首页|杜仲-牛膝药对调控软骨细胞凋亡和炎症反应治疗骨关节炎的分子机制

杜仲-牛膝药对调控软骨细胞凋亡和炎症反应治疗骨关节炎的分子机制

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目的 探讨杜仲-牛膝药对调控软骨细胞凋亡和炎症反应治疗骨关节炎的分子机制.方法 选取30只SPF级SD大鼠,随机分为空白对照组、模型组、杜仲-牛膝低剂量组、杜仲-牛膝中剂量组、杜仲-牛膝高剂量组,每组6只.除空白对照组外,其余4组大鼠进行骨关节炎造模.造模成功后,空白对照组和模型组予以生理盐水灌胃,杜仲-牛膝低、中、高剂量组分别予以相应体积的杜仲-牛膝水煎液灌胃,1次/d,共灌胃4周.治疗结束后,进行腹主动脉采血以及收集膝关节和软骨组织,HE染色观察膝关节形态变化,RT-qPCR和Western Blot检测BCL2-Associated X的蛋白质(Bax)和B淋巴细胞瘤-2基因(Bcl-2)的表达水平,ELISA检测肿瘤坏死因子-α(TNF-α)和白介素-1β(IL-1β)的血清浓度.结果 与空白对照组比较,模型组中的软骨表现出明显退变,细胞数量明显减少,经杜仲-牛膝药对处理后,软骨排列较完整,细胞数量也略微减少;与空白对照组比较,模型组中Bax表达水平升高,TNF-α和IL-1β的血清浓度升高,Bcl-2的表达水平降低,杜仲-牛膝灌胃处理后,上述基因表达水平出现相反结果,并呈剂量依赖性变化.结论 杜仲-牛膝通过抑制Bax、TNF-α和IL-1 β的表达,同时促进Bax的表达,抑制软骨细胞凋亡和炎症反应,起到延缓骨关节炎的作用.
Molecular mechanism of Duzhong-Niuxi in the treatment of osteoarthritis by regulating chondrocyte apoptosis and inflammatory response
Objective To investigate the molecular mechanism of Duzhong-Niuxi in the treatment of osteoarthritis(OA).Methods Thirty SD rats were randomly divided into blank control group,model group,low dose group of Duzhong-Niuxi,middle dose group of Duzhong-Niuxi and high dose group of Duzhong-Niuxi,with 6 rats in each group.Except for blank control group,OA models were established in the other four groups.After the model was successfully established,blank control group and model group were given normal saline by gavage,and the low,medium and high dose groups of Duzhong-Niuxi were given the corresponding volume of water decoction of Duzhong-Niuxi by gavage,once a day for 4 weeks.At the end of the treatment,abdominal aortic blood samples were collected;knee joint and cartilage tissues were collected.The morphological changes of knee joint were observed by HE staining.The expression levels of Bax and Bcl-2 were detected by RT-PCR and Western Blot,and the serum concentrations of TNF-α and IL-1 β were detected by ELISA.Results Compared with blank control group,the cartilage in model group showed obvious degeneration and the number of cells was significantly reduced.While after the administration of Duzhong-Niuxi,the cartilage was arranged more completely and the number of cells was slightly reduced.Compared with blank control group,the expression level of Bax,the serum concentrations of TNF-α and IL-1 β were increased,while the expression level of Bcl-2 was decreased in model group;the expression levels of the above genes showed opposite results in a dose-dependent manner.Conclusion Duzhong-Niuxi can delay OA by inhibiting the expression of Bax,TNF-αand IL-1 β,and promoting the expression of Bax,inhibiting the apoptosis of chondrocytes and inflammatory response.

Duzhong-NiuxiOsteoarthritisCell apoptosisInflammatory responseMolecular mechanism

胡翔宇、张伟夫、王子东、周晶

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湖北中医药大学附属医院/湖北省中医院/湖北省中医药研究院,湖北武汉 430061

湖北省襄阳市襄州区人民医院骨科,湖北襄阳 441100

杜仲-牛膝 骨关节炎 细胞凋亡 炎症反应 分子机制

国家中医药管理局"熊昌源名老中医药专家传承工作室"建设项目

国中医药人教函[2022]75号

2024

湖北中医药大学学报
湖北中医药大学

湖北中医药大学学报

CSTPCD
影响因子:0.873
ISSN:1008-987X
年,卷(期):2024.26(4)