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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Activation of liver x receptors prevents the spinal LTP induced by skin/muscle retraction in the thigh via SIRT1/NF-Kb pathway
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Activation of liver x receptors prevents the spinal LTP induced by skin/muscle retraction in the thigh via SIRT1/NF-Kb pathway

机译：肝脏X受体的激活可防止通过SIRT1 / NF-KB途径在大腿中皮肤/肌肉缩回引起的脊柱LTP

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It has been reported that skin/muscle incision and retraction (SMIR) in the thigh, produces mechanical allodynia in the hind paw, far from the site of incision/retraction. The mechanical allodynia lasts about 22 days, indicating chronic post-operative pain develops. The precise mechanisms, however, are largely unclear. In the current study, we further found that SMIR surgery induced LTP of c-fiber evoked field potentials that lasted at least 4 h. The mRNA and protein level of tumor necrosis factor-alpha (TNF alpha) and acetylated nuclear factor-kappaB p65 (ac-NF-kappa B p65) in the lumbar spinal dorsal horn was gradually increased during LTP development, while pretreatment with either TNF alpha neutralization antibody or NF-kappa B inhibitor PDTC completely prevented the induction of LTP. Moreover, the expression of Silent information regulator 1 (SIRT1) in the lumbar spinal dorsal horn was decreased and activation of SIRT1 by SRT1720 also prevented the induction of LTP. Importantly, the spinal expression of Liver X receptors (LXRs) was increased, both at mRNA and protein level following SMIR. Application of LXRs agonist T0901317 to the spinal dorsal horn prevented LTP induction following SMIR. Mechanistically, T0901317 enhanced the expression of SIRT1 and decreased the expression of ac-NF-kappa B p65 and TNF alpha. Spinal application of SIRT1 antagonist EX-527, 30 min before T0901317 administration, completely blocked the inhibiting effect of T0901317 on LTP, and on expression of ac-NF-kappa B p65 and TNF alpha. These results indicated that activation of LXRs prevented SMIR-induced LTP by inhibiting NF-kappa B/TNF alpha pathway via increasing SIRT1 expression.
机译：据报道，大腿的皮肤/肌肉切口和缩回（SMIR），在后爪中产生机械异常性疼痛，远离切口/缩回。机械异常疼痛持续约22天，表明慢性术后疼痛发展。然而，精确的机制在很大程度上不清楚。在目前的研究中，我们进一步发现，SMIR手术诱发了C-纤维的LTP诱发的现场电位，持续至少4小时。在LTP发育期间腰椎坏死因子-α和乙酰化核因子-Kappab P65（AC-NF-Kappa B P65）的mRNA和蛋白水平患者在腰椎背角中逐渐增加，同时用TNFα进行预处理中和抗体或NF-Kappa B抑制剂PDTC完全防止了LTP的诱导。此外，腰椎背角中的静音信息调节器1（SIRT1）的表达降低，SRT1720的SIRT1的激活也防止了LTP的诱导。重要的是，肝X受体（LXRS）的脊柱表达增加，在SMIR后MRNA和蛋白质水平。 LXRS激动剂T0901317在脊髓背圈防止脊髓岩后的应用。机械地，T0901317增强了SIRT1的表达并降低了AC-NF-Kappa B P65和TNFα的表达。 SIRT1拮抗剂EX-527，30分钟的脊髓施用在T0901317给药之前，完全阻断了T0901317对LTP的抑制作用，以及AC-NF-Kappa B P65和TNFα的表达。这些结果表明，通过增加SIRT1表达，通过抑制NF-Kappa B / TNFα途径阻止LXRS的激活。

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