A novel vanadium complex VO(p-dmada)inhibits neuroinflammation induced by lipopolysaccharide  

作　　者：Zhijun He Xiaoqian Li Huajie Zhang Xin Liu Shuangxue Han Anwar Abdurahman Liming Shen Xiubo Du Nan Li Xiaoda Yang Qiong Liu 

机构地区：[1]Shenzhen Key Laboratory of Marine Biotechnology and Ecology,College of Life Sciences and Oceanography,Shenzhen University,Shenzhen 518055,China [2]National R&D Center for Se-rich Agricultural Products Processing,Hubei Engineering Research Center for Deep Processing of Green Se-rich Agricultural Products,School of Modern Industry for Selenium Science and Engineering,Wuhan Polytechnic University,Wuhan 430023,China [3]Shenzhen Bay Laboratory,Shenzhen 518055,China [4]State Key Laboratories of Natural and Biomimetic Drugs,Department of Chemical Biology,School of Pharmaceutical Sciences,Peking University Health Science Center,Beijing 100191,China [5]Department of Pharmacy,Shenzhen People’s Hospital(The Second Clinical Medical College,Jinan University,The First Affiliated Hospital,Southern University of Science and Technology),Shenzhen 518020,China [6]Shenzhen-Hong Kong Institute of Brain Science-Shenzhen Fundamental Research Institutions,Shenzhen 518055,China

出　　处：《Chinese Chemical Letters》2023年第10期209-214,共6页中国化学快报（英文版）

基　　金：financially supported by grants from the National Natural Science Foundation of China(No.21877081);the China Postdoctoral Science Foundation(No.2021M692210);Guangdong Provincial Key S&T Program(No.2018B030336001);the Shenzhen Science and Technology Innovation Commission(No.JCYJ20200109110001818);the Shenzhen-Hong Kong Institute of brain Science-Shenzhen Fundamental Research institutions(No.2022SHIBS0003)。

摘　　要：Uncontrolled microglial activation is decisively involved in the neuroinflammatory pathogenesis of brain diseases. Consequently, suppression of microglial overactivation appears to be a strategy for the prevention of nerve injury. In this paper, a novel vanadium complex, vanadyl N-(p-N,Ndimethylaminophenylcarbamoylmethyl)iminodiacetate(VO(p-dmada)), was synthesized from vanadyl sulfate and N,N-dimethyl-p-phenylenediamine, which was structurally characterized by Fourier transform infrared spectrum and ESI-MS analysis. The effect of VO(p-dmada) on neuroinflammation was investigated by using the models of lipopolysaccharide(LPS)-induced BV2 microglial cells and BALB/c mice.Our data demonstrated that VO(p-dmada) significantly suppressed microglial activation by downregulating inflammatory mediators and associated proteins, and inactivating nuclear factor-κ B(NF-κ B) signaling pathway. VO(p-dmada) also upregulated peroxisome proliferator activated receptor gamma(PPARγ) by reducing transglutaminase 2 and heat shock protein 60 expression. Co-treatment with PPARγ antagonist GW9662 significantly impeded the inhibitory effect of VO(p-dmada) on LPS-induced neuroinflammation.These cumulative findings demonstrated that VO(p-dmada) is a potential new drug for the treatment of neuroinflammation-related neurodegenerative diseases.

关 键 词：Vanadium Vanadyl N-(p-N Ndimethylaminophenylcarbamoylmethyl)iminodiacetate (VO(p-dmada)) NEUROINFLAMMATION MICROGLIA Proteomics Peroxisome proliferator activated receptor gamma(PPARγ) 

分 类 号：R741[医药卫生—神经病学与精神病学] TQ460.1[医药卫生—临床医学]