This monthly, peer-reviewed journal includes studies devoted to molecular medicine, underscoring aspects including pharmacology, pathology, genetics, neurosciences, infectious diseases, molecular cardiology and molecular surgery. In vitro and in vivo studies of experimental model systems pertaining to the mechanisms of a variety of diseases offer researchers the necessary tools and knowledge with which to aid the diagnosis and treatment of human diseases.

慢性筋骨病以肝肾亏虚为病理基础,筋骨失衡为外在表现,气血失和是慢性筋骨病关键病机,其发病与气血、经络、肝肾存在着密切的联系.筋骨-经络-肝肾的功能网络影响着慢性筋骨病的发生发展,肝主筋,肝胆互为表里,少阳属胆,胆经主筋骨病,少阳主筋所生病,提示少阳为枢影响着筋骨的生理病理状态,揭示了慢性筋骨病的发生、发展和演变.因此,文章以"少阳为枢"为切入点,针对慢性筋骨病的中医病理特点,通过调节肝肾气血来纠正筋骨的失衡状态,以达治疗慢性筋骨病的目的,旨在丰富中医防治慢性筋骨病的病因病机.

This study was conducted to identify whether the TLR4/MyD88/NF-κB signalling pathway plays a vital role in osteoarthritis (OA) treatment with Duhuo Jisheng Decoction (DHJSD) on the basis of a network pharmacology approach (NPA)-integrated experiment. Two experiments were conducted as follow: NPA for DHJSD using six OA-related gene series and the key pathway was screened out using NPA. NPA identified a vital role for the TLR4/MyD88/NF-κB signalling pathway in OA treatment with DHJSD, the conventional western blot analysis and qPCR confirmed it. Furthermore, changes of miR-146a-5p and miR-34a-5p in the cellular models were recovered by DHJSD administration, which synergistically contributed to OA therapy. The toll-like receptor signalling pathway and the NF-κB signalling pathway were meaningfully enriched by the miRNA-regulated gene pathways. This study identified and confirmed the TLR4/MyD88/NF-κB signalling pathway is an essential inflammatory signalling pathway in the DHJSD underlying OA treatment. The results provide a basis for further evaluation of the regulatory mechanism of the drug’s efficacy in treating OA.

目的:探讨人参在治疗骨关节炎(OA)中发挥抗炎镇痛作用的可行性.方法:从中药系统药理数据库及分析平台(TCMSP)中筛选人参中口服生物利用度≥30％和类药性≥0.18的成分,从活性化合物专家网站中检索OA疼痛密切相关白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)的抑制剂,在Discovery studio(DS)模拟平台,分别建立人参和抑制剂分子数据集;在定量构效关系(DS QSAR)模块下,计算和分析两分子数据集的化学空间,两数据集中的化合物在空间上距离越近,代表具有相似作用的可能性越大.以IL-1β、IL-6、TNF-α为OA抗炎镇痛的治疗靶点,从蛋白质数据库(RCSB PDB)中下载其与配体的复合物结构,代码分别为6Y8M、1ALU和2AZ5,在DS LigandFit中,研究人参分子数据集中化合物与抗炎镇痛靶点IL-1β、IL-6、TNF-α之间的相互作用,从中筛选出比蛋白与各自原配体作用的DOCK-SCORE高的化合物,视为人参抗炎镇痛的活性成分.结果:人参分子数据集含有化学成分22个,抑制剂分子数据集含有化学成分26个;在三维化学空间中,人参和抑制剂分子数据集中化合物均聚集在后背部,且距离较近,具有相似的化学空间,意味着可能具有相似的作用;以IL-1β、IL-6和TNF-α与各自原配体的DOCK-SCORE为阈值,从人参中筛选出抗炎镇痛的潜在活性化合物有11个,分别为脱氧三尖杉酯碱(Deoxyharringtonine)、石竹胺(Dianthramine)、苏齐内酯(Suchilactone)、花生四烯酸(Arachidonate)、山柰酚(Kaempferol)、人参皂苷Rg5(Ginsenoside Rg5)、人参皂苷Rh2(Ginsenoside Rh2)、五味子酯乙(Gomisin B)、苯代南蛇碱(Celabenzine)、菊黄质(Chrysanthemaxanthin)和5-苯甲酰基-4-乙酰基锥序南蛇藤呋喃四醇(Malkangunin).结论:综合分析人参的化学空间及其存在抗炎镇痛的活性成分,认为人参在治疗OA方面具有抗炎镇痛的作用,本研究可为健脾法在OA临床治疗中的应用提供新依据.

Postmenopausal osteoporosis (PMOP) is an estrogen deficiency-induced bone loss, which has been shown an association with an altered gut microbiota (GM). Gut microbiota-bone axis has been recognized as a crucial mediator for bone homeostasis. Icariin (ICA) is an effective agent to delay bone loss by regulating the bone homeostasis. Thus, we hypothesize that ICA can prevent bone loss by modulating GM and regulating metabolite alterations. The effects of ICA on bone metabolism improvement in ovariectomized (OVX) rats and their relationships with the GM and fecal metabolites were investigated. Micro-computed tomography (micro-CT) and hematoxylin-eosin (HE) staining showed a typical bone boss in OVX group, while ICA or estradiol (E2) administration exhibited positive effects on bone micro-architecture improvement. The GM such as Actinobacteria, Gammaproteobacteria, Erysipelotrichi, Erysipelotrichales, Enterobacteriales, Actinomycetales, Ruminococcus and Oscillospira significantly correlated to serum bone Gla-protein (BGP), receptor activator of nuclear factor-κB (RANK), receptor activator of nuclear factor-κB ligand (RANKL), osteoprotegerin (OPG) and tartrate resistant acid phosphatase (TRACP). Further t-test revealed a substantial variation of the GM and fecal metabolites in different treatments. Among them, Lachnoclostridium, Butyricimonas, Rikenella, Paraprevolla, Adlercreutzia, Enterorhabdus, Anaerovorax, Allobaculum, Elusimicrobium, Lactococcus, Globicatella and Lactobacillus were probably the key microbial communities driving the change of bile acid, amino acid and fatty acid, thereby leading to an improvement of PMOP. The significant up-regulation of L-Saccharopine, 1-Aminocyclohexadieneacid and linoleic acid after ICA administration suggested important contributions of amino acid and fatty acid metabolisms in the prevention and treatment of PMOP. Taken together, our study has provided new perspectives to better understand the effects of ICA on PMOP improvement by regulating GM and the associated fecal metabolites. Our findings contribute to develop ICA as a potential therapy for PMOP.

目的 采用计算机模拟技术,从活性成分的角度探讨当归活血和止痛作用及其关联性.方法 ① 从中药系统药理学数据库及分析平台(TCMSP)中,检索当归的化学成分125个,以凝血酶(Thrombin)、血栓素A2受体(TXA2R)、纤溶酶原激活物抑制物1型(PAI-1)、凝血因子Ⅸa(FactorⅨa)为活血功效的靶点,以p38、肿瘤坏死因子α(TNF-α)、诱导型一氧化氮合酶(iNOS)、磷酸二酯酶4A(PDE4A)为止痛功效的靶点,在蛋白质数据库(RCSB PDB)中下载有配体结合的蛋白复合物结构,代码分别为1AWH、6IIV、7AQF、3LC3、1OUY、2AZ5、4NOS和3TVX;利用分子对接技术,筛选大于蛋白复合物结构中的原配体的DOCK-SCORE高的化合物,视为当归中活血功效和止痛功效的活性成分.② 构建当归活血功效和止痛功效的活性成分数据集,提取其全局指纹,计算其Tanimoto相似系数来反映两活性成分数据集的化学结构特征相似度.当相似系数值为0时,表示两数据集间没有相同的分子结构片段;当系数为1时,则表示有相同的字节编码,也就表示有相同的分子结构片断,即系数越接近1,代表两数据集在分子结构特征方面的关联性越好.③ 利用Cytoscape生物网络平台,构建当归活性成分与功效靶点相互作用的可视化网络,选择度值≥3的节点,视为网络中的重要活性成分和靶点.结果 ① 从当归化学成分中筛选出8个活血功效的活性成分和17个止痛功效的活性成分,其中,活血和止痛功效的共同活性成分有6个,主要属于苯肽类、磷酯类、生物碱类、有机酸类等,75％的活血功效的成分具有止痛作用,但仅约35％的止痛功效的成分具有活血作用.② 当归活血和止痛功效活性成分数据集全局指纹的Tanimoto相似系数为0.7736,显示两个功效活性成分之间在结构特征上具有很好的关联性.③ 当归活性成分-靶点网络显示了活性成分与功效靶点之间存在"一对多,多对一"的特点,活血功效的重要活性成分为异汉防己碱、欧当归内酯A和阿魏酸松柏酯,重要靶点为Thrombin、FactorⅨa和PAI-1;止痛功效的重要活性成分为欧当归内酯A和阿魏酸松柏酯,重要靶点为PDE4A、iNOS和TNF-α.结论 从活性成分的角度,计算机模拟直观显示当归的活血和止痛作用,且存在关联性;同时,活血的活性成分在很大程度上可达到止痛的功效,且当归活血功效与止痛功效的成分可通过与既能活血又能止痛活性成分的组合发挥协同作用,为理解"活血止痛"的内在联系提供依据.

This study aimed to identify whether the NF-κB signaling pathway plays a key role in the treatment of osteoarthritis (OA) with Bushen Zhuangjin Decoction (BZD) based on a typical network pharmacology approach (NPA). Four sequential experiments were performed: 1) conventional high-performance liquid chromatography (HPLC), 2) preliminary observation of the therapeutic effects of BZD, 3) NPA using three OA-related gene expression profiles, and 4) verification of the key pathway identified by NPA. Only one HPLC-verified compound (paeoniflorin) was identified from the candidate compounds discovered by NPA. The genes verified in the preliminary observation were also identified by NPA. NPA identified a key role for the NF-κB signaling pathway in the treatment of OA with BZD, which was confirmed by conventional western blot analysis. This study identified and verified NF-κB signaling pathway as the most important inflammatory signaling pathway involved in the mechanisms of BZD for treating OA by comparing the NPA results with conventional methods. Our findings also indicate that NPA is a powerful tool for exploring the molecular targets of complex herbal formulations, such as BZD.

A large volume sample stacking (LVSS) method in micellar electrokinetic chromatography (MEKC) with diode array detector was developed for the simultaneous separation and analysis of five compounds: protocatechuic acid, protocatechuic aldehyde, caffeic acid, syringetin and vanillin in Cibotium barometz. The electrophoretic separation was performed in a 10 mM sodium dodecyl sulfate (SDS) and 50 mM sodium borax-sodium dihydrogen phosphate system (pH = 8.5) with 10% methanol at a separation voltage of 30 kV after optimizing the typical parameters. The detection limits were from 32 pg to 65 pg, which were around 12–27 times lower than MEKC, and 500 times less than reported methods. Finally, the established method was validated to be applicable for the determination of protocatechuic acid and caffeic acid in Cibotium barometz. This proposed method is expected to facilitate the quality control of Cibotium barometz.

慢性筋骨病是筋骨系统动静力失衡的综合征,以脏腑气血失和、筋骨失衡为病理基础,发病过程涉及五体病机演变、肉筋骨力学失衡、五主失调等.脾(肉)-肝(筋)-肾(骨)是防治慢性筋骨病的主基线,以“和”“衡”为内核理念.经络是五体结构与功能信息物质交换的基础,五体-经络-脏腑功能网络是筋骨系统的结构与功能基础,也是慢性筋骨病治疗的关键靶点.因此,文章基于经络与五体理论,结合生物力学、分子学、细胞学等现代科学方法,从五体-经络-脏腑功能网络的角度,探索慢性筋骨病的病理基础与治疗方法,旨在丰富慢性筋骨病的病因病机,完善五体论治的科学内涵.

目的:建立高效液相色谱质谱联用(HPLC-MS)测定青风藤中生物碱的方法.方法:以70％乙醇进行索氏提取,HPLC-MS分析方法定性,HPLC分析方法定量.色谱条件为反相色谱柱Agilent ZORBAX SB-C1s(5μm,3.0mm×250mm),柱温:30℃,进样量:10μL,流动相甲醇(A)-5mmol/L醋酸铵缓冲液(B) =55:45(V:V),流速:0.5mL/min,进行线性梯度洗脱.结果:在最佳的分离条件下,5种生物碱在25min内得到很好的分离效果,且适用于青风藤中青藤碱和木兰花碱的定量分析.经测定,所购青风藤药材中青藤碱和木兰花碱的含量分别为6.11和3.22mg/g.结论:本研究建立的HPLC-MS方法具有回收率高、重现性好等优点,适用于青风藤中生物碱含量的测定.

Knee osteoarthritis (KOA) is a common disease with no specific treatment. Icariin (ICA) is considered an agent for KOA. This study aimed to confirm the pain-related neuromodulation mechanisms of ICA on KOA. Three experiments were designed: (1) verifying the therapeutic effects of ICA in vivo and in vitro, (2) exploring the potential pain-related neuromodulation pathways involved in ICA treatment by functional magnetic resonance imaging (fMRI) and virus retrograde tracing (VRT) and (3) confirming the pain-related targets by tandem mass tag (TMT)-based quantitative proteomics and bioinformatic analyses. Experiment 1 verified the efficacy of ICA in OA animal and cell models. Experiment 2 found a series of brain regions associated with KOA reversed by ICA treatment, indicating that a pain-related hypothalamic-mediated neuromodulation pathway and an endocannabinoid (EC)-related pathway contribute to ICA mechanisms. Experiment 3 explored and confirmed four pain-related genes involved in KOA and ICA treatment. We confirmed the key role of pain-related neuromodulation mechanisms in ICA treatment associated with its analgesic effect. Our findings contribute to considering ICA as a novel therapy for KOA.

目的:探讨补肾壮筋汤抑制膝骨关节炎软骨退变的作用机制.方法:选取2月龄SPF级雄性SD大鼠共45只,随机数字表法分为空白组(15只)与造模组(30只),空白组行假手术,造模组采用改良Hulth法建立动物模型.造模组随机数字表法分为模型组(15只,0.9％氯化钠溶液灌胃)和补肾壮筋汤组(15只,补肾壮筋汤10.5g·kg-1·d-1灌胃);空白组(15只,0.9％氯化钠溶液灌胃)1次/d,连续干预12周.HE染色观察关节软骨组织形态结构的变化;Mankin's评分法评估关节软骨退变程度;ELISA法检测关节滑膜组织中白细胞介素1 β(IL-1β)、肿瘤坏死因子-α(TNF-α)、基质金属蛋白酶13(MMP-13)的含量;Western Blot检测软骨组织中解聚蛋白样金属蛋白酶4(ADAMTS-4)、解聚蛋白样金属蛋白酶5(ADAMTS-5)、基质金属蛋白酶3(MMP-3)、MMP-13的表达量.结果:①HE染色显示空白组软骨结构清晰,潮线清晰可见,软骨表面光滑完整,软骨细胞分布均匀,骨小梁宽度和密度适中.模型组结构分辨不清,形态不规整,软骨变薄,潮线模糊,扭曲或中断,骨小梁稀疏.补肾壮筋汤组软骨及软骨下骨的改变介于空白组和模型组之间.②关节软骨的Mankin's评分,模型组显著高于空白组(P＜0.01),补肾壮筋汤组显著低于模型组(P＜0.05).③膝关节滑膜组织中IL-1β、TNF-α、MMP-13的表达量,模型组显著高于空白组(P＜0.05,P＜0.01),补肾壮筋汤组显著低于模型组(P＜0.05,P＜0.01).④关节软骨组织中ADAMTS-4、ADAMTS-5、MMP-3、MMP-13蛋白表达量,模型组显著高于空白组(P＜0.01),补肾壮筋汤组显著低于模型组(P＜0.05,P＜0.01).结论:补肾壮筋汤通过降低滑膜组织中TNF-α、IL-1β、MMP-13含量,抑制关节软骨组织中ADAMTS-4、ADAMTS-5、MMP-3、MMP-13蛋白的表达,从而延缓软骨退变.

背景:Wnt/β-catenin信号通路在骨关节炎的炎症反应病理过程中扮演着重要角色,而独活寄生汤拆方有效抑制软骨细胞的炎症反应有待进一步深入研究。目的:探讨独活寄生汤拆方是否可以通过调控Wnt/β-catenin信号通路抑制由脂多糖诱导的软骨细胞炎症反应。方法:（1）取SD雄性大鼠,采用机械Ⅱ型胶原酶消化法获取膝关节软骨细胞,倒置相差显微镜观察软骨细胞的形态结构,Ⅱ型胶原免疫组化鉴定软骨细胞。（2）用不同质量浓度的独活寄生汤拆方（300,400,500 mg/L）干预由脂多糖（10μg/L）诱导的软骨细胞炎症模型,干预8 h后,采用酶联免疫吸附（ELISA）法测定各组软骨细胞培养液中白细胞介素1β、肿瘤坏子因子α水平,确定独活寄生汤拆方干预浓度。（3）将第2代软骨细胞分为4组:空白组含正常培养液;模型组培养液中含10μg/L脂多糖;独活寄生汤拆方组培养液中含10μg/L脂多糖和400 mg/L独活寄生汤拆方;抑制剂组培养液中含10μg/L脂多糖和10 mg/L Dickkopf-1。干预8 h后,采用Western blot法检测β-catenin、Wnt-4、Frizzled-2、GSK-3β、CKI-ε的蛋白表达量。结果与结论:（1）软骨细胞鉴定:获取的软骨细胞Ⅱ型胶原免疫组化染色胞浆呈棕黄色,具备软骨细胞典型特征;（2）ELISA结果显示:模型组培养液中白细胞介素1β和肿瘤坏子因子α水平均高于空白组,400 mg/L独活寄生汤拆方干预后两种炎症因子水平较模型组显著降低,所以确定独活寄生汤拆方干预浓度为400 mg/L;（3）Western blot结果显示:模型组β-catenin、Wnt-4、Frizzled-2、CKI-ε的蛋白表达量均高于空白组,而GSK-3β蛋白表达量低于空白组;独活寄生汤拆方组和抑制剂组β-catenin、Wnt-4、Frizzled-2、CKI-ε蛋白表达量低于模型组,而GSK-3β蛋白表达量高于模型组。（4）结果表明:独活寄生汤拆方通过调控Wnt/β-catenin信号通路抑制由脂多糖诱导的软骨细胞炎症反应。

An enzyme-catalyzed fluorescence "switch" type sensor was constructed for the determination of alkaline phosphatase (ALP) activity by combining the fluorescence quenching effect of Ag+ on ultrathin g-C3N4 nanosheets (CNNSs) with the simple redox reaction of AA and Ag+. Briefly, Ag+ exhibits a significant quenching effect on the fluorescence of CNNSs. Thus the fluorescence signal of the CNNS-Ag+ system is extremely weak even in the presence of l-ascorbic acid-2-phosphate (AAP) ("off" state). When ALP coexists in the system, the enzyme can specifically catalyze the hydrolysis of AAP to form ascorbic acid (AA), which reduces Ag+ to Ag0. In this case, the fluorescence signal of the system is recovered ("on" state). Based on this principle, a signal-enhanced CNNS fluorescence sensor was developed to determine the activity of alkaline phosphatase. The experimental results show that the detection range of alkaline phosphatase is 0.5-20 U L-1, and the detection limit is 0.05 U L-1 (S/N = 3). Meanwhile, this method was used to assay ALP in serum samples.

膝为筋之府,以筋骨失衡为重要病理基础,临床以骨关节炎为多发.经筋是软组织复合结构的平衡体,足三阳、三阴经筋深聚于膝关节,从而维持关节的结构与功能.肌筋膜是维持肌肉-骨骼系统力学分配协调性及膝关节动静力平衡的整体结构.膝骨关节炎病理特点是筋骨失衡、以筋为先,筋-骨-筋失衡的恶性循环是其迁延进展的的主要因素.经筋与肌筋膜理论为膝骨关节炎的诊疗提供了理论依据,两者的核心理念一致,从整体观来揭示膝骨关节炎的生理、病理变化,为膝骨关节炎辨-防-治的一体化提供新的思路.因此,文章以经筋理论为切入点,借助肌筋膜理论,初探膝骨关节炎点-线-面的治疗方案,旨在为膝骨关节炎的防治提供新策略.

Objective:To explore the pharmacodynamic material basis, action targets and modes of Achyranthis Bidentatae Radix (Niuxi in Chinese) on the simultaneous treatment of Wei syndrome and Bi syndrome in osteoarthritis (OA) from the molecular level.Methods:①Seventy-three chemical components of Niuxi were retrieved from the databases of China National Knowledge Infrastructure (CNKI) and PubMed, and to built molecular dataset of Niuxi. Meanwhile, three drugs related to articular cartilage proteoglycan synthesis stimulation (the treatment for Wei syndrome) and twenty-eight drugs related to anti-inflammation analgesia (the treatment for Bi syndrome) on OA were searched from the DrugBank database, and their corresponding molecular datasets of treating Wei syndrome and Bi syndrome were also built. Based on the platforms of quantitative structure-activity relationship and principal component analysis, the distributions of the above datasets were analyzed in the chemical space.②Matrix metalloproteinase-1 (MMP-1), matrix metalloproteinase-3 (MMP-3), and transforming growth factor beta-1 (TGF-β1) were chosen as the targets of treating Wei Syndrome of OA, while interleukine-1 beta (IL-1β), interleukine-6 (IL-6), tumor necrosis factor-alpha (TNF-α) were chosen as the targets of treating Bi syndrome of OA. The platforms of molecular docking and biological network were used to study the interactions between the Niuxi compounds and above targets, and Niuxi compound-target networks related to the treatment of Wei syndrome and Bi syndrome were constructed to analyze the pharmacodynamic material basis, action targets and modes of Niuxi in the therapy of OA.Results:①Comparison of the chemical space distributions between molecular datasets of Niuxi and drugs indicated that the chemical space distributions of the former were more diverse than those of the latter, and the former were the same, or close to the latter with the treatment of Wei syndrome at the back of chemical space, while the former were the same, or close to the latter with the treatment of Bi syndrome at the bottom back corner of chemical space. These revealed the possible effects of Niuxi on Wei syndrome and Bi syndrome of OA.②The compound-target networks showed that the main pharmacodynamic material basis of Niuxi contained saponins, phytosterones, flavonoids and alkaloids. Meanwhile, the Niuxi compound numbers of treating Bi syndrome and Wei syndrome were thirty-seven and twenty-six, respectively. Among them, twenty compounds could simultaneously treating Bi syndrome and Wei syndrome of OA. The maximum number of targets interacting with them was six. Furthermore, in the compound-target network of Niuxi in treating Bi syndrome of OA, the key compound nodes of Niuxi were puerarin, baicalin, quercetin-3-O-rutinose and kaempferol-3-O-glucoside, which belonged to flavonoids, and the key target nodes were IL-1β and TNF-α. In the compound-target network of Niuxi in treating Wei syndrome of OA, the key compound node of Niuxi was baicalin, which belonged to flavonoids, and the key target node was MMP-1.Conclusion:Computer simulation intuitively showed the multi-target effects of Niuxi in simultaneously treating Wei syndrome and Bi syndrome of OA through the modes like promiscuous drug and combination drug. This could provide a basis for Niuxi therapeutic for OA and new drug development from Niuxi.

学科是高校教育的基本功能单位,其学术水平与影响力在一定程度上标志高校的地位.研究生培养是学科内涵建设的重要组成部分,既依托于学科发展,又能加快学科的内涵建设,且研究生培养质量与高素质的师资队伍、良好的教学环境与严谨的学术氛围等因素密切相关.正确认识研究生培养与学科内涵建设之间的内在关系,实现协调发展、互动共融,为学科的可持续发展提供原动力.因此,本文基于中西医结合研究院的研究生培养发展历程与现状,从相离、相切、相交、相融等四种类型,探讨了研究生培养与学科内涵建设的相辅相成,从互动共融的角度,揭示了研究生培养与学科内涵建设的内在关系.

ETHNOPHARMACOLOGICAL RELEVANCE:Tougu Xiaotong capsules (TXC) are an herbal compound commonly used to treat osteoarthritis (OA) in China. AIM OF THE STUDY:We attempted to verify TXC's therapeutic effects and mechanisms related to the p38 mitogen-activated protein kinase (MAPK) pathway in vivo and in vitro. MATERIALS AND METHODS:TXC's therapeutic effects were assessed by observing cartilage degeneration and inflammatory factors in a modified Hulth's model (in vivo) and a lipopolysaccharides (LPS)-exposed cellular model (in vitro). The expression of biomarkers related to p38 MAPK pathway-mediated inflammation was also investigated. RESULTS:TXC treatment reversed cartilage degeneration related biomarkers (ADAMTS 4, ADAMTS 5, Col I, Col V, MMP 3, MMP 9, and MMP 13) and inflammation factors (IL-1β, TNF-α, and IL-6) in both the animal and cellular OA models. Expression of p-p38 MAPK was downregulated following TXC administration, and changes to microRNAs in the cellular models were recovered. These results indicated that the p38 MAPK pathway-related mechanism may involve therapeutic effects of TXC. CONCLUSIONS:This study verified TXC's efficacy to treat OA in vivo and in vitro and suggests that p38 MAPK pathway-related mechanisms may be involved in TXC's therapeutic effects.

骨关节炎是影响中老年人健康的常见疾病,明确本病的病因病机是提高中医疗效的关键.软骨下骨重建稳态,为肾所主,肾气亏虚,髓生化乏源,一是骨失所养,则发骨痿,以软骨下骨重建失衡为病理表现;二是脑失所充,则神经环路功能紊乱,从而参与骨关节炎肾虚的病理调控.鉴于骨关节炎软骨下骨重建失衡以肾虚为关键诱因,与下丘脑-垂体-靶腺轴有关.因此,在肾通于脑的中医理论指导下,以骨关节炎软骨下骨重建失衡为研究对象,综合国内外相关文献,采用数据挖掘的方法,初探下丘脑-垂体-靶腺轴与骨关节炎的关系,旨在丰富肾虚的病因病机理论,进一步诠释肾通于脑的科学内涵.

基于中西医结合研究生传统培养模式的科研创新思维缺乏、实践操作能力不足等亟待解决的问题,中西医结合学科创新中西医结合研究生培养的模式,建立"科研思维-实验技能-SCI论文写作"的三位一体多元化培养模式,以培养中西医结合创新型人才为目的,合理设置课程,采用以问题为核心、以学生为主导、以教师为引导的培养方法,突出培养中西医结合思维、科研能力与创新能力,推动中西医结合研究生培养与中西医结合学科建设的互动共融,从而实现中西医结合学科的可持续发展战略.