基于近10年文献数据挖掘中药内服治疗强直性脊柱炎方剂用药规律

目的:基于文献数据挖掘中药内服治疗强直性脊柱炎的用药规律,为中医药辨证论治强直性脊柱炎提供理论基础和遣方用药的参考依据。方法:检索中国知网、万方、维普等数据库中中药内服治疗强直性脊柱炎近10年临床研究文献,整理、统计和分析中药内服治疗强直性脊柱炎的用药规律。结果:获得有效文献458篇,方剂458首,中药134种,统计出30味高频中药,聚类分析发现3个有效聚类群,关联规则分析获得牛膝、狗脊、杜仲、当归、熟地黄5味核心中药。结论:中药内服治疗强直性脊柱炎以补肾强督为本,兼顾祛邪,与强直性脊柱炎本虚标实的病机具有一致性。

利用CT图像和ADINA软件建立新型正常中国男性腰椎运动节段三维有限元模型

目的探讨多节段腰椎有限元模型的建立方法,为脊柱生物力学的研究提供条件。方法选取一正常男性自愿者L3～L5节段为研究对象,通过CT断层扫描、图像数字化分析及ADINA软件处理建立多节段腰椎有限元模型,并模拟力学作用进行模型真实性验证。结果建立了正常中国男性L3～L5运动节段三维有限元模型,模型总结点数为16 532个,包括12 130个Solid单元,208个Truss单元,16个planar单元。结论利用CT图像和ADINA软件建立新型腰椎运动节段三维有限元模型,为腰椎运动节段有限元模型的建立提供了一种简便、准确的方法,为探究腰椎多个运动节段三维有限元模型在各种应力应变状态下的生物力学特性创造了条件。

Discussion on the application principle of tuina manipulations for lumbar intervertebral disc herniation in Chinese literatures in recent 30 years

Objective: To discuss the application principle in tuina manipulation for lumbar intervertebral disc herniation (LIDH) in Chinese literatures published in recent 30 years. Methods: The three major Chinese databases, Wanfang Academic Journal Full-text Database (Wanfang), Chongqing VIP Database (CQVIP) and China National Knowledge Infrastructure (CNKI), were searched to collect the studies of tuina man ipulati ons in treatment of LIDH published in rece nt 30 years. Clusteri ng an alysis was applied to an a lyze the top 20 tuina manipulati ons for LIDH. Results: The top 20 most frequently used manipulations for LIDH were Gun-rolling, Rou-kneading, Dian-digital pressing, oblique Ban-pulli ng, An-pressi ng, Tan bo-plucki ng,*Bashe rvpulli ng and exte nding, horiz on tai Tui-pushi ng, Na-graspi ng, Anrou-pressing and kneading, Dou-shaking, Yao-rocking, Ca-scrubbing, Pai-patting, post-extension Ban-pulling, Mo-rubbing, Zhen-vibrating, Nie-pinching, fist-back Ji-tapping, and dorsal Shen-extending methods. The involved manipulations can be divided into two categories by the treated body areas. One category is applied to the soft tissues, including Gun-rolling, Rou-k neading, Dian-digital pressi ng, An-pressi ng, Tan bo-plucking, horiz ontal Tui-pushi ng, Na-graspi ng, An rou-pressi ng and kneading, Ca-scrubbing, Pai-patting, Mo-rubbing, Zhervvibrating, Nie-pinching, and fist-back Ji-tapping methods. The other category is applied to bones and joints, including oblique Ban-pulling, Bashen-pulling and extending, Dou-shaking, Yao-rocking, post-extension Ban-pulling, and dorsal Shen-extending methods. Conclusion: Based on the treated body area, the tuina manipulations applied to treat LIDH are predominated by the ones performed on soft tissues, assisted by those on bones and joints. From the way of force exertion, the involved manipulations are majorly the swinging methods, followed by squeezing and pressing ones. The manipulations applied to bones and joints are predominated by the Ban-pulling ones, followed by the Bashepulling and extending ones.

独活寄生汤对膝骨性关节炎退变软骨细胞Aggrecan和Collagen Ⅹ mRNA表达的影响

目的:观察独活寄生汤血清对膝骨性关节炎退变软骨细胞Aggrecan和Collagen X mRNA表达的影响。方法:选择6例患者标本均来源于云南省中医医院骨科膝骨性关节炎住院患者,行手术截取的新鲜退变软骨组织,采用组织块法培养原代细胞;MTT法检测传代第一代细胞生长情况,并绘制生长曲线;制备独活寄生汤大鼠含药血清;均取传代第一代的退变软骨细胞,配制5%、10%、20%独活寄生汤含药血清及相应体积比浓度的生理盐水血清作为对照;MTT法检测不同浓度的独活寄生汤血清对退变软骨细胞增殖的影响;实时荧光定量PCR检测不同给药时间点各组退变软骨细胞Aggrecan和Collagen Ⅹ mRNA的表达。结果:退变软骨细胞传代第一代生长曲线见传代第8天时细胞增殖达到顶峰,故选择细胞传代第8天为给药干预时间点;与含同体积比的生理盐水血清组比较,不同浓度的独活寄生汤血清可对退变软骨细胞增殖产生促进作用(P<0.01),尤以10%独活寄生汤血清更为明显(P<0.05);与含同体积比生理盐水血清组比较,不同时间点的5%、10%、20%独活寄生汤血清干预后的退变软骨细胞Aggrecan mRNA的表达均上调(P<0.01),Collagen Ⅹ mRNA的表达均下调(P<0.01),且以10%独活寄生汤血清组的作用最为明显(P<0.05)。结论:独活寄生汤可能通过调节退变软骨组织的胶原及其蛋白多糖的表达而产生延缓膝骨性关节炎退变软骨组织的部分作用。

骨痹合剂对膝关节骨性关节炎原代软骨细胞PI3K/AKT信号通路的影响

目的:探究骨痹合剂对膝关节骨性关节炎(KOA)模型鼠软骨细胞PI3K/AKT信号通路的影响。方法:体外培养小鼠KOA软骨细胞凋亡模型,予骨痹合剂含药血清进行干预,通过MTT检测细胞生长情况,运用免疫荧光染色、RT-PCR、Western Blot法检测软骨细胞Bad、Caspase-3、Caspase-9、NF-κB蛋白水平的表达。结果:与5%和20%含药血清浓度比较,10%含药血清更加促进细胞增殖;与第4、6、8天比较,第2天的时间点各组增殖变化最为明显。与正常对照组比较,KOA模型组软骨细胞Bad、Caspase-3、Caspase-9、NF-κB蛋白表达上调,mRNA表达显著上调(P<0.01);与KOA模型组比较,KOA+骨痹合剂组软骨细胞Bad、Caspase-3、Caspase-9、NF-κB蛋白表达下调,Bad、NF-κB mRNA表达显著下调(P<0.05,P<0.01)。与正常对照组比较,KOA模型组软骨细胞PI3K、AKT、mTOR蛋白表达均显著上调(P<0.05);与KOA模型组比较,KOA+骨痹合剂组软骨细胞PI3K、mTOR蛋白表达显著下调(P<0.01)。结论:骨痹合剂能通过抑制PI3K/AKT/mTOR信号通路,增加软骨细胞的自噬能力,抑制Bad、Caspase-3、Caspase-9、NF-κB相关蛋白及基因的表达,从而减少软骨细胞的凋亡。