Huang Lingxiao, Du Wanchun, Jin Xing, Chen Bo, Meng Zhaoxiang
Medical College, Yangzhou University, Yangzhou, Jiangsu, 225001, China.
Rehabilitation Medicine Department, Northern Jiangsu People's Hospital Afliated to Yangzhou University, Yangzhou, 225001, Jiangsu, China.
BMC Musculoskelet Disord. 2025 Jul 5;26(1):657. doi: 10.1186/s12891-025-08903-6.
The efficacy of swimming in managing knee osteoarthritis (KOA) is well documented. However, the potential of swimming to regulate the Hif-1α/VEGFa pathway and thereby hindering the formation of subchondral bone H-type vessels, remains to be fully elucidated.
A mouse model of KOA was established by intra-articular injection of papain solution, followed by a swimming intervention. Symptomatic changes were observed by measuring body weight and knee joint diameter. Behavioural tests were used to assess exercise-related functions. HE staining was used to observe bone tissue morphology, while immunofluorescence staining was used to observe variations in H-type vessels of the subchondral bone. Quantitative PCR and western blotting were used to determine the expression levels of the pathway mRNA and protein.
The results obtained from this study revealed that KOA mice exhibited activation of the Hif-1α/VEGFa pathway in the tibial plateau bone, increased H-type vessels in the subchondral bone, and significant cartilage degeneration. In contrast, mice in the swimming exercise group demonstrated faster recovery from body weight and knee swelling, and exhibited superior performance in the balance beam test, rotarod test, and open field test. The swimming exercise group exhibited reduced articular cartilage destruction, diminished formation of H-type vessels in the subchondral bone, and decreased mRNA and protein expression of the Hif-1α/VEGFa pathway.
Articular cartilage in KOA mice exhibited signs of degradation and joint function was impaired. The findings of this study demonstrate that swimming exercise led to a down-regulation of the Hif-1α/VEGFa pathway in the tibial plateau bone of KOA mice, an inhibition of H-type vessels in the subchondral bone, and an improvement in cartilage morphology.
The online version contains supplementary material available at 10.1186/s12891-025-08903-6.
游泳对膝关节骨关节炎（KOA）的治疗效果已有充分记录。然而，游泳调节Hif-1α/VEGFa通路从而阻碍软骨下骨H型血管形成的潜力，仍有待充分阐明。
通过关节内注射木瓜蛋白酶溶液建立KOA小鼠模型，随后进行游泳干预。通过测量体重和膝关节直径观察症状变化。行为测试用于评估运动相关功能。HE染色用于观察骨组织形态，免疫荧光染色用于观察软骨下骨H型血管的变化。定量PCR和蛋白质印迹法用于测定该通路mRNA和蛋白质的表达水平。
本研究结果显示，KOA小鼠胫骨平台骨中Hif-1α/VEGFa通路激活，软骨下骨中H型血管增多，且软骨明显退变。相比之下，游泳运动组小鼠体重和膝关节肿胀恢复更快，在平衡木试验、转棒试验和旷场试验中表现更优。游泳运动组关节软骨破坏减少，软骨下骨中H型血管形成减少，Hif-1α/VEGFa通路的mRNA和蛋白质表达降低。
KOA小鼠的关节软骨出现退变迹象，关节功能受损。本研究结果表明，游泳运动导致KOA小鼠胫骨平台骨中Hif-1α/VEGFa通路下调，抑制软骨下骨中H型血管，并改善软骨形态。
在线版本包含可在10.1186/s12891-025-08903-6获取的补充材料。
