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骨保护素的上调抑制叔丁基过氧化氢诱导的人软骨细胞凋亡。

Upregulation of osteoprotegerin inhibits -butyl hydroperoxide-induced apoptosis of human chondrocytes.

作者信息

Ren Qifeng, Zhang Wenfei, Li Ping, Zhou Jianli, Li Zhonghao, Zhou Yang, Li Ming

机构信息

Department of Joint Surgery, Dezhou People's Hospital, Dezhou, Shandong 253014, P.R. China.

Department of Clinical Psychology, Dezhou People's Hospital, Dezhou, Shandong 253014, P.R. China.

出版信息

Exp Ther Med. 2022 May 26;24(1):470. doi: 10.3892/etm.2022.11397. eCollection 2022 Jul.

DOI:10.3892/etm.2022.11397
PMID:35747145
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9204554/
Abstract

Necrosis of the femoral head (NFH) is an orthopedic disease characterized by a severe lack of blood supply to the femoral head and a marked increase in intraosseous pressure. NFH is associated with numerous factors, such as alcohol consumption and hormone levels. The present study focused on the expression levels of osteoprotegerin (OPG) in NFH and the effect of overexpression on chondrocyte apoptosis. The results demonstrated that expression was markedly decreased in the femoral head of patients with NFH compared with normal femoral heads. Lentivirus-mediated overexpression of in human chondrocytes reversed the decrease in cell viability and the increase in reactive oxygen species production induced by an oxidative stress-inducing factor, -butyl hydroperoxide. Flow cytometry and TUNEL assays revealed that overexpression inhibited the apoptosis of chondrocytes. In addition, it was revealed that exerted its anti-apoptotic effect mainly by promoting Bcl-2 expression and Akt phosphorylation and inhibiting caspase-3 cleavage and Bax expression. The present study revealed that may be an important regulator of NFH.

摘要

股骨头坏死(NFH)是一种骨科疾病,其特征是股骨头严重供血不足且骨内压显著升高。NFH与多种因素相关,如饮酒和激素水平。本研究聚焦于NFH中骨保护素(OPG)的表达水平以及过表达对软骨细胞凋亡的影响。结果表明,与正常股骨头相比,NFH患者股骨头中OPG的表达明显降低。慢病毒介导的人软骨细胞中OPG过表达逆转了由氧化应激诱导因子叔丁基过氧化氢诱导的细胞活力下降和活性氧生成增加。流式细胞术和TUNEL分析显示,OPG过表达抑制了软骨细胞的凋亡。此外,研究表明,OPG主要通过促进Bcl-2表达和Akt磷酸化以及抑制caspase-3裂解和Bax表达发挥其抗凋亡作用。本研究表明,OPG可能是NFH的重要调节因子。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1794/9204554/b3152da7fe41/etm-24-01-11397-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1794/9204554/379b6b4e36b0/etm-24-01-11397-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1794/9204554/263ef4a35e37/etm-24-01-11397-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1794/9204554/13a7cb6e2fa8/etm-24-01-11397-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1794/9204554/7152fef8ca90/etm-24-01-11397-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1794/9204554/2d2157ab6ae9/etm-24-01-11397-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1794/9204554/b3152da7fe41/etm-24-01-11397-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1794/9204554/379b6b4e36b0/etm-24-01-11397-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1794/9204554/263ef4a35e37/etm-24-01-11397-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1794/9204554/13a7cb6e2fa8/etm-24-01-11397-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1794/9204554/7152fef8ca90/etm-24-01-11397-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1794/9204554/2d2157ab6ae9/etm-24-01-11397-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1794/9204554/b3152da7fe41/etm-24-01-11397-g05.jpg

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