Following the publication of the above article, and a Corrigendum (doi: 10.3892/mmr.2025.13581) that was published to rectify errors associated with the published versions of Figs. 5, 8, 9 and 10, an interested reader contacted the Editorial Office to explain that they had identified additional issues in need of further investigation. Subsequently, the authors recognized that there were further problems associated with the manuscript requiring attention which arose while they were organizing materials related to this manuscript. To ensure the scientific integrity of the work, the authors have requested that this article now be retracted from the Journal. In view of these additional issues, the Editor of Molecular Medicine Reports has agreed to the authors' request to retract this paper. Note that all the authors agree to this retraction, and the Editor and the authors apologize to the readership of the Journal for any inconvenience caused. [Molecular Medicine Reports 29: 102, 2024; DOI: 10.3892/mmr.2024.13226].

Knee osteoarthritis (KOA) is a chronic degenerative disease that affects the quality of life of middle‑aged and elderly individuals, and is one of the major factors leading to disability. Rongjin Niantong Fang (RJNTF) can alleviate the clinical symptoms of patients with KOA, but the molecular mechanism underlying its beneficial effects on KOA remains unknown. Using pharmacological analysis and in vitro experiments, the active components of RJNTF were analyzed to explore their potential therapeutic targets and mechanisms in KOA. The potential targets and core signaling pathways by which RJNTF exerts its effects on KOA were obtained from databases such as Gene Expression Omnibus, Traditional Chinese Medicine Systems Pharmacology and Analysis Platform. Subsequently, chondrocyte apoptosis was modeled using hydrogen peroxide (H2O2). Cell Counting Kit‑8 assay involving a poly [ADP‑ribose] polymerase‑1 (PARP1) inhibitor, DAPI staining, reverse transcription‑quantitative PCR, Annexin V‑FITC/PI staining and flow cytometry, western blotting and co‑immunoprecipitation analysis were used to determine the therapeutic efficacy of RJNTF on KOA and to uncover the molecular mechanism. It was found that PARP1‑knockdown lentivirus, incubation with PARP1 inhibitor PJ34, medium and high doses of RJNTF significantly reduced H2O2‑induced chondrocyte apoptosis. Medium and high doses of RJNTF downregulated the expression of cleaved caspase‑3, cleaved PARP1 and PAR total proteins, as well as nucleus proteins of apoptosis‑inducing factor (AIF) and migration inhibitory factor (MIF), and upregulated the expression of caspase‑3, PARP1 total protein, as well as the cytoplasmic expression of AIF and MIF, suggesting that RJNTF may inhibit chondrocyte apoptosis through the PARP1/AIF signaling pathway.

探讨五输穴之输穴与筋伤的关系,以及输穴对应五行中的"木"和"土",提出五脏中的肝、脾与筋伤的病因病机密切相关,阐明肝、脾生理病理的相互联系,说明肝脾同调理论防治筋伤的有效性,为筋伤疾病的病因病机提供理论依据,旨在为临床中医治疗筋伤疾病提供新的思路.

背景:课题组前期动物实验研究表明,荣筋拈痛方可通过LncRNA GAS5/miR-21影响软骨基质分解和合成代谢,以达到防治膝骨关节炎的作用.LncRNA GAS5/miR-21能否作为防治膝骨关节炎的靶点,仍需从细胞水平研究验证.目的:从细胞水平探讨荣筋拈痛方防治膝骨关节炎的作用机制.方法:①8周龄SPF级雄性SD大鼠40只,随机分组后给予生理盐水、荣筋拈痛方(0.45 g/mL)、盐酸氨基葡萄糖胶囊(0.015 g/mL)灌胃,制备含药血清.②分离培养SD大鼠膝关节软骨细胞,采用白细胞介素1β干预软骨细胞,诱导退变软骨细胞模型,采用CCK-8法明确含药血清干预软骨细胞的量效时效关系.③将第2代软骨细胞分为空白组(空白血清)、模型组(白细胞介素1β+空白血清)、治疗组(白细胞介素1β+荣筋拈痛方含药血清)、对照组(白细胞介素1β+盐酸氨基葡萄糖胶囊含药血清)诱导干预48 h,Real-time PCR法和Western blot法检测各组软骨细胞血清干预后LncRNA GAS5、miR-21、基质金属蛋白酶抑制物3(tissue inhibitor of metalloproteinases 3,TIMP-3)、基质金属蛋白酶(matrix metalloproteinase,MMP)3、MMP-9、MMP-13和解聚蛋白样金属蛋白酶5(a disintegrin and metalloproteinase with thrombospondin motifs,ADAMTS-5)基因及蛋白表达.④慢病毒转染软骨细胞过表达LncRNA GAS5,分为LncRNA GAS5空载体+空白血清组、LncRNA GAS5空载体+荣筋拈痛方含药血清组、LncRNA GAS5过表达+空白血清组、LncRNA GAS5过表达+荣筋拈痛方含药血清组,各组干预后Real-time PCR检测LncRNA GAS5、miR-21、TIMP-3、MMP-9、MMP-13、ADAMTS-5基因表达.结果 与结论:①荣筋拈痛方含药血清体积分数为10％、培养48 h;盐酸氨基葡萄糖胶囊含药血清体积分数为15％、培养48 h,能显著提高软骨细胞活性;②干预48 h后,与模型组相比,荣筋拈痛方含药血清和盐酸氨基葡萄糖胶囊含药血清均能抑制LncRNA GAS5、MMP-3、MMP-9、MMP-13、ADAMTS-5基因和蛋白的表达(P<0.05),促进miR-21、TIMP-3基因和蛋白表达(P<0.05);③与空载体组相比,LncRNA GAS5过表达组LncRNA GAS5、MMP-9、MMP-13、ADAMTS-5基因表达量明显升高(P<0.05),miR-21、TIMP-3基因表达量明显降低(P<0.05);与LncRNA GAS5过表达+空白血清组相比,LncRNA GAS5过表达+荣筋拈痛方含药血清组MMP-9、MMP-13和ADAMTS-5 mRNA表达量均降低(P<0.05),miR-21、TIMP-3基因表达量升高(P<0.05);④结果表明,荣筋拈痛方通过调控LncRNA GAS5/miR-21,促进TIMP-3的表达,抑制MMP-3、MMP-9、MMP-13、ADAMTS-5等表达,从而延缓退变软骨细胞外基质降解,起到防治膝骨关节炎的作用.

背景:前期研究发现荣筋拈痛方能有效抑制软骨基质降解.长链非编码RNA GAS5可作为竞争性内源性RNA吸附miR-21-5p调控基质金属蛋白酶的表达,进而影响关节软骨基质代谢.但荣筋拈痛方是否通过长链非编码RNA GAS5/miR-21调控软骨基质代谢,发挥防治骨关节炎的作用机制有待深入研究.目的:从长链非编码RNA GAS5/miR-21调控软骨基质合成与分解代谢角度,探讨荣筋拈痛方治疗SD大鼠膝骨关节炎的作用机制.方法:SPF级8周龄雄性SD大鼠60只,随机分为4组,即空白组、模型组、治疗组及对照组,每组15只.后3组采用改良Hulth法建立大鼠膝骨关节炎模型.造模后2周,空白组和模型组予生理盐水,治疗组予荣筋拈痛方汤剂,对照组予盐酸氨基葡萄糖胶囊水溶液,每天灌胃一次,共干预12周.药物干预结束后取材,采用苏木精-伊红染色、改良番红O-固绿染色观察软骨组织显微结构形态变化,实时荧光定量PCR法检测长链非编码RNA GAS5、miR-21的表达及基质代谢因子mRNA的表达,Western blot法检测软骨组织中基质代谢因子蛋白的表达.结果 与结论:①软骨显微结构观察,模型组软骨4层结构紊乱,排列不规律,潮线及黏合线不规则或消失,软骨细胞增生肥大且排列紊乱,软骨下骨增生,胶原、蛋白多糖大量丢失;治疗组和对照组软骨4层结构、潮线可辨,软骨细胞排列较规律,软骨下骨结构较完整,胶原、蛋白多糖部分丢失;②与空白组相比,模型组软骨组织中长链非编码RNA GAS5及基质金属蛋白酶3、基质金属蛋白酶9、基质金属蛋白酶13、血小板反应蛋白解整合素金属肽酶5 mRNA表达量升高(P<0.01或P<0.05),治疗组、对照组与模型组相比表达量降低(P<0.01或P<0.05);模型组软骨组织中miR-21及组织金属蛋白酶抑制因子3、Ⅱ型胶原和聚集蛋白聚糖mRNA表达量降低(P<0.01或P<0.05),治疗组、对照组与模型组相比表达量升高(P<0.05);③与空白组相比,模型组软骨组织中组织金属蛋白酶抑制因子3、Ⅱ型胶原和聚集蛋白聚糖蛋白表达降低(P<0.01或P<0.05),治疗组和对照组中表达升高(P<0.01或P<0.05);模型组软骨组织中基质金属蛋白酶3、基质金属蛋白酶9、基质金属蛋白酶13、血小板反应蛋白解整合素金属肽酶5蛋白表达升高(P<0.01或P<0.05),治疗组和对照组中表达降低(P<0.01或P<0.05);④提示荣筋拈痛方下调膝骨关节炎大鼠软骨组织中长链非编码RNA GAS5、基质金属蛋白酶3、基质金属蛋白酶9等的表达,上调miR-21、组织金属蛋白酶抑制因子3、Ⅱ型胶原和聚集蛋白聚糖的表达,影响软骨基质分解和合成代谢,减少软骨基质中胶原、蛋白多糖的丢失,延缓软骨基质降解,减轻软骨组织形态结构的破坏.

病理学是中医学专业的必修课程.在中医学专业病理学教学实践中引入以团队为基础的教学法(Team-based learn-ing,TBL),将专业教育与人文教育进行有效融合,将超星学习通平台与传统课堂相结合,以临床案例为导向,围绕"线上线下混合式"教学理念,建立科学的综合性考评机制,旨在探索以学生为中心、培养高素质应用型中医专业人才的教学模式.

目的:探讨荣筋拈痛方调控NOD样受体热蛋白结构域相关蛋白3(NLRP3)/半胱氨酸天冬氨酸蛋白酶1(caspase-1)/消皮素D(GSDMD)通路减轻软骨细胞焦亡,改善骨关节炎炎性病变的作用机制.方法:将二代软骨细胞随机分为正常组、模型组[脂多糖(LPS)+三磷酸腺苷(ATP)]、荣筋拈痛方组(LPS+ATP+荣筋拈痛方)和抑制剂组(LPS+ATP+MCC950)oHoechst 33342/PI双染检测软骨细胞膜的完整性;双转盘活细胞共聚焦实时成像分析系统观察NLRP3和caspase-1的定位与表达;ELISA检测白细胞介素(IL)-1 β和IL-18的水平;RT-PCR检测NLRP3、caspase-1、GSDMD、Ⅱ 型胶原蛋白(collagen Ⅱ)和聚集蛋白聚糖(aggrecan)mRNA水平;Western Blot检测NLRP3、pro-caspase-1、caspase-1、GSDMD、GSDMD-N、collagen Ⅱ、aggrecan、基质金属蛋白酶(MMP)-3和MMP-13蛋白表达.结果:与模型组比较,荣筋拈痛方可降低因细胞膜完整性丧失而染上的PI红色荧光强度;降低NLRP3和caspase-1蛋白表达的绿色荧光强度(P＜0.01);降低软骨细胞上清液中炎症因子IL-1 β和IL-18水平(P＜0.01);降低NLRP3、caspase-1、GSDMD mRNA水平(P＜0.05,P＜0.01),提高collagen Ⅱ和aggrecan mRNA水平(P＜0.01);降低NLRP3、pro-caspase-1、caspase-1、GSDMD、GSDMD-N、MMP-3和MMP-13蛋白表达(P＜0.05,P＜0.01),提高collagen Ⅱ和aggrecan蛋白表达(P＜0.05).结论:荣筋拈痛方可通过调控软骨细胞NLRP3/caspase-1/GSDMD途径,减轻因细胞焦亡而导致的炎症反应,改善骨关节炎炎性病变.

目的：观察荣筋拈痛方对白细胞介素-1β（IL-1β）诱导的体外大鼠软骨细胞自噬相关基因表达的影响，探讨其防治膝骨关节炎的作用机制。方法：取4周龄SD大鼠膝关节软骨，进行软骨细胞的体外分离培养，选取第2代软骨细胞甲苯胺蓝染色进行细胞鉴定。经IL-1β 10 ng·mL -1 诱导建立体外软骨细胞炎症模型，诱导成功后，给予荣筋拈痛方(50，100，200 μg·mL -1 )孵育48 h。将细胞分为空白对照组，模型对照组，荣筋拈痛方低、中、高剂量组。分别采用CCK-8法检测荣筋拈痛方对软骨细胞活性的影响，qPCR法检测软骨细胞中LC3Ⅱ、Beclin 1的mRNA表达，Western Blot法观察自噬蛋白LC3Ⅱ/Ⅰ比值、Beclin 1的蛋白表达水平。结果：与模型对照组比较，荣筋拈痛方低、中、高剂量组均显著提高细胞活力，呈剂量依赖性增加（P ＜ 0.01）；模型对照组较空白对照组LC3Ⅱ、Beclin 1的mRNA及LC3Ⅱ/Ⅰ、Beclin 1的蛋白表达水平升高（P ＜ 0.05）；经100 μg·mL -1 荣筋拈痛方干预后LC3Ⅱ、Beclin 1的mRNA及LC3Ⅱ/Ⅰ、Beclin 1的蛋白表达水平降低（P ＜ 0.05）。结论：荣筋拈痛方可能通过抑制自噬水平，从而具有延缓膝骨关节炎退变的作用。

目的:观察荣筋拈痛方对白细胞介素-1β(IL-1β)诱导的体外大鼠软骨细胞自噬相关基因表达的影响,探讨其防治膝骨关节炎的作用机制.方法:取4周龄SD大鼠膝关节软骨,进行软骨细胞的体外分离培养,选取第2代软骨细胞甲苯胺蓝染色进行细胞鉴定.经IL-1β10 ng·mL-1诱导建立体外软骨细胞炎症模型,诱导成功后,给予荣筋拈痛方(50,100,200μg·mL-1)孵育48 h.将细胞分为空白对照组,模型对照组,荣筋拈痛方低、中、高剂量组.分别采用CCK-8法检测荣筋拈痛方对软骨细胞活性的影响,qPCR法检测软骨细胞中LC3Ⅱ、Beclin 1的mRNA表达,Western Blot法观察自噬蛋白LC3Ⅱ/Ⅰ比值、Beclin 1的蛋白表达水平.结果:与模型对照组比较,荣筋拈痛方低、中、高剂量组均显著提高细胞活力,呈剂量依赖性增加(P<0.01);模型对照组较空白对照组LC3Ⅱ、Beclin 1的mRNA及LC3Ⅱ/Ⅰ、Beclin 1的蛋白表达水平升高(P<0.05);经100μg·mL-1荣筋拈痛方干预后LC3Ⅱ、Beclin 1的mRNA及LC3Ⅱ/Ⅰ、Beclin 1的蛋白表达水平降低(P<0.05).结论:荣筋拈痛方可能通过抑制自噬水平,从而具有延缓膝骨关节炎退变的作用.

基于骨关节炎"本痿标痹"的核心病机,提出骨关节炎的治疗原则——内养外休.内养围绕骨关节炎与"肾藏精,主骨生髓""肝主筋,肾主骨""少阳主骨""脾为后天之本"四大理论的相关性进行阐述,外休涵盖了外养以实腠理、理疗以助关节运动、制动以促关节功能恢复三个方面,充分体现骨关节炎内外兼治的治疗理念.

目的:利用数据挖掘软件与网络药理学分析陈可冀院士主编的清宫系列书籍中治疗骨关节炎外用方的用药规律.方法:从清宫系列书籍中筛选出治疗骨关节炎的外用方剂,利用Excel软件建立数据库,基于中医传承辅助平台(V3.0)统计中药使用频次及其性味、归经、功效,再对方剂进行关联规则和聚类分析.在此基础上结合专业知识组出新方(荣筋祛痹方),再用网络药理学验证荣筋祛痹方治疗骨关节炎的可行性.结果:从清宫系列书籍中筛选出治疗骨关节炎的外用方剂103首,频数统计显示常见外用药物以乳香、当归、没药、防风等为主,多用性温、平,味辛、苦,入肝、脾经的中药,基于此分析中药的关联规则聚类出核心组合.综合上述结果组出新方(荣筋祛痹方).结论:清宫系列书籍治疗骨关节炎的外用药主要以活血化瘀、祛风除湿为主,兼以补益肝肾.用药规律符合骨关节炎外因感受风寒湿邪、内因肝肾亏虚从而产生中间病理产物-瘀血的中医发病特点.由此分析聚类出的中药核心组合对骨关节炎的治疗用药具有参考价值,在此基础上用网络药理学验证过的新方(荣筋祛痹方)对骨关节炎具有治疗价值.

目的:通过生物信息学、网络药理学和分子对接技术探讨洗腿又方治疗骨关节炎的药理学机制.方法:从基因表达综合数据库(GEO)中获取骨关节炎滑膜的差异表达基因,使用TCMSP、HERB、TCMID等数据库搜集洗腿又方的活性成分及其作用靶点,并与疾病靶点取交集.通过STRING数据库及Cytoscape 3.8.2软件对交集靶点进行蛋白互作和富集分析,最终将关键活性成分与关键靶点进行分子对接.结果:获得骨关节炎滑膜的差异表达基因2 072个,洗腿又方的活性成分20种,其治疗骨关节炎的靶点30个,进一步通过蛋白互作筛选获得HIF1A、CASP8、RAF1等关键靶点,富集分析发现洗腿又方主要通过干预细胞周期、炎症和内分泌等信号通路治疗骨关节炎,分子对接结果显示,关键有效成分芹黄素、槲皮素分别与关键靶点HIF1A、CASP8有良好的对接活性.结论:对洗腿又方治疗骨关节炎的可能活性成分、靶点及作用通路有了初步认识,为其应用于骨关节炎的治疗提供了理论依据.

Context Rongjin Niantong Fang (RJNTF) is a Traditional Chinese Medicine formulation with a good therapeutic effect on osteoarthritis (OA). However, the underlying mechanisms remain unclear. Objective This study investigates whether RJNTF could delay OA cartilage degeneration by regulating the SDF-1/CXCR4-p38MAPK signalling pathway. Materials and methods The Sprague-Dawley (SD) rats were used to establish the OA model by a modified Hulth's method. SD rats were divided into three groups (n = 10): blank group, model group (0.9% saline, 10 mL/kg/day), and treatment group (RJNTF, 4.5 g/kg/day). After 12 weeks of treatment, each group was analysed by H&E, Safranine-O solid green, ELISA, Immunohistochemistry, and Western blot. An in vitro model was induced with 100 ng/mL SDF-1 by ELISA, the blank group, model group, RJNTF group, and inhibitor group with intervention for 12 h, each group was analysed by Immunofluorescence staining and Western blot. Results SDF-1 content in the synovium was reduced in RJNTF treatment group compared to non-treatment model group (788.10 vs. 867.32 pg/mL) and down-regulation of CXCR4, MMP-3, MMP-9, MMP-13 protein expression, along with p38 protein phosphorylated were observed in RJNTF treatment group. In vitro results showed that RJNTF (IC50 = 8.925 mg/mL) intervention could down-regulate SDF-1 induced CXCR4 and p38 protein phosphorylated and reduce the synthesis of MMP-3, MMP-9, and MMP-13 proteins of chondrocytes from SD rat cartilage tissues. Discussion and conclusion RJNTF alleviates OA cartilage damage by SDF-1/CXCR4-p38MAPK signalling pathway inhibition. Our ongoing research focuses on Whether RJNTF treats OA through alternative pathways.

目的:观察独活寄生汤含药血清对白细胞介素-1 β(IL-1β)诱导大鼠退变软骨细胞外基质代谢的影响.方法:制备含药血清,提取大鼠软骨细胞,分为空白组、模型组、治疗组、对照组.构建LncRNA GAS5过表达退变软骨细胞,分为空载体组、空载体治疗组、LncRNA GAS5过表达组、LncRNA GAS5过表达治疗组.Q-PCR检测LncRNA GAS5、miR-21、基质金属蛋白酶(MMP)-3、MMP-9、MMP-13、ADAMTS-5 mRNA表达.Western blot检测MMP-3、MMP-9、MMP-13、ADAMTS-5蛋白表达.结果:与模型组比较,治疗组和对照组LncRNA GAS5 mRNA表达显著降低(P＜0.05),miR-21 基因表达升高(P＜0.05),MMP-3、MMP-9、MMP-13、ADAMTS-5 mRNA及蛋白表达显著降低(P＜0.05).与空载体治疗组比较,LncRNA GAS5过表达治疗组LncRNA GAS5、MMP-3、MMP-9、MMP-13、ADAMTS-5 mRNA表达显著升高(P＜0.05),miR-21 mRNA表达显著降低(P＜0.05).结论:独活寄生汤可通过调控LncRNA GAS5/miR-21起到延缓软骨细胞外基质降解的作用.

Taking advantage of an exquisite hairpin DNA for strand displacement amplification (SDA) and the magnetic Fe3O4-graphene oxide nanosheets (MGN) as the carrier, an immobilization-free ECL biosensor was constructed for ultra-trace detection of Cd2+. Firstly, the ECL probe Ru (phen)(3)(2+) easily diffuses in the solution and reaches the electrode surface to induce strong ECL signal. This is because the pre-designed hairpin DNA is constrained by MGN in the absence of Cd2+. The presence of Cd2+ releases cDNA by binding to its corresponding aptamer, leading to removal of hairpin DNA away from the surface of MGN. In this case, SDA amplification was evoked and generated numerous dsDNA which further trapped Ru (phen)(3)(2+) in its groove. It is difficult for the embedded ECL probe to touch the electrode surface to generate ECL signal. Therefore, the concentration of Cd2+ was monitored according to the attenuation of ECL signal. This method showed high sensitivity to Cd2+ with a detection limit of 1.1 x 10(-4) ppb. Moreover, it not only avoids many condition optimizations required in the conventional SDA method, but also circumvent the modification and immobilization of DNA probe. This sensor is further applied in the detection of Cd2+ in the sample of traditional Chinese medicine.

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:探讨独活寄生汤治疗大鼠膝骨关节炎(knee osteoarthritis,KOA)的作用机制.方法:从66只大鼠中随机选取48只,采用改良Hulth法建立大鼠KOA模型,随机选择3只正常大鼠和3只建模大鼠进行鉴定.证实建模成功后,将剩余的15只正常大鼠纳入正常对照组,采用随机数字表将剩余的45只KOA模型大鼠分为KOA模型组、独活寄生汤治疗组、盐酸氨基葡萄糖治疗组,每组15只.正常对照组、KOA模型组、独活寄生汤治疗组、盐酸氨基葡萄糖治疗组大鼠均按每天10 mL·kg-1分别以0.9％生理盐水、0.9％生理盐水、独活寄生汤(浓度为0.93 g·mL-1)、盐酸氨基葡萄糖溶液(浓度为0.015 g·mL-1)灌胃,连续干预12周.12周后,切取大鼠双侧胫骨近端和股骨下端的软骨组织.采用实时定量PCR检测大鼠胫骨近端软骨组织中miR-675-3p、长链非编码RNA(long non-coding RNA,lncRNA)H19及聚集蛋白聚糖(Aggrecan)mRNA、Ⅱ型胶原蛋白(CollagenⅡ)mRNA的表达量,采用蛋白印迹法检测大鼠股骨远端软骨组织中Aggrecan、CollagenⅡ的蛋白表达量.结果:①大鼠饲养结果.KOA模型组大鼠因肺栓塞死亡2只,独活寄生汤治疗组大鼠因腹泻死亡1只,盐酸氨基葡萄糖治疗组大鼠因肺栓塞死亡1只.②大鼠胫骨近端软骨组织中KOA相关基因的RNA表达结果.正常对照组、KOA模型组、独活寄生汤治疗组、盐酸氨基葡萄糖治疗组大鼠胫骨近端软骨组织中miR-675-3p、lncRNA H19、Aggrecan mRNA、CollagenⅡmRNA的表达量比较,组间差异均有统计学意义(F=83.050,P=0.000;F=436.003,P=0.000;F=129.212,P=0.000;F=135.844,P=0.000).KOA模型组、独活寄生汤治疗组、盐酸氨基葡萄糖治疗组大鼠胫骨近端软骨组织中miR-675-3p、Aggrecan mRNA、CollagenⅡmRNA的表达量均低于正常对照组(miR-675-3p:P=0.000;P=0.003;P=0.002;Aggrecan mRNA:P=0.000;P=0.000;P=0.000;CollagenⅡmRNA:P=0.000;P=0.000;P=0.000);KOA模型组大鼠胫骨近端软骨组织中lncRNA H19的表达量低于正常对照组(P=0.002),独活寄生汤治疗组、盐酸氨基葡萄糖治疗组大鼠胫骨近端软骨组织中lncRNA H19的表达量与正常对照组比较,差异无统计学意义(P=0.058,P=0.069);独活寄生汤治疗组、盐酸氨基葡萄糖治疗组大鼠胫骨近端软骨组织中miR-675-3p、Aggrecan mRNA、CollagenⅡmR-NA的表达量均高于KOA模型组(miR-675-3p:P=0.000;P=0.000;Aggrecan mRNA:P=0.000;P=0.000;CollagenⅡmRNA:P=0.000;P=0.000);独活寄生汤治疗组大鼠胫骨近端软骨组织中miR-675-3p、lncRNA H19、Aggrecan mRNA、CollagenⅡmR-NA的表达量与盐酸氨基葡萄糖治疗组比较,组间差异均无统计学意义(P=0.922;P=0.778;P=0.857;P=0.904).③大鼠股骨远端软骨组织中软骨组成相关基因的蛋白表达结果.正常对照组、KOA模型组、独活寄生汤治疗组、盐酸氨基葡萄糖治疗组的大鼠股骨远端软骨组织中Aggrecan和CollagenⅡ的蛋白表达量比较,组间差异均有统计学意义(F=58.118,P=0.002;F=16.625,P=0.001).KOA模型组、独活寄生汤治疗组大鼠股骨远端软骨组织中Aggrecan的蛋白表达量均低于正常对照组(P=0.003;P=0.004),盐酸氨基葡萄糖治疗组大鼠股骨远端软骨组织中Aggrecan的蛋白表达量与正常对照组相比,差异无统计学意义(P=0.078),KOA模型组、独活寄生汤治疗组、盐酸氨基葡萄糖治疗组大鼠股骨远端软骨组织中CollagenⅡ的蛋白表达量均低于正常对照组(P=0.000;P=0.028;P=0.018),独活寄生汤治疗组、盐酸氨基葡萄糖治疗组大鼠股骨远端软骨组织中Aggrecan和Colla-genⅡ的蛋白表达量均高于KOA模型组(Aggrecan:P=0.025;P=0.034;CollagenⅡ:P=0.003;P=0.004),独活寄生汤治疗组大鼠股骨远端软骨组织中Aggrecan和CollagenⅡ的蛋白表达量与盐酸氨基葡萄糖治疗组比较,组间差异均无统计学意义(P=0.999;P=0.775).结论:独活寄生汤治疗大鼠KOA的作用机制,可能与其能够上调miR-675-3p、lncRNA H19的表达进而促进Aggrecan、CollagenⅡ的表达有关.

Doxorubicin (Dox), an effective antineoplastic drug, was limited use for cardiotoxicity. Xinshuitong Capsule (XST), a patented herbal formula, showed desirable beneficial effects in the treatment of chronic heart failure (CHF) patients. However, the drug on Dox-induced cardiotoxicity remains unclear. Ninety male Sprague-Dawley rats were randomized into two groups: 15 rats were selected as the normal group and 75 rats were injected intraperitoneally with Dox to establish CHF rat models, the success ones were randomly divided into five groups: low XST (LXST), medium XST (MXST) or high XST (HXST) (4.9, 9.8, or 19.6 g/kg d) administrated intragastrically twice a day for 4 weeks, with the captopril-treated group and the model group as comparison. The model group showed the cardiac functions generally impaired, and CHF mortality rate higher (47%) than those in the XST-treated groups (averaged 24%, P < 0.05). Compared with XST-treated groups, myocardial remodeling, inflammation and desarcomerization, and higher water content more severe in the cardiac tissue in the model group (P < 0.05), which was associated with higher expressions of mRNA or protein levels of AQP1, 4 and 7. Dox-impaired cardiac functions, cardiac remodeling and myocardial edema could be dose-dependently reverted by XST treatment. XST could inhibit AQP1, 4 and 7 at mRNA levels or at protein levels, which was associated with the attenuation of myocardial edema and cardiac remodeling, decreasing the ventricular stiffness and improving the cardiac functions and rats' survival. AQPs is involved in cardiac edema composed one of the mechanisms of Dox-induced cardiotoxicity, XSTvia inhibition of AQPs relieved the Dox-induced side effects.

目的:比较洗腿又方联合推拿和单纯推拿治疗瘀血阻滞证膝骨关节炎的临床疗效.方法:将44例瘀血阻滞证膝骨关节炎患者采用随机数字表法分为观察组和对照组各22例,观察组采用洗腿又方联合推拿治疗.对照组仅采用单纯推拿治疗,治疗4周后观察治疗前后疼痛评分、运动功能评分的变化.结果:观察组总有效率为90.48％,优于对照组的80.95％(P<0.05);治疗后,观察组疼痛评分、运动功能评分改善幅度均优于对照组(P<0.05).结论:洗腿又方联合推拿治疗瘀血阻滞证膝骨关节炎疗效显著,值得临床推广运用.