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脉冲电磁场治疗通过激活过氧化物酶体增殖物激活受体γ减轻骨质疏松性骨关节炎模型大鼠的自噬和凋亡。

Protective effects of pulsed electromagnetic field therapy attenuates autophagy and apoptosis in osteoporotic osteoarthritis model rats by activating PPARγ.

机构信息

The First Affiliated Hospital, Rehabilitation Medicine Center, Hengyang Medical School, University of South China, Hengyang, Hunan, China.

The First Affiliated Hospital, Department of Rehabilitation, Hengyang Medical School, University of South China, Hengyang, Hunan, China.

出版信息

Electromagn Biol Med. 2024 Apr 2;43(1-2):61-70. doi: 10.1080/15368378.2024.2314108. Epub 2024 Feb 12.

DOI:10.1080/15368378.2024.2314108
PMID:38347683
Abstract

Osteoporotic osteoarthritis (OPOA) is a specific phenotype of OA with high incidence and severe cartilage damage. This study aimed to explore the protective efficacy of PEMF on the progression of OPOA and observed the effects of PEMF on PPARγ, autophagy- and apoptosis-related proteins in OPOA rats. Rats were randomly divided into three groups: control group, OPOA group, and PEMF group ( = 6). One week after surgery, the rats in PEMF group were subjected to PEMF (3.82 mT, 8 Hz, 40 min/day and 5 day/week) for 12 weeks. Results showed that PEMF retarded cartilage degeneration and bone loss, as evidenced by pathological staining image, decreased MMP-13 expression and increased bone mineral density. PEMF inhibited the serum levels of inflammatory cytokines, and the expressions of caspase-3 and caspase-8, while upregulated the expression of PPARγ. Moreover, PEMF significantly improved the autophagy disorders, represented by decrease expressions of Beclin-1, P62, and LC3B. The research demonstrates that PEMF can effectively prevent cartilage and subchondral bone destruction in OPOA rats. The potential mechanism may be related to upregulation of PPARγ, inhibition of chondrocyte apoptosis and inflammation, and improvement of autophagy disorder. PEMF therapy thus shows promising application prospects in the treatment of postmenopausal OA.

摘要

骨质疏松性骨关节炎(OPOA)是一种具有高发病率和严重软骨损伤的特定 OA 表型。本研究旨在探讨 PEMF 对 OPOA 进展的保护作用,并观察 PEMF 对 OPOA 大鼠中 PPARγ、自噬和凋亡相关蛋白的影响。大鼠随机分为三组:对照组、OPOA 组和 PEMF 组(n=6)。手术后 1 周,PEMF 组大鼠接受 PEMF(3.82 mT、8 Hz、40 min/天和 5 天/周)治疗 12 周。结果表明,PEMF 可延迟软骨退变和骨丢失,这体现在病理染色图像上,表现为 MMP-13 表达减少和骨密度增加。PEMF 抑制了血清中炎症细胞因子的表达,降低了 caspase-3 和 caspase-8 的表达,同时上调了 PPARγ 的表达。此外,PEMF 还显著改善了自噬紊乱,表现在 Beclin-1、P62 和 LC3B 的表达减少。该研究表明,PEMF 可有效预防 OPOA 大鼠的软骨和软骨下骨破坏。其潜在机制可能与上调 PPARγ、抑制软骨细胞凋亡和炎症以及改善自噬紊乱有关。因此,PEMF 治疗在治疗绝经后 OA 方面具有广阔的应用前景。

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