摘要
急性脊髓损伤(spinal cord injury,SCI)发生时,损伤部位具有神经保护作用的M2型小胶质细胞/巨噬细胞转换成具有神经毒性的M1型,并分泌大量炎性介质,同时上调犬尿氨酸信号通路(kynurenine pathway,KP)的犬尿氨酸3-羟化酶,引起兴奋性毒素喹啉酸(quinolinic acid,QUIN)分泌,进一步促进神经炎症,最终加重脊髓继发性损伤。这一过程还涉及血红素氧化酶1(heme oxygenase-1,HO-1)和红细胞相关因子2(nuclear factor erythroid 2-related factor 2,Nrf2)信号通路。近年大量的研究发现,通过调节KP抑制QUIN可用于治疗神经性疾病和SCI,本文就以上内容做一简要综述。
Following the occurrence of acute spinal cord injury(SCI),M2 microglia/macrophages,which have neuroprotective function,convert into neurotoxic M1 type and secrete a large number of inflammatory mediators.Meanwhile,M1 microglia/macrophages upregulate the kynurenine 3-monooxygenase(KMO)branch of the kynurenine pathway(KP),resulting in the production of excess excitotoxin quinolinic acid(QUIN),which promotes neurotoxicity and aggravates secondary injury of SCI finally.In addition,heme oxygenase-1(HO-1)and nuclear factor erythroid 2-related factor 2(Nrf2)pathways are also involved in this process.Recent studies have acknowledged that inhibition of QUIN through regulating KP pathway can be used to treat neurological diseases and SCI.This article briefly reviews the related researches mentioned above.
作者
钟佳师
郭祥
刘亦恒
符策岗
Zhong Jiashi;Guo Xiang;Liu Yiheng;Fu Cegang(Department of The Spinal Surgery,People’s Hospital of Lingao County in Hainan Province,Lingao 571800;Department of orthopedics,Haikou People‘s Hospital,Xiangya Medical College,Central South University,Haikou 570208;Department of orthopedics,Orthopedics and Diabetes Hospital in Haikou,Shanghai sixth People’s Hospital,Haikou 570000)
出处
《中国组织化学与细胞化学杂志》
CAS
CSCD
2019年第6期547-551,共5页
Chinese Journal of Histochemistry and Cytochemistry
基金
海南省卫计委科教项目(18A200115)。
