Naloxone Protects against Lipopolysaccharide-Induced Neuroinflammation and Microglial Activation via Inhibiting ATP-Sensitive Potassium Channel
Autor: | Xue Xue, Chunyan Liu, Zhang Anyu, Binbin Yuan, Fei Xu, Xiaobao Shao, Yijun Li, Shiwei Li, Zhijia Tang, Jun Wu, He Ping, Hucheng Chen |
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Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
0301 basic medicine
Lipopolysaccharides Article Subject Lipopolysaccharide ATP-sensitive potassium channel Narcotic Antagonists Computer applications to medicine. Medical informatics R858-859.7 Inflammation (+)-Naloxone Pharmacology General Biochemistry Genetics and Molecular Biology Proinflammatory cytokine Cell Line Glibenclamide 03 medical and health sciences chemistry.chemical_compound Mice 0302 clinical medicine KATP Channels medicine Animals Neuroinflammation Cell Proliferation Mice Inbred BALB C General Immunology and Microbiology Microglia Behavior Animal Chemistry Naloxone Applied Mathematics Anti-Inflammatory Agents Non-Steroidal Computational Biology Neurodegenerative Diseases General Medicine Disease Models Animal 030104 developmental biology medicine.anatomical_structure Modeling and Simulation medicine.symptom 030217 neurology & neurosurgery medicine.drug Research Article |
Zdroj: | Computational and Mathematical Methods in Medicine Computational and Mathematical Methods in Medicine, Vol 2021 (2021) |
ISSN: | 1748-6718 1748-670X |
Popis: | 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-1β, 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. |
Databáze: | OpenAIRE |
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