目的:观察蒙药润僵汤对KOA模型小鼠膝关节组织形态学的影响,探讨其治疗膝骨关节炎的作用机理,为临床运用以及进一步探索蒙药润僵汤治疗膝骨关节炎的机制提供依据。方法:将40只C57BL/6小鼠随机区组法分为空白组、模型组、实验组(蒙药润僵汤)、阳性对照组(中药海桐皮汤),每组10只。空白组膝关节腔内注射生理盐水处理,模型组、实验组、阳性对照组通过膝关节腔内注射胶原酶的方式建立KOA动物模型。术后1周开始用药,实验组以蒙药润僵汤浸泡治疗,阳性对照组以中药海桐皮汤浸泡治疗,空白组及模型组温水浸泡治疗。隔日1次,连续治疗2周。2周后行小动物膝关节MRI检查并处死动物后取股骨内髁关节软骨及部分软骨下骨标本,分别经HE染色。结果:小鼠膝关节MRI显示润僵汤组膝关节结构完整,关节腔内可见少量液体高信号影,所见肌肉组织信号正常。HE染色光镜下观察实验组大体同阳性对照组,关节软骨破坏较模型组明显轻;结论:蒙药润僵汤可能减少膝关节处炎症反应,减轻关节软骨破坏,减缓软骨下骨硬化,延缓骨关节炎的发展进程,但同时也表明其不能停止或逆转关节软骨的退变。Objective: To observe the effect of Mongolian medicine Runjiang Tang on the morphology of knee joint tissue in KOA model mice, explore its mechanism of action in treating knee osteoarthritis, and provide a basis for clinical application and further exploration of the mechanism of Mongolian medicine Runjiang Tang in treating knee osteoarthritis. Method: Forty C57BL/6 mice were randomly divided into a blank group, a model group, an experimental group (Mongolian medicine Runjiang Tang), and a positive control group (Chinese medicine Haitong Pi Tang), with 10 mice in each group. The blank group was treated with injecting physiological saline into the knee joint cavity, while the model group, experimental group, and positive control group were established with KOA animal models by injecting collagenase into the knee joint cavity. Medication started one week after surgery. The experimental group was treated with Mongolian medicine Runjiang Tang soaking, while the positive control group was treated with traditional Chinese medicine Haitongpi Tang soaking. The blank group and model group were treated with warm water soaking. Once every other day, continuous treatment for 2 weeks. Two weeks later, a small animal’s knee joint MRI examination was performed and the animal was euthanized. The femoral medial condylar joint cartilage and some subchondral bone specimens were taken and stained with HE, respectively. Result: MRI of the mouse knee joint showed that the knee joint structure of the Runjiang Tang group was intac
目的观察补肾强督方对自发性强直性脊柱炎模型DBA/1小鼠关节韧带及附着点骨化程度和DKK1/Wnt通路的影响,探讨补肾强督方防治强直性脊柱炎的作用机制。方法将30只12周龄的雄性DBA/1小鼠随机分为模型组、阳性药物组、补肾强督方低、中、高剂量组,每组6只,另设6只同周龄C57BL/6小鼠作为空白组。补肾强督方低、中及高剂量组分别灌胃低、中、高浓度的补肾强督方,所含生药重量分别为11.25、22.5、45 g/(kg·d),0.2 m L/只,每日1次;阳性药物组灌胃塞来昔布胶囊0.8 mg/只,0.2 m L/只,每日1次;模型组及空白组灌胃等量的生理盐水。连续饲养、灌胃12周。定期观察小鼠体重、饮食、大便、毛发等情况。每两周评价1次小鼠关节炎体征。处死后取小鼠跟腱部位进行大体观察,对跟腱组织行HE染色,用免疫组化法检测小鼠跟腱中碱性磷酸酶(alkaline phosphatase,ALP)、骨钙素(bone gamma-carboxyglutamicacid-containing proteins,BGP)、DKK1、Wnt5a的蛋白表达。结果与空白对照组比较,模型组关节炎体征评分明显升高,而补肾强督方各剂量组及阳性药物组评分均低于模型组(P<0.05)。跟腱组织病理观察显示,正常组无炎性细胞及成纤维细胞浸润,组织形态结构正常;模型组出现不同程度的软骨及骨形成、炎性细胞及附着点成纤维样细胞浸润;各给药组小鼠跟腱组织多见散在淋巴细胞浸润,软骨及骨形成较少见。与空白组比较,模型组组织标本骨化评分升高,补肾强督方各剂量组及阳性药物组评分均低于模型组,差异有统计学意义(P<0.05)。与空白组比较,模型组DKK1蛋白表达降低,Wnt5a蛋白表达升高(P<0.05);与模型组比较,补肾强督方高、中剂量组DKK1蛋白表达升高,Wnt5a蛋白降低,差异有统计学意义(P<0.05)。结论补肾强督方可能通过抑制经典Wnt通路来延缓自发性强直性脊柱炎模型DBA/1小鼠关节炎及骨化程度的发生与发展。
暂无评论