文献类型：期刊文献

中文题名：机械应力刺激对关节软骨代谢的调控影响

英文题名：Effect of Mechanical Stress Stimulation on the Regulation of Articular Cartilage Metabolism

作者：李陆[1];许佳强[2];赵中亭[3];敬艳[4]

第一作者：李陆

机构：[1]内蒙古大学体育学院,呼和浩特010021;[2]广州民航职业技术学院人文社科学院,广州510403;[3]甘肃中医药大学针灸推拿学院,兰州730000;[4]武汉体育学院体育教育学院,武汉430079

第一机构：内蒙古大学体育学院,呼和浩特010021

年份：2019

卷号：36

期号：5

起止页码：619

中文期刊名：西安体育学院学报

外文期刊名：Journal of Xi'an Physical Education University

收录：CSTPCD;;北大核心:【北大核心2017】；CSSCI:【CSSCI2019_2020】；

基金：国家自然科学基金项目(81560791)

语种：中文

中文关键词：机械应力;关节软骨;炎症;运动医学

外文关键词：mechanical stress;articular cartilage;inflammation;sports medicine

摘要：目的研究机械应力加载对软骨细胞基质合成代谢及炎性介质产生的影响。方法Ⅱ型胶原酶法消化C57/BL6乳鼠肋软骨提取原代软骨细胞,将纯化后的软骨细胞接种于BioFlex细胞拉力板,并对生长于柔性基底膜表面的软骨细胞固定0.5 Hz频率施加不同强度的应力加载(对照、4%、8%、12%、16%及20%加载组),48 h后实时荧光定量PCR检测软骨合成代谢基因的表达情况,酶联免疫吸附ELISA试剂盒检测炎性因子PGE2和TNF-α表达水平,Western Blot检测软骨细胞Collagen II及Aggrecan蛋白表达量。结果 4%加载组各项指标与对照组无明显差异(P>0.05),8%加载组能够促进软骨细胞的增殖,对软骨细胞外基质的合成降解及炎性因子释放影响不大(P>0.05)。但随着拉伸强度的增加,应力刺激对细胞的增殖影响由促进转为抑制,加速细胞外基质降解减少蛋白聚糖合成,并促进炎性因子合成释放,与对照组形成显著差异(P<0.05),且在16%加载组达到峰值。结论机械应力刺激信号可能参与软骨细胞合成代谢及炎症相关免疫调节,8%强度应力加载有助于维持软骨细胞正常生理状态。
Objective To study the effect of mechanical stress on the synthesis and metabolism of chondrocyte matrix and the production of inflammatory mediators.Methods The primary cartilage cells were extracted from the rib cartilage of C57/BL6 newborn mice by enzymatic digestion of typeⅡcollagen.The purified chondrocytes were inoculated into BioFlex membrane and were subjected to stress loading with different intensities at a frequency of 0.5 Hz(control,4%,8%,12%,16%,and 20%load group).The expression of cartilage anabolic genes was detected by real-time fluorescence quantitative PCR 48 h later.The expression of inflammatory cytokines PGE2 and TNF-αwere measured by enzyme-linked immunosorbent assay(ELISA)kit,and the expression of Collagen II and Aggrecan protein detected by Western Blot assay.Results There was no significant difference between the 4%loading group and the control group(P>0.05).The 8%loading group could promote the proliferation of chondrocytes but had limited effect on the synthesis and degradation of cartilage extracellular matrix and the release of inflammatory factors(P>0.05).However,with the increase of tensile strength,the effect of stress stimuli on cell proliferation was changed from promotion to inhibition,accelerated degradation of extracellular matrix,decreased proteoglycan synthesis,and promoted the synthesis and release of inflammatory factors,which was significantly different from the control group(P<0.05),and peaks in the 16%loading group.Conclusions Our findings reveal that mechanically stress-stimulated signals may be involved in chondrocytes anabolism and inflammation-related immunomodulation.8%intensity stress loading helps maintain the normal physiological state of chondrocytes.