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

Zhijia Tang | Zendy; Xiaobao Shao | Zendy; Jun Wu | Zendy; Hucheng Chen | Zendy; Anyu Zhang | Zendy; Fei Xu | Zendy; Ping He | Zendy; Shiwei Li | Zendy; Chunyan Liu | Zendy; Yijun Li | Zendy; Xue Xue | Zendy; Yuan Bin-bin | Zendy

Open Access

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

Author(s) -

Zhijia Tang,

Xiaobao Shao,

Jun Wu,

Hucheng Chen,

Anyu Zhang,

Fei Xu,

Ping He,

Shiwei Li,

Chunyan Liu,

Yijun Li,

Xue Xue,

Yuan Bin-bin

Publication year - 2021

Publication title -

computational and mathematical methods in medicine

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.462

H-Index - 48

eISSN - 1748-6718

pISSN - 1748-670X

DOI - 10.1155/2021/7731528

Subject(s) - neuroinflammation , potassium channel , lipopolysaccharide , (+) naloxone , pharmacology , atp sensitive potassium channel , microglia , chemistry , potassium channel blocker , potassium , neuroscience , medicine , endocrinology , inflammation , biology , biochemistry , antagonist , receptor , glibenclamide , diabetes mellitus , organic chemistry

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- α , IL-1 β , 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.

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