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首页> 外文期刊>Brain research >Effects of dexmedetomidine on P2X4Rs, p38-MAPK and BDNF in spinal microglia in rats with spared nerve injury
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Effects of dexmedetomidine on P2X4Rs, p38-MAPK and BDNF in spinal microglia in rats with spared nerve injury

机译：右美托咪定对神经损伤大鼠脊髓小胶质细胞P2X4Rs，p38-MAPK和BDNF的影响

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Microglia in the spinal cord is evidenced to play a crucial role in neuropathic pain. Spinal P2X4 receptors (P2X4Rs), which are mainly expressed in microglia, have been investigated for their roles in neuropathic pain. Dexmedetomidine (DEX), a highly selective agonist of a2-adrenergic receptors, is clinically applied to sedation and analgesia. Despite the proposed mechanisms underlying DEX-induced analgesia, the possible interactions between DEX and P2X4Rs at a molecular level have not been elucidated. We designated the spared nerve injury (SNI) to establish the neuropathic pain model. Mechanical paw withdrawal threshold (MWT) was measured to evaluate the sensitivity of neuropathic pain in rats. MWT was significantly decreased in SNI rats versus control rats. Expressions of spinal P2X4Rs, phosphorylated p38-mitogen-activated protein kinase (p-p38-MAPK) and brain-derived neurotrophic factor (BDNF) were upregulated in SNI rats. Immunofluores-cence assay indicated higher densities of microglia and P2X4Rs, which appeared yellow in colour, suggesting they were co-labelled. Intraperitoneal injections of DEX 40 ng/kg for 14 consecutive days markedly reversed the SNI-induced decline of MWT; the activation of microglia was markedly inhibited; in addition, the protein expressions of P2X4Rs, p-p38-MAPK and BDNF were significantly downregulated. Thus, DEX could attenuate the neuropathic pain in SNI rats, of which the mechanism might be related to the down-expressed P2X4Rs, p-p38 and BDNF in microglia of spinal dorsal horn.
机译：脊髓中的小胶质细胞被证明在神经性疼痛中起关键作用。已经研究了主要在小胶质细胞中表达的脊髓P2X4受体（P2X4Rs）在神经性疼痛中的作用。右美托咪定（DEX）是α2-肾上腺素能受体的高度选择性激动剂，临床上已用于镇静和镇痛。尽管提出了DEX诱导的镇痛的潜在机制，但尚未阐明DEX和P2X4R在分子水平上的可能相互作用。我们指定了备用的神经损伤（SNI）以建立神经性疼痛模型。测量机械爪退缩阈值（MWT）以评估大鼠神经性疼痛的敏感性。与对照组相比，SNI大鼠的MWT明显降低。在SNI大鼠中，脊髓P2X4Rs，磷酸化p38-促分裂原活化蛋白激酶（p-p38-MAPK）和脑源性神经营养因子（BDNF）的表达上调。免疫荧光法检测表明小胶质细胞和P2X4Rs的密度较高，颜色呈黄色，表明它们是共标记的。连续14天腹腔注射DEX 40 ng / kg明显逆转了SNI引起的MWT下降;小胶质细胞的激活被明显抑制。此外，P2X4Rs，p-p38-MAPK和BDNF的蛋白表达明显下调。因此，DEX可以减轻SNI大鼠的神经性疼痛，其机制可能与脊髓背角小胶质细胞中P2X4Rs，p-p38和BDNF的下调有关。

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