PMID- 29514562
OWN - NLM
STAT- MEDLINE
DCOM- 20200226
LR  - 20200226
IS  - 1476-8305 (Electronic)
IS  - 1028-415X (Linking)
VI  - 22
IP  - 11
DP  - 2019 Nov
TI  - Evaluation of antioxidant and anti-inflammatory efficacy of caffeine in rat model 
      of neurotoxicity.
PG  - 789-796
LID - 10.1080/1028415X.2018.1446812 [doi]
AB  - Objective: The present study aims to investigate the neuroprotective effect of 
      caffeine against aluminum chloride (AlCl(3))-induced neurotoxicity in rats. 
      Methods: Twenty-one male albino rats were divided into 3 groups: control, 
      AlCl(3)-intoxicated group that received daily oral administration of AlCl(3) 
      (100 mg/kg for 30 days) and protected group injected daily with caffeine 
      (20 mg/kg intraperitoneally) one hour before oral administration of AlCl(3) for 
      30 days. Levels of lipid peroxidation, reduced glutathione, and nitric oxide and 
      the activities of acetylcholinesterase (AchE) and Na(+)/K(+)-ATPase were measured 
      spectrophotometrically. Tumor necrosis factor-alpha (TNF-alpha) was evaluated by ELISA 
      kit. Results: The data revealed evidence of oxidative and nitrosative stress in 
      the cerebral cortex, hippocampus, and striatum of AlCl(3)-intoxicated rats. This 
      was indicated from the increased levels of lipid peroxidation and nitric oxide 
      together with the decreased level of reduced glutathione. Moreover, the daily 
      AlCl(3) administration increased AchE and Na(+)/K(+)-ATPase activities and the 
      level of TNF-alpha in the selected brain regions. Protection with caffeine 
      ameliorated the oxidative stress induced by AlCl(3) in the cerebral cortex, 
      hippocampus, and striatum. In addition, caffeine restored the elevated level of 
      TNF-alpha in the hippocampus and striatum. This was accompanied by an improvement in 
      the activities of AchE and Na(+)/K(+)-ATPase in the studied brain regions. 
      Discussion and conclusions: The present findings clearly indicate that caffeine 
      provides a significant neuroprotection against AlCl(3)-induced neurotoxicity 
      mediated by its antioxidant, anti-inflammatory, and anticholinesterase 
      properties.
FAU - Hosny, Eman N
AU  - Hosny EN
AD  - Medical Physiology Department, Medical Division, National Research Centre , Giza 
      , Egypt.
FAU - Sawie, Hussein G
AU  - Sawie HG
AUID- ORCID: 0000-0001-6112-7580
AD  - Medical Physiology Department, Medical Division, National Research Centre , Giza 
      , Egypt.
FAU - Elhadidy, Mohamed E
AU  - Elhadidy ME
AD  - Department of Research on Children with Special Needs, National Research Centre , 
      Giza , Egypt.
FAU - Khadrawy, Yasser A
AU  - Khadrawy YA
AD  - Medical Physiology Department, Medical Division, National Research Centre , Giza 
      , Egypt.
LA  - eng
PT  - Journal Article
DEP - 20180307
PL  - England
TA  - Nutr Neurosci
JT  - Nutritional neuroscience
JID - 100892202
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Antioxidants)
RN  - 0 (Neuroprotective Agents)
RN  - 3CYT62D3GA (Aluminum Chloride)
RN  - 3G6A5W338E (Caffeine)
SB  - IM
MH  - Aluminum Chloride/toxicity
MH  - Animals
MH  - Anti-Inflammatory Agents, Non-Steroidal/*administration & dosage
MH  - Antioxidants/*administration & dosage
MH  - Brain/*drug effects/metabolism
MH  - Caffeine/*administration & dosage
MH  - Lipid Peroxidation/drug effects
MH  - Male
MH  - Neuroprotective Agents/*administration & dosage
MH  - Neurotoxicity Syndromes/*drug therapy
MH  - Oxidative Stress/drug effects
MH  - Rats
MH  - Rats, Wistar
OTO - NOTNLM
OT  - Acetylcholinesterase
OT  - Aluminum
OT  - Caffeine
OT  - Neuroinflammation
OT  - Oxidative stress
EDAT- 2018/03/09 06:00
MHDA- 2020/02/27 06:00
CRDT- 2018/03/09 06:00
PHST- 2018/03/09 06:00 [pubmed]
PHST- 2020/02/27 06:00 [medline]
PHST- 2018/03/09 06:00 [entrez]
AID - 10.1080/1028415X.2018.1446812 [doi]
PST - ppublish
SO  - Nutr Neurosci. 2019 Nov;22(11):789-796. doi: 10.1080/1028415X.2018.1446812. Epub 
      2018 Mar 7.