Naloxone Protects against Lipopolysaccharide-Induced Neuroinflammation and Microglial Activation via Inhibiting ATP-Sensitive Potassium Channel

被引：5

作者：

Tang, Zhijia ^{[1
]}

Shao, Xiaobao ^{[2
]}

Wu, Jun ^{[3
,4
]}

Chen, Hucheng ^{[5
]}

Zhang, Anyu ^{[5
]}

Xu, Fei ^{[6
]}

Ping, He ^{[5
]}

Li, Shiwei ^{[5
]}

Liu, Chunyan ^{[5
]}

Li, Yijun ^{[5
]}

Xue, Xue ^{[5
]}

Yuan, Binbin ^{[7
]}

机构：

[1] Tongling Technol Coll, Dept Med, Tongling 244061, Anhui, Peoples R China

[2] Nanjing Univ Chinese Med, Affiliated Nanjing Tradit Chinese Med Hosp, Dept Transfus Med, Nanjing 210022, Peoples R China

[3] Nanjing Med Univ, Dept Clin Lab, Nanjing Brain Hosp, Nanjing 210029, Peoples R China

[4] Nanjing Med Univ, Affiliated Brain Hosp, Nanjing 210029, Peoples R China

[5] Nanjing Med Univ, Nanjing Hosp 1, Dept Nucl Med, Nanjing 210006, Peoples R China

[6] Nanjing Med Univ, Nanjing Hosp 1, Dept Transfus Med, Nanjing 210006, Peoples R China

[7] Haimen Peoples Hosp, Dept Neurosurg, Nantong 226100, Peoples R China

来源：

COMPUTATIONAL AND MATHEMATICAL METHODS IN MEDICINE | 2021年 / 2021卷

基金：

中国国家自然科学基金;

关键词：

ALZHEIMERS-DISEASE; OXIDATIVE STRESS; INFLAMMATION; REDUCTION;

D O I：

10.1155/2021/7731528

中图分类号：

Q [生物科学];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Aim. The aim of this study was to evaluate the anti-inflammatory effects and underlying mechanism of naloxone on lipopolysaccharide- (LPS-) induced neuronal inflammation and microglial activation. Methods. LPS-treated microglial BV-2 cells and mice were used to investigate the anti-inflammatory effects of naloxone. Results. The results showed that naloxone dose-dependently promoted cell proliferation in LPS-induced BV-2 cells, downregulated the expression of proinflammatory cytokines (TNF-alpha, IL-1 beta, and IL-6) and proinflammatory enzymes iNOS and COX-2 as well as the expression of free radical molecule NO, and reduced the expression of Iba-1-positive microglia in LPS-stimulated BV-2 cells and mouse brain. Moreover, naloxone improved LPS-induced behavior degeneration in mice. Mechanically, naloxone inhibited LPS-induced activation in the ATP-sensitive potassium (KATP) channel. However, the presence of glibenclamide (Glib), an antagonist of KATP channel, ameliorated the suppressive effects of naloxone on inflammation and microglial activation. Conclusion. Naloxone prevented LPS-induced neuroinflammation and microglial activation partially through the KATP channel. These findings might highlight the potential of naloxone in neuroinflammation therapy.

引用

页数：9

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