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首页> 外文期刊>Molecular medicine reports >Chronic sciatic nerve compression induces fibrosis in dorsal root ganglia
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Chronic sciatic nerve compression induces fibrosis in dorsal root ganglia

机译:慢性坐骨神经受压导致背根神经节纤维化

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In the present study, pathological alterations in neurons of the dorsal root ganglia (DRG) were investigated in a rat model of chronic sciatic nerve compression. The rat model of chronic sciatic nerve compression was established by placing a 1 cm Silastic tube around the right sciatic nerve. Histological examination was performed via Masson's trichrome staining. DRG injury was assessed using Fluoro Ruby (FR) or Fluoro Gold (FG). The expression levels of target genes were examined using reverse transcription-quantitative polymerase chain reaction, western blot and immunohistochemical analyses. At 3 weeks post-compression, collagen fiber accumulation was observed in the ipsilateral area and, at 8 weeks, excessive collagen formation with muscle atrophy was observed. The collagen volume fraction gradually and significantly increased following sciatic nerve compression. In the model rats, the numbers of FR-labeled DRG neurons were significantly higher, relative to the sham-operated group, however, the numbers of FG-labeled neurons were similar. In the ipsilateral DRG neurons of the model group, the levels of transforming growth factor-1 (TGF-1) and connective tissue growth factor (CTGF) were elevated and, surrounding the neurons, the levels of collagen type I were increased, compared with those in the contralateral DRG. In the ipsilateral DRG, chronic nerve compression was associated with significantly higher levels of phosphorylated (p)-extracellular signal-regulated kinase 1/2, and significantly lower levels of p-c-Jun N-terminal kinase and p-p38, compared with those in the contralateral DRGs. Chronic sciatic nerve compression likely induced DRG pathology by upregulating the expression levels of TGF-1, CTGF and collagen type I, with involvement of the mitogen-activated protein kinase signaling pathway.
机译:在本研究中,在慢性坐骨神经压迫的大鼠模型中研究了背根神经节(DRG)神经元的病理改变。慢性坐骨神经受压的大鼠模型是通过在右坐骨神经周围放置1厘米的硅橡胶管而建立的。组织学检查通过Masson三色染色进行。使用Fluoro Ruby(FR)或Fluoro Gold(FG)评估DRG损伤。使用逆转录-定量聚合酶链反应,蛋白质印迹和免疫组化分析检查靶基因的表达水平。压缩后3周,在同侧区域观察到胶原纤维积聚,并且在8周时,观察到过量胶原形成与肌肉萎缩。坐骨神经受压后胶原蛋白的体积分数逐渐增加。在模型大鼠中,与假手术组相比,FR标记的DRG神经元的数量明显多,但是FG标记的神经元的数量相似。在模型组的同侧DRG神经元中,转化生长因子1(TGF-1)和结缔组织生长因子(CTGF)的水平升高,并且在神经元周围,I型胶原的水平与对侧DRG中的那些。在同侧DRG中,与正常人相比,慢性神经压迫与磷酸化(p)-细胞外信号调节激酶1/2的水平显着升高,pc-Jun N端激酶和p-p38的水平显着降低有关。对侧DRG。慢性坐骨神经压迫可能通过上调TGF-1,CTGF和I型胶原的表达水平来诱导DRG病理,并参与有丝分裂原激活的蛋白激酶信号通路。

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