Spinal cord injury (SCI) is a severe central nervous system trauma. The present study aimed to evaluate the effect of HIF-1α on inflammation in spinal cord injury (SCI) to uncover the molecular mechanisms of anti-inflammation. HIF-1α was reduced in SCI model rats and HIF-1α activation reduced TNF-α, IL-1β, IL-6 and IL-18 levels in SCI model rats. Meanwhile, Circ 0001723 expression was down-regulated and miR-380-3p expression was up-regulated in SCI model rats. In vitro model, down-regulation of Circ 0001723 promoted TNF-α, IL-1β, IL-6 and IL-18 levels, compared with control negative group. However, over-expression of Circ 0001723 reduced TNF-α, IL-1β, IL-6 and IL-18 levels in vitro model. Down-regulation of Circ 0001723 suppressed HIF-1α protein expressions and induced NLRP3 and Caspase-1 protein expressions in vitro model by up-regulation of miR-380-3p. Next, inactivation of HIF-1α reduced the pro-inflammation effects of Circ 0001723 in vitro model. Then, si-NLRP3 also inhibited the pro-inflammation effects of Circ 0001723 in vitro model via promotion of autophagy. We concluded that HIF-1α reduced inflammation in spinal cord injury via miR-380-3p/ NLRP3 by Circ 0001723.

中文翻译：

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缺氧诱导因子-1（HIF-1α）通过miR-380-3p / NLRP3通过Circ 0001723减轻了脊髓损伤中的炎症。

脊髓损伤（SCI）是严重的中枢神经系统创伤。本研究旨在评估HIF-1α对脊髓损伤（SCI）中炎症的影响，以揭示抗炎症的分子机制。在SCI模型大鼠中，HIF-1α降低，而在SCI模型大鼠中，HIF-1α激活降低TNF-α，IL-1β，IL-6和IL-18的水平。同时，SCI模型大鼠中Circ 0001723表达下调，miR-380-3p表达上调。在体外模型中，与对照组相比，Circ 0001723的下调促进了TNF-α，IL-1β，IL-6和IL-18的水平。然而，Circ 0001723的过表达降低了体外模型中的TNF-α，IL-1β，IL-6和IL-18水平。通过上调miR-380-3p，在体外模型中Circ 0001723的下调抑制了HIF-1α蛋白的表达，并诱导NLRP3和Caspase-1的蛋白表达。接下来，HIF-1α的失活降低了Circ 0001723体外模型的促炎作用。然后，si-NLRP3还通过促进自噬而抑制了Circ 0001723体外模型的促炎作用。我们得出结论，Circ 0001723证实，HIF-1α通过miR-380-3p / NLRP3减轻了脊髓损伤中的炎症。