TREM-1在大鼠脑出血后继发性脑损伤中的作用机制  被引量:2

Role of TREM-1 in the formation of secondary brain injury after intracerebral hemorrhage in rats

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作  者:段红玲 孙新刚[2] 张咪咪[1] 侯雅芝 DUAN Hongling;SUN Xingang;ZHANG Mimi;HOU Yazhi(Shanxi Medical University,Taiyuan 030001,China;Second Hospital of Shanxi Medical University,Taiyuan 030001,China;Shanxi Cardiovascular Hospital,Taiyuan 030024,China)

机构地区:[1]山西医科大学,山西太原030001 [2]山西医科大学第二医院,山西太原030001 [3]山西省心血管病医院,山西太原030024

出  处:《临床医药实践》2020年第7期523-525,共3页Proceeding of Clinical Medicine

基  金:山西省应用基础研究项目(项目编号:201701D221269)

摘  要:目的:观察髓系细胞触发受体-1(TREM-1)在大鼠脑出血(ICH)后继发性脑损伤形成中的作用机制。方法:采用自体注血法制作大鼠ICH组,ICH+LP17组及假手术组模型,比较各组大鼠脑组织含水量,以实时荧光定量PCR(RT-PCR)法检测各组大鼠脑组织中TREM-1和P38丝裂原活化蛋白激酶(p38MAPK)及细胞外信号调节激酶1/2(ERK1/2)的表达。结果:与假手术组相比,ICH组大鼠脑组织中TREM-1及其下游p38MAPK/ERK1/2的表达明显升高,脑组织含水量明显增加;抑制TREM-1的表达可使其下游p38MAPK/ERK1/2的表达明显减少,脑组织含水量明显减轻。结论:TREM-1可能会通过p38MAPK/ERK1/2途径来调控ICH后继发性脑损伤的形成。Objective:To observe the mechanism of triggering receptor expressed on myeloid cell-1(TREM-1)in the formation of secondary brain injury after intracerebral hemorrhage(ICH)in rats.Methods:The rat models of ICH group,ICH+LP17 group and sham were established by autologous blood injection.The water content of brain tissue in each group was compared,and the expression of TREM-1,p38 mitogen-activated protein kinase(p38MAPK)and extracellular signal-regulated kinase 1/2(ERK1/2)in brain tissue of each group was detected by RT-PCR method.Results:Compared with the sham,the expression of TREM-1 and its downstream p38MAPK/ERK1/2 in ICH group was significantly increased,and the brain water content was significantly increased.Inhibition of TREM-1 expression could significantly decrease the expression of p38MAPK/ERK1/2 downstream and reduce the water content of brain.Conclusion:TREM-1 may regulate the formation of secondary brain injury after ICH through p38MAPK/ERK1/2 pathway.

关 键 词:脑出血 髓系细胞触发受体-1 继发性脑损伤 

分 类 号:R743.34[医药卫生—神经病学与精神病学]

 

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