GPR30激活通过抑制NLRP3炎症小体形成改善蛛网膜下腔出血后早期脑损伤  

Protective effect of GPR30 activation inhibiting NLRP3 inflammasome on early brain injury after subarachnoid hemorrhage

作　　者：陈立刚 蒋琳 孔睿 李侑埕 梁国标 CHEN Ligang;JIANG Lin;KONG Rui;LI Youcheng;LIANG Guobiao(Hospital of Northern Theater Command,Shenyang,110016,China;Department of Gynaecology,Department of Maternal and Child Health Care,Lanzhou,730050,China)

机构地区：[1]北部战区总医院神经外科,辽宁沈阳110016 [2]甘肃省妇幼保健院妇科,甘肃兰州730050

出　　处：《沈阳药科大学学报》2022年第11期1362-1367,共6页Journal of Shenyang Pharmaceutical University

基　　金：国家自然科学基金资助项目(81971133)。

摘　　要：目的探讨GPR30激活对蛛网膜下腔出血的影响及其对NLRP3炎性小体形成的影响。方法采用SD大鼠随机分成三组:假手术组、SAH模型组和SAH模型+GPR30激活剂G1组,每组24只,颈内动脉穿刺法构建SAH模型。SAH 24 h小时后进行神经功能评分;检测脑水肿和Evans Blue渗出率;并利用Western blot和ELISA方法检测NLRP3、ASC、caspase1、IL-1β和IL-18的表达水平;TUNEL染色观察蛛网膜下腔出血后神经元的凋亡情况。结果GPR30激活能够降低NLRP3、caspase1、ASC、IL-1β和IL-18的表达(P<0.05),减少神经元凋亡。结论GPR30激活能够抑制NLRP3炎症小体的形成和神经元凋亡而改善蛛网膜下腔出血后的早期脑损伤。Objective To investigate the effect of GPR30 activation on subarachnoid hemorrhage and its relationship with NLRP3 inflammasome activation.Methods SD rats were randomly divided into three groups(sham group,SAH model group,SAH model+GPR30 activator G1 group)with 24 rats in each group.SAH model was established by internal carotid artery puncture.Neurological score was performed at 24 hours after SAH.Brain edema and Evans Blue exudation rate were detected.Western blot and ELISA were used to detect the expression levels of NLRP3,ASC,caspase1,IL-1βand IL-18.TUNEL staining was used to observe neuronal apoptosis after subarachnoid hemorrhage.Results Activation of GPR30 could reduce the expressions of NLRP3,caspase1,ASC,IL-1βand IL-18(P<0.05),and reduce neuronal apoptosis.Conclusion GPR30 activation can inhibit the formation of NLRP3 inflammasome and neuronal apoptosis,thus improving brain injury after subarachnoid hemorrhage.

关 键 词：GPR30 NLRP3炎症小体 蛛网膜下腔出血 神经元凋亡 

分 类 号：R737.14[医药卫生—肿瘤]