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Effects of Brilliant Blue G on Serum Tumor Necrosis Factor-alpha Levels and Depression-like Behavior in Mice after Lipopolysaccharide Administration
Article in En | WPRIM | ID: wpr-53120
Responsible library: WPRO
ABSTRACT
OBJECTIVE: Accumulating evidence suggests that inflammation plays a role in the pathophysiology of major depression. The adenosine triphosphate (ATP)-sensitive P2X7 receptor (P2X7R) plays a crucial role in microglial activation caused by inflammation. The dye brilliant blue G (BBG) is a P2X7R antagonist. This study examined whether BBG shows antidepressant effects in an inflammation-induced model of depression. METHODS: We examined the effects of BBG (12.5, 25, or 50 mg/kg) on serum tumor necrosis factor-alpha (TNF-alpha) levels after administering the bacterial endotoxin lipopolysaccharide (LPS; 0.5 mg/kg) and the effects of BBG (50 mg/kg) on depression-like behavior in the tail-suspension test (TST) and forced swimming test (FST). RESULTS: Pretreatment with BBG (12.5, 25, or 50 mg/kg) significantly blocked the increase in serum TNF-alpha levels after a single dose of LPS (0.5 mg/kg). Furthermore, BBG (50 mg/kg) significantly attenuated the increase in immobility time in the TST and FST after LPS (0.5 mg/kg) administration. CONCLUSION: The results suggest that BBG has anti-inflammatory and antidepressant effects in mice after LPS administration. Therefore, P2X7R antagonists are potential therapeutic drugs for inflammation-related major depression.
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Full text: 1 Database: WPRIM Main subject: Adenosine Triphosphate / Tumor Necrosis Factor-alpha / Depression / Physical Exertion / Receptors, Purinergic P2X7 / Inflammation Type of study: Prognostic_studies Limits: Animals Language: En Journal: Clinical Psychopharmacology and Neuroscience Year: 2014 Document type: Article
Full text: 1 Database: WPRIM Main subject: Adenosine Triphosphate / Tumor Necrosis Factor-alpha / Depression / Physical Exertion / Receptors, Purinergic P2X7 / Inflammation Type of study: Prognostic_studies Limits: Animals Language: En Journal: Clinical Psychopharmacology and Neuroscience Year: 2014 Document type: Article