PMID- 28388365
OWN - NLM
STAT- MEDLINE
DCOM- 20180301
LR  - 20181202
IS  - 1205-7541 (Electronic)
IS  - 0008-4212 (Linking)
VI  - 95
IP  - 7
DP  - 2017 Jul
TI  - Protective effects of telmisartan and tempol on lipopolysaccharide-induced 
      cognitive impairment, neuroinflammation, and amyloidogenesis: possible role of 
      brain-derived neurotrophic factor.
PG  - 850-860
LID - 10.1139/cjpp-2017-0042 [doi]
AB  - Angiotensin II has pro-inflammatory and pro-oxidant potentials. We investigated 
      the possible protective effects of the Angiotensin II receptor blocker 
      telmisartan, compared with the superoxide scavenger tempol, on lipopolysaccharide 
      (LPS)-induced cognitive decline and amyloidogenesis. Briefly, mice were allocated 
      into a normal control group, an LPS control group, a tempol treatment group, and 
      2 telmisartan treatment groups. A behavioral study was conducted followed by a 
      biochemical study via assessment of brain levels of beta amyloid (Abeta) and 
      brain-derived neurotropic factor (BDNF) as amyloidogenesis and neuroplasticity 
      markers, tumor necrosis factor alpha (TNF-alpha), nitric oxide end products (NOx), 
      neuronal and inducible nitric oxide synthase (nNOS and 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 routine and special Congo red stains. 
      Tempol and telmisartan improved cognition, decreased brain Abeta deposition and BDNF 
      depletion, decreased TNF-alpha, NOx, nNOS, iNOS, MDA, and NT brain levels, and 
      increased brain SOD and GSH contents, parallel to confirmatory histopathological 
      evidences. In conclusion, tempol and telmisartan are promising drugs in managing 
      cognitive impairment and amyloidogenesis, at least via upregulation of BDNF with 
      inhibition of neuroinflammation and oxido-nitrosative stress.
FAU - Khallaf, Waleed A I
AU  - Khallaf WAI
AD  - a Department of Pharmacology and Toxicology, Faculty of Pharmacy, Beni-Suef 
      University, Beni Suef, Egypt.
FAU - Messiha, Basim A S
AU  - Messiha BAS
AD  - a Department of Pharmacology and Toxicology, Faculty of Pharmacy, Beni-Suef 
      University, Beni Suef, Egypt.
FAU - Abo-Youssef, Amira M H
AU  - Abo-Youssef AMH
AD  - a Department of Pharmacology and Toxicology, Faculty of Pharmacy, Beni-Suef 
      University, Beni Suef, Egypt.
FAU - El-Sayed, Nesrine S
AU  - El-Sayed NS
AD  - b Department of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo 
      University, Giza, Egypt.
LA  - eng
PT  - Journal Article
DEP - 20170407
PL  - Canada
TA  - Can J Physiol Pharmacol
JT  - Canadian journal of physiology and pharmacology
JID - 0372712
RN  - 0 (Amyloid)
RN  - 0 (Benzimidazoles)
RN  - 0 (Benzoates)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Cyclic N-Oxides)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Spin Labels)
RN  - U5SYW473RQ (Telmisartan)
RN  - U78ZX2F65X (tempol)
SB  - IM
MH  - Amyloid/*metabolism
MH  - Animals
MH  - Benzimidazoles/*pharmacology/therapeutic use
MH  - Benzoates/*pharmacology/therapeutic use
MH  - Brain-Derived Neurotrophic Factor/*metabolism
MH  - Cognitive Dysfunction/chemically induced/*drug therapy
MH  - Cyclic N-Oxides/*pharmacology/therapeutic use
MH  - Cytoprotection/drug effects
MH  - Inflammation/chemically induced/drug therapy
MH  - Lipopolysaccharides/*adverse effects
MH  - Male
MH  - Mice
MH  - Oxidative Stress/drug effects
MH  - Spin Labels
MH  - Telmisartan
OTO - NOTNLM
OT  - amyloidogenesis
OT  - amyloidogenese
OT  - brain-derived neurotropic factor
OT  - facteur neurotrophique derive du cerveau
OT  - neuro-inflammation
OT  - neuroinflammation
OT  - telmisartan
OT  - tempol
EDAT- 2017/04/08 06:00
MHDA- 2018/03/02 06:00
CRDT- 2017/04/08 06:00
PHST- 2017/04/08 06:00 [pubmed]
PHST- 2018/03/02 06:00 [medline]
PHST- 2017/04/08 06:00 [entrez]
AID - 10.1139/cjpp-2017-0042 [doi]
PST - ppublish
SO  - Can J Physiol Pharmacol. 2017 Jul;95(7):850-860. doi: 10.1139/cjpp-2017-0042. 
      Epub 2017 Apr 7.