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Jun, 2016;389 (6): 637-56.

Tempol and perindopril protect against lipopolysaccharide-induced cognition impairment and amyloidogenesis by modulating brain-derived neurotropic factor, neuroinflammation and oxido-nitrosative stress.

Mohammed Ragab Abdel-Aziz Ali, Amira Morad Hussein Abo-Youssef, Basim Anwar Shehata Messiha, Mahmoud Mohamed Khattab
Author Information
  1. Mohammed Ragab Abdel-Aziz Ali: Department of Pharmacology and Toxicology, Faculty of Pharmacy, Beni-Suef University, Beni Suef, Beni Suef Governorate, Egypt.
  2. Amira Morad Hussein Abo-Youssef: Department of Pharmacology and Toxicology, Faculty of Pharmacy, Beni-Suef University, Beni Suef, Beni Suef Governorate, Egypt.
  3. Basim Anwar Shehata Messiha: Department of Pharmacology and Toxicology, Faculty of Pharmacy, Beni-Suef University, Beni Suef, Beni Suef Governorate, Egypt. drbasimanwar2006@yahoo.com.
  4. Mahmoud Mohamed Khattab: Department of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Cairo University Rd, Oula, Giza Governorate, Egypt.
PMID: 27026404 DOI: 10.1007/s00210-016-1234-6

Abstract

We aim to evaluate the protective role of the central angiotensin-converting enzyme (ACE) inhibitor perindopril, compared with the standard reactive oxygen species (ROS) scavenger tempol, against lipopolysaccharide (LPS)-induced cognition impairment and amyloidogenesis in a simulation to Alzheimer's disease (AD). mice were allocated into a control group, an LPS control group (0.8 mg/kg, i.p., once), a tempol (100 mg/kg/day, p.o., 7 days) treatment group, and two perindopril (0.5 and 1 mg/kg/day, p.o., 7 days) treatment groups. A behavioral study was conducted to evaluate spatial and nonspatial memory in mice, followed by a biochemical study involving assessment of brain levels of Aβ and BDNF as Alzheimer and neuroplasticity markers; tumor necrosis factor-alpha (TNF-α), nitric oxide end-products (NOx), neuronal nitric oxide synthase (nNOS), and inducible nitric oxide synthase (iNOS) as inflammatory markers; and superoxide dismutase (SOD), malondialdehyde (MDA), glutathione reduced (GSH), and nitrotyrosine (NT) as oxido-nitrosative stress markers. Finally, histopathological examination of cerebral cortex, hippocampus, and cerebellum sections was performed using both routine and special staining. tempol and perindopril improved spatial and nonspatial memory in mice without affecting locomotor activity; decreased brain Aβ deposition and BDNF depletion; decreased brain TNF-α, NOx, nNOS, iNOS, MDA, and NT levels; and increased brain SOD and GSH contents, parallel to confirmatory histopathological findings. tempol and perindopril may be promising agents against AD progression via suppression of Aβ deposition and BDNF decline, suppression of TNF-α production, support of brain antioxidant status, and amelioration of oxido-nitrosative stress and NT production.

Keywords

Amyloidogenesis Brain-derived neurotropic factor Neuroinflammation Oxido-nitrosative stress Perindopril Tempol

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MeSH Term

Alzheimer Disease
Amyloid beta-Peptides
Angiotensin-Converting Enzyme Inhibitors
Animals
Antioxidants
Behavior, Animal
Biomarkers
Brain
Brain-Derived Neurotrophic Factor
Cognition
Cognition Disorders
Cyclic N-Oxides
Disease Models, Animal
Inflammation Mediators
Lipopolysaccharides
Male
Maze Learning
Mice, Inbred BALB C
Motor Activity
Neuroprotective Agents
Oxidative Stress
Perindopril
Reactive Nitrogen Species
Recognition, Psychology
Spatial Memory
Spin Labels
Time Factors

Chemicals

Amyloid beta-Peptides
Angiotensin-Converting Enzyme Inhibitors
Antioxidants
Biomarkers
Brain-Derived Neurotrophic Factor
Cyclic N-Oxides
Inflammation Mediators
Lipopolysaccharides
Neuroprotective Agents
Reactive Nitrogen Species
Spin Labels
tempol
Perindopril
Comparative Study Journal Article

Word Cloud

Created with Highcharts 10.0.0perindoprilbrainstressTempolgrouppAβBDNFmarkersTNF-αnitricoxideNToxido-nitrosativeevaluatetempolLPScognitionimpairmentamyloidogenesisADcontrol0o7 daystreatmentstudyspatialnonspatialmemorymicelevelsNOxsynthasenNOSiNOSSODMDAGSHhistopathologicaldecreaseddepositionsuppressionproductionneurotropicfactoraimprotectiverolecentralangiotensin-convertingenzymeACEinhibitorcomparedstandardreactiveoxygenspeciesROSscavengerlipopolysaccharide-inducedsimulationAlzheimer'sdiseaseMiceallocated8 mg/kgi100 mg/kg/daytwo51 mg/kg/daygroupsbehavioralconductedfollowedbiochemicalinvolvingassessmentAlzheimerneuroplasticitytumornecrosisfactor-alphaend-productsneuronalinducibleinflammatorysuperoxidedismutasemalondialdehydeglutathionereducednitrotyrosineFinallyexaminationcerebralcortexhippocampuscerebellumsectionsperformedusingroutinespecialstainingimprovedwithoutaffectinglocomotoractivitydepletionincreasedcontentsparallelconfirmatoryfindingsmaypromisingagentsprogressionviadeclinesupportantioxidantstatusameliorationprotectlipopolysaccharide-inducedmodulatingbrain-derivedneuroinflammationAmyloidogenesisBrain-derivedNeuroinflammationOxido-nitrosativePerindopril

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