Nerve decompression surgery suppresses TNF-a; expression and T cell infiltration in a rat sciatic nerve chronic constriction injury model
Nerve decompression surgery suppresses TNF-a; expression and T cell infiltration in a rat sciatic nerve chronic constriction injury model
复制标题
神经减压手术抑制TNF-a；
作者：
Mukai M;Uchida K;Inoue G;Satoh M;Miyagi M;Yokozeki Y;Hirosawa N;Matsuura Y;Ohtori S;Takaso M
减压手术（DS）是慢性神经压迫损伤的标准治疗方法；然而，其影响的机制仍不清楚。在这里，我们研究了 DS 对大鼠坐骨神经 (SN) 慢性缩窄性损伤 (CCI) 模型中肿瘤坏死因子-α (TNF-α) 信使 RNA (mRNA) 表达和 T 细胞募集的影响。雄性Wistar大鼠经CCI建立SN损伤模型（CCI组）。 CCI手术后3天进行DS，其中所有结扎线均被移除（CCI + dec组）。 CCI 手术后 3、7 和 14 天使用 von Frey 试验评估机械敏感性。分别使用定量聚合酶链反应 (qPCR) 和免疫组织化学评估 Tnfa、Cd3、Cxcl10 的基因表达以及 TNF-α 和泛 T 细胞标记物 CD3 的免疫定位。此外，在 SN 细胞培养物中使用 qPCR 和酶联免疫吸附测定评估了 TNF-α 对 Cxcl10 表达和 CXCL10 蛋白产生的影响。接受 DS 的大鼠的戒断阈值水平显着高于 CCI 组的大鼠。此外，CCI 后 Tnfa、Cd3 和 Cxcl10 mRNA 表达增加。 DS 抑制了这种升高的表达，与 CCI 组相比，CCI + dec 组的表达水平显着降低。此外，TNF-α 在 SN 细胞培养物中诱导 Cxcl10 表达和 CXCL10 蛋白产生。因此，DS 减少了大鼠 SN CCI 模型中 TNF-α 的表达和 T 细胞的募集。这些观察结果可能部分解释了 DS 治疗效果的机制。
Decompression surgery (DS) is a standard treatment for chronic nerve compression injuries; however, the mechanisms underlying its effects remain unclear. Here, we investigated the effects of DS on messenger RNA (mRNA) expression of tumor necrosis factor‐α (TNF‐α) and T cell recruitment in a rat sciatic nerve (SN) chronic constriction injury (CCI) model. Male Wistar rats were subjected to CCI to establish a model of SN injury (CCI group). DS, in which all ligatures were removed, was performed 3 days after CCI surgery (CCI + dec group). Mechanical sensitivity was assessed using the von Frey test 3, 7, and 14 days after the CCI surgery. Gene expression ofTnfa, Cd3, Cxcl10, and immunolocalization of TNF‐α and the pan T cell marker, CD3, was evaluated using quantitative polymerase chain reaction (qPCR) and immunohistochemistry, respectively. In addition, the effects of TNF‐α onCxcl10expression and CXCL10 protein production were evaluated using qPCR and enzyme‐linked immunosorbent assay in SN cell culture. Rats that received DS had significantly higher withdrawal threshold levels than those in the CCI group. In addition,Tnfa, Cd3, andCxcl10mRNA expression increased following CCI. DS suppressed this elevated expression, with the CCI + dec group showing significantly reduced expression levels compared to the CCI group. Furthermore, TNF‐α inducedCxcl10expression and CXCL10 protein production in SN cell culture. Therefore, DS reduced TNF‐α expression and T cell recruitment in the rat SN CCI model. These observations may partly explain the mechanism underlying the therapeutic effects of DS.