription-polymerase chain reaction,RT-PCR)、蛋白免疫印迹法(Western blot)、免疫组化和酶联免疫吸附试验(enzyme linked immunosorbent assay,ELISA)检测大鼠PGC-1α、IL-1β、RANTES基因和蛋白表达水平.结果与正常对照组比较,6周时和8周时模型组PGC-1α 蛋白表达水平及8周时PGC-1α基因转录水平显著下调,6周时IL-1β基因转录、蛋白表达水平和RANTES蛋白表达水平及8周时两者水平显著上调(P<0.05,P<0.01).与模型组比较,6周时秦苓液各剂量组PGC-1α蛋白表达水平及8周时中、小剂量组PGC-1α基因水平及蛋白表达水平显著上调,6周时秦苓液各剂量组IL-1β基因转录及大、中剂量组IL-1β蛋白表达水平以及各剂量组RANTES蛋白表达水平显著下调,8周时秦苓液小剂量组IL-1β及中、小剂量组RANTES基因转录及中、小剂量组IL-1β、RANTES蛋白表达水平显著下调(P<0.05,P<0.01).结论秦苓液抑制UN模型大鼠免疫炎性损伤,其分子机制可能与上调PGC-1α的水平,抑制IL-1β、RANTES的生物学活性有关.

目的:通过观察虎杖对胶原诱导性关节炎(CIA)模型大鼠滑膜组织、血清中抑癌基因p53突变型(mt-p53)、增殖诱导配体(APRIL)、肿瘤坏死因子-α(TNF-α)表达的影响,探讨虎杖抑制类风湿关节炎滑膜免疫炎性损伤的作用机制.方法:采用大鼠尾根部注射牛Ⅱ型胶原方法制备CIA模型,将成模大鼠按随机数字表法分为模型组、阳性对照组、虎杖2倍剂量组、虎杖常量组,另设正常对照组,每组6只.正常对照组与模型组予去离子水10mL·kg-1·d-1灌胃,阳性对照组予来氟米特1.87mg·kg-1·d-1灌胃,虎杖2倍剂量组、虎杖常量组分别以虎杖颗粒8、4g·kg-1·d-1灌胃,连续干预12周.观察各组大鼠偶数周体质量、AI评分及各组大鼠滑膜组织中APRIL、mt-p53、TNF-αmRNA,mt-p53、TNF-α蛋白及血清中TNF-α蛋白表达情况.结果:与正常对照组比较,模型组大鼠体质量及AI评分有明显变化(P＜0.05,P＜0.01);与模型组比较,各治疗组大鼠体质量及AI评分有明显改善.与正常对照组比较,模型组APRIL、mt-P53、TNF-α mRNA转录水平显著上调(P＜0.01),mt-P53、TNF-α蛋白表达水平显著上调(P＜0.01);与模型组比较,各治疗组APRIL、mt-p53、TNF-αmRNA转录水平显著下调(P＜0.01);mt-p53、TNF-α蛋白表达水平显著下调(P＜0.01).结论:虎杖改善CIA大鼠关节滑膜免疫炎性损伤的机制可能与抑制滑膜细胞增殖相关.

目的:探讨三金合八正散与诺氟沙星对湿热型石淋大鼠的疗效分析.方法:将雄性SD大鼠分为空白组,模型组,西药组(诺氟沙星),中西药联合组和中药高、中、低剂量组,造模后第14日,分别给予空白组、模型组生理盐水灌胃,其他各组给予相应药物灌胃治疗.每3 d监测各组大鼠尿液pH值,于手术前、治疗前、治疗完成时分别对各组大鼠进行泌尿系统超声检查.造模后第28日,收集、称重各组大鼠的尿路结石.结果:尿液pH值检测结果显示,模型组大鼠尿液pH值持续上升,呈碱性;中西药联合组及中药高、中、低剂量组尿液出现酸化.超声影像检查显示,空白组仅见膀胱形态不规则;各治疗组超声影像主要表现为肾脏增大、肾门处出现强回声伴声影、膀胱形态不规则、膀胱壁增厚、膀胱内出现回声.模型组上述改变较为典型,中药低剂量组无肾脏改变,中西药联合组及中药高、中剂量组仅见膀胱形态不规则、膀胱壁增厚.膀胱内大鼠结石重量检测显示各治疗组结石重量与模型组比较,差异均有统计学意义(P<0.01).其中西药组、中西药联合组及中药中剂量组结石重量比较,差异均无统计学意义(P>0.05);中药高剂量组与西药组、中西药联合组、中药中剂量组、中药低剂量组大鼠结石重量比较,差异均有统计学意义(P<0.01).结论:三金合八正散能够减轻湿热型石淋大鼠泌尿系统病理改变,酸化尿液,促进结石溶解及排出,其治疗效果优于单纯使用诺氟沙星,且与中西药联合治疗比较,治疗效果无明显差异.

目的:探究汉黄芩素对巨噬细胞炎症反应的抑制作用.方法:设正常对照组,LPS和ATP联合刺激组(LPS刺激4 h后加ATP刺激30 min),汉黄芩素干预组(刺激的同时加入汉黄芩素).利用免疫荧光法观察各组细胞NF-κB的核定位,荧光定量PCR法检测各组细胞IL-1β、IL-18、IL-6、TNF-α、NLRP3及Caspase-1的mRNA水平,流式细胞术检测各组细胞活性氧(ROS)水平,酶联免疫吸附法检测胞外IL-6和TNF-α 水平.结果:与LPS和ATP刺激组相比,汉黄芩素干预组细胞胞内NF-κB核定位明显减少,胞内IL-1β、IL-18、IL-6、TNF-α、NLRP3和Caspase-1的mRNA,胞内ROS及胞外IL-6和TNF-α 水平都显著降低(P<0.01).结论:汉黄芩素可能通过减少巨噬细胞ROS的产生,降低NF-κB的核定位,进而弱化NF-κB调控的炎症相关分子的基因转录来干预巨噬细胞的炎症反应.

目的 探究参芪瓜蒌薤白半夏汤治疗肝肾阴虚型冠状动脉粥样硬化性心脏病(简称冠心病)合并糖尿病的临床效果.方法 将100例肝肾阴虚型冠心病合并糖尿病患者,随机分为观察组(50例)和对照组(50例).对照组采用常规西药治疗,观察组在对照组基础上联用参芪瓜蒌薤白半夏汤进行治疗.比较两组患者的生活质量、血脂、血管内皮功能和疗效.结果 经卡方检验,观察组的总有效率(84.00％)显著高于对照组(64.00％),差异具有统计学意义(P<0.05).治疗后两组患者的甘油三酯(triglyceride,TG)、胆固醇(cholesterol,TC)、低密度脂蛋白胆固醇(low-density lipoprotein cholesterol,LDL-C)及内皮素(Endothelin,ET)水平均降低(P<0.05),且观察组患者的TG、TC、LDL-C及ET水平低于对照组(P<0.05).治疗后两组患者的生理功能(physiological Function,PF)、社会职能(social function,SF)、躯体疼痛(bodily pain,BP)、精力(vitality,VT)、 总体健康(general health,GH)、情感职能(role emotional,RE)、生理职能(role physical,RP)、精神健康(Mental Health,MH)评分、高密度脂蛋白胆固醇(high density lipoprotein cholesterol,HDL-C)、一氧化氮(nitric oxide,NO)水平均升高,且观察组患者的的PF、RP、BP、GH、VT、RE、SF、MH评分、HDL-C及NO水平高于对照组(P<0.05).结论 在常规西药基础上,参芪瓜蒌薤白半夏汤治疗冠心病合并糖尿病肝肾阴虚证的临床效果较好,可有效调节血脂代谢,减轻血管内皮损伤,改善患者生活质量,值得临床推广应用.

The aim of the present study was designed to investigate that Platycodon grandiflorum saponins (PGS) exerted protective effects against testicular injury induced by scrotal hyperthermia. PGS (15, 30 mg/kg) were administered intragastrically to mice for 14 days, then exposed to a single scrotal heat treatment at 43 °C for 18 min on the 7th day. Heat stress (HS) induced spermatogenic damage was associated with a significant loss of leydig cells and the changes of serum testosterone, oxidative stress and apoptosis markers, and activated MAPK signaling pathway. In contrast, PGS treatment normalized HS-induced histopathological changes and prevented the activation of MAPK signaling pathway, which was contributed to oxidative stress and apoptosis in the testis of treated mice. In conclusion, our findings clearly demonstrated that PGS exhibited a significant protective effect against HS-induced testicular dysfunction, largely dependent upon the inhibition of oxidative stress associated apoptosis via partly regulation of MAPK signaling pathway.

目的 通过观察虎杖对胶原诱导性关节炎(CIA)大鼠踝关节病理及滑膜组织、血清中过氧化物酶体增殖物激活受体-γ(PPARγ)、p65、白细胞介素17(IL-17)表达的影响,探讨虎杖抑制类风湿关节炎(RA)滑膜免疫炎性损伤的作用机制.方法 采用大鼠尾根部注射牛CⅡ方法制备CIA模型,将成模大鼠按随机数字表法分为模型组、阳性对照组、虎杖2倍剂量组、虎杖常量组,另设正常对照组,每组6只.正常对照组与模型组每天予去离子水10 mL/kg灌胃,阳性对照组每天予来氟米特1.87 mg/kg灌胃,虎杖2倍剂量组、常量组每天分别以8、4 g/kg灌胃,连续干预12周.采用光镜观察各组大鼠踝关节病理改变.运用RTPCR、Western Blot及ELISA检测技术,观察各组大鼠滑膜组织、血清中PPARγ、p65、IL-17 mRNA及蛋白表达情况.结果 与正常对照组比较,模型组大鼠踝关节关节周围纤维组织增生,炎性细胞浸润;与模型组比较,虎杖常量组大鼠关节软骨、关节腔未见明显病变.与正常对照组比较,模型组PPARγ、p65、IL-17 mRNA及蛋白表达上调(P＜0.01).与模型组比较,虎杖2倍剂量组及常量组p65、IL-17 mRNA及蛋白表达均下调(P＜0.01);PPARγ mRNA蛋白表达水平上调(P＜0.01).结论 虎杖改善CIA模型大鼠关节滑膜免疫炎性损伤的机制,可能与调节PPARγ/NF-κB信号途径相关.

骨关节炎(osteoarthritis,OA)是一种以慢性关节软骨的退行性变和丢失为主,以及关节边缘和软骨下骨骨质增生为主要特征的关节炎疾病.膝骨关节炎(knee osteoarthritis,KOA)是40岁以后的最常见的慢性、进展性、退行性OA.KOA 的常见症状多有局部疼痛、晨僵、关节肿胀、畸形伴有活动受限,最终可导致残疾[1].研究发现体质量指数、关节外伤史、家族史、居住环境潮湿、关节负重、职业运动过度锻炼、代谢系统疾病是膝骨关节炎的重要危险因素[2].对于KOA晚期患者会出现明显的功能障碍及活动受限,最终出现关节变形,失去关节功能,由此导致的关节置换手术治疗不仅增加医疗费用更增加患者痛苦.

强直性脊柱炎( ankylosing spondylitis, AS)是一种原因不明的,以骶髂关节及脊柱中轴关节为主要病变部位的炎症性疾病,其主要病理改变是肌腱、韧带及骨附着点炎症. AS患者常常出现腰背部僵直和疼痛,夜间痛明显,活动后症状缓解,疾病发展最终导致关节畸形、活动受限甚至功能障碍. AS多见于青壮年,发病年龄多在10～40 岁,男性发病率明显高于女性,目前我国患病率约为0. 3％ [1].

OBJECTIVE To optimize the preparation methods of harpagide of Scrophularia ningpoensis. METHODS Orthogonal test was adopted to optimize extraction technology of harpagide with extraction capacity as the index. The macroporous resin was employed to enrich the harpagide. Taking the adsorption and desorption rates as the indexes, the best type of macroporous adsorption resin was screened and the enrichment technology was optimized. The purification technology of harpagide was optimized using column chromatography by investigating the stationary phase, eluting solvents, loading amount of sample, the diameter height ratio of chromatographic column and eluting volumns. RESULTS The optimized extraction technology of harpagide was that Scrophularia ningpoensis was extracted with water for 3 times, 1.5 h for each time. The optimized enrichment technology was that the SP825 type of macroporous adsorption resin was employed to enrich the harpagide with the following parameters: the sample concentration at 0.07 g·mL-1, 1: 6 of the ratio of diameter and height, the absorptive flow rate at 1.0 mL·min-1, and 0.40 g·mL-1 of the maximum adsorption capacity. The optimized purification process using silica gel and C18 column chrimatography was as follows: 1: 70 of the ratio of loading sample amount and silica gel, 1: 15 of the ratio of diameter and height, the eluant solvent of a mixture solvent system of chloroform and methanol, eluting with 2 BV of chloroform/methanol (4: 1), then eluting with 1 BV of chloroform/methanol (2: 1); the final purification using C18 column chrimatography (the ratio of diameter and height was 1: 9). CONCLUSION The established preparation method of harpagide is convenient and good repeatability with a better effect. The purity of prepared harpagide is over 98％, and the yield is high. And the preparetion methods can be used for bulk production. It provides a reference for the further application and product development of Scrophularia ningpoensis.

Objective] To explore the effect of modified Simiao Yong’an decoction on collagen induced arthritis about arthritis index (AI), the joint tissue inflammatory pathological manifestations, and effect on protein expression of IL-6,IL-17,TNF-αin rats. [Methods] The successful CIA models of SD rats were randomly divided into model group, positive group (leflunomide), and high, medium, low dose group of Chinese medicine, and normal control group, 6 rats in each group. The intervention and treatment period was 12 weeks. AI val-ues of each rat were evaluated every week. At 12 weeks, rats were executed and right ankle joint of each group of rats was taken. Joint pathlological changes of each right ankle were observed. At the same time levels of IL-6, IL-17 and TNF-αin serum were examined by ELISA, mRNA transcription levels of IL-6, IL-17and TNF-αin synovial were detected by RT-PCR. [Results] AI scores of the three Chi-nese medicine groups decreased significantly (P﹤0.05 or P﹤0.01) in 6~12 weeks compared with the model group, and in the 8~10 weeks AI scores were even improved significantly than positive group (P﹤0.05 or P﹤0.01). Histological examination showed that the ankle joint cartilage pathological had an improvement in the medium dose of modified Simiao Yong’an decoction group compared with the control model group. Compared with the model group, mRNA and protein expression of IL-6, IL-17and TNF-αwere down regulated in all treat-ment groups significantly (P﹤0.01). [Conclusion] The anti-inflammatory action mechanism on CIA rats of modified Simiao Yong’an de-coction might achieve by reducing expression of IL-6, IL-17 and TNF-α.

Objective:To explore the effects of Astragalus glycoproteins on collagen-induced arthritis mice′s specific transcription factors, T-bet and GATA-3, expression, and to clarify the immune mechanism of Astragalus glycoprotein on the treatment in collagen-induced arthritis mice.Methods:CIA model was induced by bovine Ⅱcollagen in mice.Mice were randomly divided into a CIA model group, a hydrocortisone positive control group, a Astragalus glycoprotein low dose group, a middle dose group and a high dose group.HE was used to observe the CIA mice spleen tissues damage.IFN-γ and IL-4 level were measured with flow cytometry in CIA mice.Western blot was used to analyze T-bet and GATA-3 protein expression.Results:Compared with the model group, Astragalus glycoprotein improved spleen tissue damage in CIA mice, and inhibited the infiltration of inflammatory cells.Astragalus glycoprotein reduced IFN-γand IL-4 level (P<0.05) and T-bet and GATA-3 protein expression (P<0.05).Conclusion:The mechanisms of action of Astragalus glycoprotein on CIA mice may be related to the decrease of T-bet and GATA-3 expression and function balance of the Th1 and Th2 cells.