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被动吸烟导致大鼠椎间盘内细胞凋亡和基质退变的检测。

Detection of apoptosis and matrical degeneration within the intervertebral discs of rats due to passive cigarette smoking.

机构信息

Department of Orthopaedic Surgery, Nihon University School of Medicine, Itabashi-ku, Tokyo, Japan.

Department of Therapeutics for Aging Locomotive Disorders, Nihon University School of Medicine, Itabashi-ku, Tokyo, Japan.

出版信息

PLoS One. 2019 Aug 27;14(8):e0218298. doi: 10.1371/journal.pone.0218298. eCollection 2019.

DOI:10.1371/journal.pone.0218298
PMID:31454348
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6711513/
Abstract

Although low-back pain is considered to be associated with cigarette smoking, the influence of cigarette smoking on the intervertebral discs (IVD) has not been confirmed. We established a rat model of passive cigarette smoking-induced IVD degeneration, and investigated the cytohistological changes in the IVD and the accompanying changes in gene expression. IVD from rats exposed to 8 weeks of passive cigarette smoking were stained with Elastica van Gieson, and exhibited marked destruction of the supportive structure of the reticular matrix in the nucleus pulposus (NP). Positive signals on safranin O, alcian blue, type II collagen and aggrecan staining were decreased in the destroyed structure. Safranin O and type II collagen signals were also decreased in the cartilage end-plate (CEP) after 4- and 8-weeks of cigarette smoking. In the CEP, the potential for apoptosis was increased significantly, as demonstrated by staining for single-strand DNA. However, there were no signs of apoptosis in the NP or annulus fibrosus cells. Based on these findings, we hypothesized that passive cigarette smoking-induced stress stimuli first affect the CEP through blood flow due to the histological proximity, thereby stimulating chondrocyte apoptosis and reduction of the extracellular matrix (ECM). This leads to reduction of the ECM in the NP, destroying the NP matrix, which can then progress to IVD degeneration.

摘要

虽然腰痛被认为与吸烟有关,但吸烟对椎间盘(IVD)的影响尚未得到证实。我们建立了一个被动吸烟诱导的椎间盘退行性变大鼠模型,研究了椎间盘的细胞组织学变化及其伴随的基因表达变化。用弹性Van Gieson 染色被动吸烟 8 周的大鼠的椎间盘,显示核髓质(NP)网状基质的支持结构明显破坏。破坏结构中硫酸软骨素、阿利新蓝、II 型胶原和聚集蛋白染色的阳性信号减少。在吸烟 4 周和 8 周后,软骨终板(CEP)中的软骨素 O 和 II 型胶原信号也减少。CEP 中,通过单链 DNA 染色,细胞凋亡的可能性显著增加。然而,在 NP 或纤维环细胞中没有凋亡的迹象。基于这些发现,我们假设被动吸烟引起的应激刺激首先通过血流影响 CEP,因为组织学上的接近,从而刺激软骨细胞凋亡和细胞外基质(ECM)减少。这导致 NP 中 ECM 的减少,破坏 NP 基质,然后进展为 IVD 退行性变。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06b8/6711513/6661c6f94202/pone.0218298.g006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06b8/6711513/6661c6f94202/pone.0218298.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06b8/6711513/0565dc936218/pone.0218298.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06b8/6711513/e189004ead1c/pone.0218298.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06b8/6711513/3d60c9410f95/pone.0218298.g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/06b8/6711513/6661c6f94202/pone.0218298.g006.jpg

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