Curcumin amends Ca2+ dysregulation in microglia by suppressing the activation of P2X7 receptor
Autor: | Kui Jia, Zhen Wang, Caili Liu, Ren Weihua, Fucheng Zhao, Yanru Han |
---|---|
Rok vydání: | 2020 |
Předmět: |
0301 basic medicine
Clinical chemistry Clinical Biochemistry Pharmacology 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine mental disorders medicine Post-stroke depression Middle cerebral artery occlusion Molecular Biology P2x7 receptor Neuroinflammation Microglia musculoskeletal neural and ocular physiology Sucrose preference Cell Biology General Medicine 030104 developmental biology medicine.anatomical_structure nervous system chemistry 030220 oncology & carcinogenesis Curcumin psychological phenomena and processes |
Zdroj: | Molecular and Cellular Biochemistry. 465:65-73 |
ISSN: | 1573-4919 0300-8177 |
DOI: | 10.1007/s11010-019-03668-8 |
Popis: | Curcumin (Cur) is widely used as an anti-inflammation agent and has anti-depression potential. Neuroinflammation mediated by Ca2+ channel activation is closely associated with the progression of post-stroke depression (PSD). In the current study, the role of P2X7 receptor (P2X7R) in the anti-PSD function of Cur was explored. Rats were subjected to middle cerebral artery occlusion (MCAO) surgery and chronic mild stress administration to induce PSD symptoms and then treated with Cur. The behaviors of rats were assessed with sucrose preference and forced swim tests. The accumulation of Ca2+ and the systemic inflammatory response in rats were detected. To determine the role of P2X7R in the anti-PSD function of curcumin, the PSD mice were further administrated with P2X7R agonist and antagonist. The administration of Cur attenuated behavior disorders associated with PSD. Moreover, the Ca2+ accumulation and the inflammatory response associated with PSD were also blocked by Cur. Cur also inhibited the activation of Ca2+ channel. The induced activity of P2X7R blocked the function of Cur by maintaining the symptoms of PSD in Cur-treated rats. Collectively, the anti-PSD function of Cur was dependent on the inhibition of P2X7R, which then deactivated Ca2+ channel-mediated inflammatory response associated with PSD progression. |
Databáze: | OpenAIRE |
Externí odkaz: |