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Inhibition of AGEs/RAGE/Rho/ROCK pathway suppresses non-specific neuroinflammation by regulating BV2 microglial M1/M2 polarization through the NF-κB pathway.

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收录情况： ◇ SCIE

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机构： [1]School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China [2]International Joint Laboratory (SYSU-PolyU HK) of Novel Anti-dementia Drugs of Guangdong, Guangzhou 510006, China [3]National and Local United Engineering Lab of Drug ability and New Drugs Evaluation, Sun Yat-sen University, Guangzhou 510080, China [4]Department of TCM, the First Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510080, China [5]Department of Applied Biology and Chemical Technology, Hong Kong Polytechnic University, Hong Kong, China [6]Guangdong Province Key Laboratory of Brain Function and Disease, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China

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关键词： Alzheimer's disease BV2 cells Neuroinflammation Advanced glycation end products Rho kinase

摘要：

The microglia-mediated neuroinflammation plays an important role in the pathogenesis of Alzheimer's disease (AD). Advanced glycation end products (AGEs)/receptor for advanced glycation end products (RAGE) or Rho/Rho kinase (ROCK) are both involved in the development of non-specific inflammation. However, there are few reports about their effects on neuroinflammation. Here, we explored the mechanism of AGEs/RAGE/Rho/ROCK pathway underlying the non-specific inflammation and microglial polarization in BV2 cells. AGEs could activate ROCK pathway in a concentration-dependent manner. ROCK inhibitor fasudil and RAGE-specific blocker FPS-ZM1 significantly inhibited AGEs-mediated activation of BV2 cells and induction of reactive oxygen species (ROS). FPS-ZM1 and fasudil exerted their anti-inflammatory effects by downregulating inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), NLRP3 and nuclear translocation of nuclear factor kappa B (NF-κB) p65. In addition, AGEs induced both M1 (CD16/32, M1 marker) and M2 (CD206, M2 marker) phenotype in BV2 cells. Fasudil and FPS-ZM1 led to a decreased M1 and increased M2 phenotype. Together, these results indicate that the AGEs/RAGE/Rho/ROCK pathway in BV2 cells could intensify the non-specific inflammation of AD, which will provide novel strategies for the development of anti-AD drugs. Copyright © 2017 Elsevier B.V. All rights reserved.

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出版当年[2016]版：

大类 | 3 区医学

小类 | 4 区免疫学 4 区神经科学

最新[2025]版：

大类 | 4 区医学

小类 | 4 区免疫学 4 区神经科学

JCR分区：

出版当年[2015]版：

Q3 NEUROSCIENCES Q3 IMMUNOLOGY

最新[2023]版：

Q2 NEUROSCIENCES Q3 IMMUNOLOGY

影响因子： 2.9 最新[2023版] 3 最新五年平均 2.536 出版当年[2015版] 2.67 出版当年五年平均 2.467 出版前一年[2014版] 2.72 出版后一年[2016版]

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第一作者机构： [1]School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China [2]International Joint Laboratory (SYSU-PolyU HK) of Novel Anti-dementia Drugs of Guangdong, Guangzhou 510006, China [3]National and Local United Engineering Lab of Drug ability and New Drugs Evaluation, Sun Yat-sen University, Guangzhou 510080, China [6]Guangdong Province Key Laboratory of Brain Function and Disease, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China

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通讯作者：

通讯机构： [1]School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China [2]International Joint Laboratory (SYSU-PolyU HK) of Novel Anti-dementia Drugs of Guangdong, Guangzhou 510006, China [3]National and Local United Engineering Lab of Drug ability and New Drugs Evaluation, Sun Yat-sen University, Guangzhou 510080, China [6]Guangdong Province Key Laboratory of Brain Function and Disease, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China [*1]School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China.

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Inhibition of AGEs/RAGE/Rho/ROCK pathway suppresses non-specific neuroinflammation by regulating BV2 microglial M1/M2 polarization through the NF-κB pathway.

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