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Curcumin Confers Neuroprotection Against Alcohol-Induced Hippocampal Neurodegeneration Via Creb-Bdnf Pathway in Rats Publisher Pubmed



Motaghinejad M1 ; Motevalian M1 ; Fatima S2 ; Hashemi H1 ; Gholami M3
Authors
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Authors Affiliations
  1. 1. Razi Drug Research Center & Department of Pharmacology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran
  2. 2. Department of Physiology, Tehran University of Medical Sciences, International Campus, Tehran, Iran
  3. 3. Department of Medical Chemistry, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran

Source: Biomedicine and Pharmacotherapy Published:2017


Abstract

Background Alcohol abuse causes severe damage to the brain neurons. Studies have reported the neuroprotective effects of curcumin against alcohol-induced neurodegeneration. However, the precise mechanism of action remains unclear. Methods Seventy rats were equally divided into 7 groups (10 rats per group). Group 1 received normal saline (0.7 ml/rat) and group 2 received alcohol (2 g/kg/day) for 21 days. Groups 3, 4, 5 and 6 concurrently received alcohol (2 g/kg/day) and curcumin (10, 20, 40 and 60 mg/kg, respectively) for 21 days. Animals in group 7 self- administered alcohol for 21 days. Group 8 treated with curcumin (60 mg/kg, i.p.) alone for 21 days. Open Field Test (OFT) was used to investigate motor activity in rats. Hippocampal oxidative, antioxidative and inflammatory factors were evaluated. Furthermore, brain cyclic adenosine monophosphate (cAMP) response element binding protein (CREB) and brain derived neurotrophic factor (BDNF) levels were studied at gene level by reverse transcriptase polymerase chain reaction (RT-PCR). In addition, protein expression for BDNF, CREB, phosphorylated CREB (CREB-P), Bax and Bcl-2 was determined by western blotting. Result Voluntary and involuntary administration of alcohol altered motor activity in OFT, and curcumin treatment inhibited this alcohol-induced motor disturbance. Also, alcohol administration augmented lipid peroxidation, mitochondrial oxidized glutathione (GSSG), interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α) and Bax levels in isolated hippocampal tissues. Furthermore, alcohol-induced significant reduction were observed in reduced form of glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione reductase (GR) activities and CREB, BDNF and Bcl-2 levels. Also curcumin alone did not change the behavior and biochemical and molecular parameters. Conclusion Curcumin can act as a neuroprotective agent against neurodegenerative effects of alcohol abuse, probably via activation of CREB-BDNF signaling pathway. © 2017 Elsevier Masson SAS
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