TUG-891 inhibits neuronal endoplasmic reticulum stress and pyroptosis activation and protects neurons in a mouse model of intraventricular hemorrhage  

作　　者：Hao-Xiang Wang Chang Liu Yuan-You Li Yi Cao Long Zhao Yan-Jie Zhao Zi-Ang Deng Ai-Ping Tong Liang-Xue Zhou 

机构地区：[1]Department of Neurosurgery,West China Hospital,Sichuan University,Chengdu,Sichuan Province,China [2]Department of Neurosurgery,The First Affiliated Hospital of Chongqing Medical University,Chongqing,China [3]Department of Neurosurgery,Chengdu Second People’s Hospital,Chengdu,Sichuan Province,China [4]Department of Neurosurgery,Affiliated Hospital of North Sichuan Medical College,Nanchong,Sichuan Province,China [5]State Key Laboratory of Biotherapy,West China Medical School,Sichuan University,Chengdu,Sichuan Province,China

出　　处：《Neural Regeneration Research》2023年第10期2278-2284,共7页中国神经再生研究（英文版）

摘　　要：Pyroptosis plays an important role in hemorrhagic stroke.Excessive endoplasmic reticulum stress can cause endoplasmic reticulum dysfunction and cellular pyroptosis by regulating the nucleotide-binding oligomerization domain and leucine-rich repeat pyrin domain-containing protein 3(NLRP3)pathway.However,the relationship between pyroptosis and endoplasmic reticulum stress after intraventricular hemorrhage is unclear.In this study,we established a mouse model of intraventricular hemorrhage and found pyroptosis and endoplasmic reticulum stress in brain tissue.Intraperitoneal injection of the selective GPR120 agonist TUG-891 inhibited endoplasmic reticulum stress,pyroptosis,and inflammation and protected neurons.The neuroprotective effect of TUG-891 appears related to inhibition of endoplasmic reticulum stress and pyroptosis activation.

关 键 词：ameliorating inflammation endoplasmic reticulum stress GPR120 GSDMD hemorrhagic stroke neurological function NLRP3 PYROPTOSIS TUG-891 unfolded protein response 

分 类 号：R741[医药卫生—神经病学与精神病学]