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在兔椎间盘退变模型中，电针通过抑制细胞凋亡刺激细胞外基质重塑。

Electroacupuncture stimulates remodeling of extracellular matrix by inhibiting apoptosis in a rabbit model of disc degeneration.

作者信息

Huang Guo-Fu, Zou Jing, Shi Jing, Zhang Dong-You, Peng Hong-Fen, Zhang Qi, Gao Yu, Wang Bo-Yi, Zhang Tang-Fa

机构信息

Department of Neurobiology, School of Basic Medicine, Tongji Medical College of Huazhong University of Science and Technology, 13 Hangkong Road, Wuhan 430030, China ; Department of Acupuncture & Moxibustion, Wuhan Hospital of Integrated Chinese & Western Medicine, Tongji Medical College of Huazhong University of Science & Technology, 215 Zhongshan Road, Wuhan 430022, China.

Department of Acupuncture & Moxibustion, Wuhan Hospital of Integrated Chinese & Western Medicine, Tongji Medical College of Huazhong University of Science & Technology, 215 Zhongshan Road, Wuhan 430022, China.

出版信息

Evid Based Complement Alternat Med. 2015;2015:386012. doi: 10.1155/2015/386012. Epub 2015 Feb 11.

DOI:10.1155/2015/386012
PMID:25763091
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4339975/
Abstract

The present study was designed to determine whether EA stimulates remodeling of extracellular matrix by inhibiting apoptosis in degenerated disc. 40 rabbits were randomly assigned to one of the four groups. Animal model was established by a loading device. Magnetic resonance imaging and Pfirrmann's classification were obtained to evaluate both the model and the EA treatment on disc degeneration. The ultrastructure of discs was observed by TEM. Apoptosis involvement was determined with TUNEL staining and western blot for the protein expression of Bax and Bcl-2. The results indicated that EA intervention decreased the MRI grades. TEM analysis showed an apparent remodeling and rearrangement of disc ECM after EA intervention for 28 days. The number of TUNEL-positive cells in the EA group was significantly lower than that in the compression group. The protein expression demonstrated an antiapoptosis effect mediated by EA. Increased expression of Bcl-2 proteins and reduced Bax protein expression were detected after 28 days treatment. It was concluded that antiapoptosis pathway probably participates in the mechanism of EA stimulating the remodeling of ECM in disc degeneration.

摘要

本研究旨在确定电针是否通过抑制退变椎间盘细胞凋亡来刺激细胞外基质重塑。40只兔子被随机分为四组。通过加载装置建立动物模型。采用磁共振成像和Pfirrmann分级来评估模型以及电针对椎间盘退变的治疗效果。通过透射电子显微镜观察椎间盘的超微结构。采用TUNEL染色以及蛋白质免疫印迹法检测Bax和Bcl-2蛋白表达来确定细胞凋亡情况。结果表明，电针干预降低了磁共振成像分级。透射电子显微镜分析显示，电针干预28天后，椎间盘细胞外基质出现明显重塑和重排。电针组TUNEL阳性细胞数量显著低于压迫组。蛋白质表达显示电针具有抗细胞凋亡作用。治疗28天后，检测到Bcl-2蛋白表达增加，Bax蛋白表达减少。得出的结论是，抗细胞凋亡途径可能参与了电针刺激退变椎间盘中细胞外基质重塑的机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e790/4339975/4832a75a35f4/ECAM2015-386012.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e790/4339975/e3e612308db0/ECAM2015-386012.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e790/4339975/f3fa9c997906/ECAM2015-386012.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e790/4339975/219a2e0a618d/ECAM2015-386012.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e790/4339975/721f055ded12/ECAM2015-386012.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e790/4339975/8ff2493e5ebd/ECAM2015-386012.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e790/4339975/4832a75a35f4/ECAM2015-386012.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e790/4339975/e3e612308db0/ECAM2015-386012.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e790/4339975/f3fa9c997906/ECAM2015-386012.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e790/4339975/219a2e0a618d/ECAM2015-386012.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e790/4339975/721f055ded12/ECAM2015-386012.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e790/4339975/8ff2493e5ebd/ECAM2015-386012.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e790/4339975/4832a75a35f4/ECAM2015-386012.006.jpg

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Why do some intervertebral discs degenerate, when others (in the same spine) do not?为什么一些椎间盘会发生退变，而（同一脊柱中的）其他椎间盘却不会呢？
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