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Inhibition of Neurogenic Inflammation Attenuates the Inflammatory Response Following Traumatic Brain Injury in Rats

机译:神经源性炎症的抑制减轻了大鼠创伤性脑损伤后的炎症反应

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A profound inflammatory response is initiated following traumatic brain injury (TBI). It has been proposed that serum IL-6 levels may serve as a marker for the severity of the injury. Using the rat impact-acceleration model of TBI, the study examined whether drugs which are able to inhibit neurogenic inflammation (capsaicin, NK1 antagonist), might influence the post-traumatic inflammatory response. In non-treated animals, TBI resulted in a significant increase in serum IL-6 levels. However, in animals pre-treated with capsaicin prior to injury, or treated with an NK1 antagonist following injury, this rise in IL-6 levels was not observed. We conclude that the inhibition of neurogenic inflammation may attenuate the inflammatory reaction associated with TBI, and help improve outcome.
机译:在创伤性脑损伤(TBI)后开始引发深度炎症反应。已经提出,血清IL-6水平可以作为损伤严重程度的标志物。使用TBI的大鼠冲击加速模型,研究检查了能够抑制神经源性炎症(辣椒素,NK1拮抗剂)的药物是否可能影响创伤后炎症反应。在未治疗的动物中,TBI导致血清IL-6水平显着增加。然而,在损伤前用辣椒素预处理的动物,或用损伤后的NK1拮抗剂处理,未观察到IL-6水平的这种升高。我们得出结论,神经源性炎症的抑制可以衰减与TBI相关的炎症反应,并有助于改善结果。

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