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

机译:被动吸烟引起的大鼠椎间盘内细胞凋亡和基质变性的检测

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摘要

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.
机译:尽管认为腰痛与吸烟有关,但尚未确认吸烟对椎间盘(IVD)的影响。我们建立了被动吸烟引起的IVD变性的大鼠模型,并研究了IVD的细胞组织学变化以及伴随的基因表达变化。暴露于被动吸烟8周的大鼠的IVD用Elastica van Gieson染色,并显示髓核(NP)中网状基质支持结构的明显破坏。藏红素O,阿尔辛蓝,II型胶原蛋白和聚集蛋白聚糖染色的阳性信号在破坏的结构中降低。抽烟4周和8周后,软骨终板(CEP)中的藏红素O和II型胶原信号也降低了。在CEP中,凋亡的潜力显着增加,如单链DNA染色所示。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由于组织学上的接近性而通过血流影响CEP,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,破坏了NP基质,然后可能发展为IVD变性。

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