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首页> 外文期刊>eNeurologicalSci >Intrathecal Noggin administration in rats temporally ameliorates mechanical allodynia induced by a chronic constriction injury
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Intrathecal Noggin administration in rats temporally ameliorates mechanical allodynia induced by a chronic constriction injury

机译：大鼠鞘内注射Noggin可暂时改善慢性收缩损伤所致的机械性异常性疼痛

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Chronic intractable neuropathic pain after central or peripheral nervous system injury remains refractory to therapeutic intervention. Using microarray and RT-qPCR methods, we found that Noggin mRNA is downregulated in the lumbar enlargement 2 weeks after chronic constriction injury (CCI) in rats. Eight-week-old female Sprague Dawley rats were used for the CCI model. Two weeks after CCI, rats underwent a laminectomy at L5 under halothane anesthesia, and a silicone tube connected to an osmotic minipump was inserted intrathecally for 14 days. Rats were administered Noggin ranging from 10 ng/ml to 10 μg/ml. Phosphate buffered saline (PBS) was used as a control. The time course of mechanical allodynia was assessed for 5 weeks using von Frey filaments. An ANOVA showed that rats administered Noggin at 2 μg/ml had significantly less mechanical allodynia compared with controls. We next compared the effect of intrathecal administration (14 days) of Noggin (2 μg/ml), bone morphogenetic protein 4 (BMP4; 2 μg/ml), or BMP4 (μg/ml) + Noggin (μg/ml) with controls. Only Noggin administration significantly reduced mechanical allodynia in the CCI model. Fluorescence immunohistochemistry indicated that Noggin administration decreased astrocyte accumulation in the dorsal horn compared with PBS after administration for one week. BMP4-driven conversion of oligodendrocyte progenitor cells (OPCs) to type 2 astrocytes is inhibited by Noggin Hampton et al. (2007) . We speculated that Noggin administration inhibits the conversion of OPCs to astrocytes, and decreases glial fibrillar acidic protein expression. This histological condition could decrease neuropathic pain. Highlights ? Noggin mRNA is significantly down-regulated two weeks after CCI in rats. ? The mechanical allodynia was decreased in Noggin administration at seven days. ? Noggin administration influenced GFAP expression and reduced mechanical allodynia.
机译：中枢或周围神经系统损伤后的慢性顽固性神经性疼痛仍难于治疗干预。使用微阵列和RT-qPCR方法，我们发现大鼠慢性收缩性损伤（CCI）后2周，腰部肿胀中Noggin mRNA的表达下调。将八周大的雌性Sprague Dawley大鼠用于CCI模型。 CCI后两周，大鼠在氟烷麻醉下于L5进行椎板切除术，并将与渗透性微型泵相连的硅胶管鞘内插入14天。给大鼠施用范围从10ng / ml至10μg/ ml的头蛋白。磷酸盐缓冲盐水（PBS）用作对照。使用von Frey细丝评估了机械性异常性疼痛的时程为5周。方差分析表明，与对照组相比，以2μg/ ml的剂量施用Noggin的大鼠具有明显更少的机械异常性疼痛。接下来，我们比较了鞘内注射Noggin（2μg/ ml），骨形态发生蛋白4（BMP4; 2μg/ ml）或BMP4（μg/ ml）+ Noggin（μg/ ml）鞘内给药（14天）的效果。仅Noggin给药可显着降低CCI模型中的机械异常性疼痛。荧光免疫组织化学表明，与施用PBS相比，Noggin施用1周后减少了背角中星形胶质细胞的积累。 Noggin Hampton等人抑制了BMP4驱动的少突胶质祖细胞（OPC）向2型星形胶质细胞的转化。 （2007）。我们推测，Noggin给药抑制了OPC向星形胶质细胞的转化，并降低了神经胶质原纤维酸性蛋白的表达。这种组织学状况可以减轻神经性疼痛。强调 ？大鼠CCI后两周，Noggin mRNA显着下调。 ？ Noggin给药第7天使机械性异常性疼痛减少。 ？ Noggin的使用影响了GFAP的表达并减少了机械性异常性疼痛。

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