• Je něco špatně v tomto záznamu ?

14-3-3ζ protein protects against brain ischemia/reperfusion injury and induces BDNF transcription after MCAO in rat

Naeemeh Khalesi, Mojgan Bandehpour, Mohammad Reza Bigdeli, Hassan Niknejad, Ali Dabbagh, Bahram Kazemi

. 2019 ; 17 (2) : 99-106.

Jazyk angličtina Země Česko

Typ dokumentu práce podpořená grantem

Perzistentní odkaz   https://www.medvik.cz/link/bmc19032531

Brain ischemia is a leading cause of death and disability worldwide that occurs when blood supply of the brain is disrupted. Brain-derived neurotrophic factor (BDNF) is a protective factor in neurodegenerative conditions. Nevertheless, there are some problems when exogenous BDNF is to be used in the clinic. 14-3-3ζ is a pro-survival highly-expressed protein in the brain that protects neurons against death. This study evaluates 14-3-3ζ effects on BDNF transcription at early time point after ischemia and its possible protective effects against ischemia damage. Human 14-3-3ζ protein was purified after expression. Rats were assigned into four groups, including sham, ischemia, and two treatment groups. Stereotaxic cannula implantation was carried out in the right cerebral ventricle. After one week, rats underwent middle cerebral artery occlusion (MCAO) surgery and received 14-3-3ζ (produced in our laboratory or standard form as control) in the middle of ischemia time. At 6 h of reperfusion after ischemia, brain parts containing the hippocampus, the cortex, the piriform cortex-amygdala and the striatum were collected for real time PCR analysis. At 24 h of reperfusion after ischemia, neurological function evaluation and infarction volume measurement were performed. The present study showed that 14-3-3ζ could up-regulate BDNF mRNA at early time point after ischemia in the hippocampus, in the cortex and in the piriform cortex-amygdala and could also improve neurological outcome and reduce infarct volume. It seems that 14-3-3ζ could be a candidate factor for increasing endogenous BDNF in the brain and a potential therapeutic factor against brain ischemia.

Citace poskytuje Crossref.org

Bibliografie atd.

Literatura

000      
00000naa a2200000 a 4500
001      
bmc19032531
003      
CZ-PrNML
005      
20200420112719.0
007      
ta
008      
190923s2019 xr ad f 000 0|eng||
009      
AR
024    7_
$a 10.32725/jab.2019.007 $2 doi
040    __
$a ABA008 $d ABA008 $e AACR2 $b cze
041    0_
$a eng
044    __
$a xr
100    1_
$a Khalesi, Naeemeh $u Shahid Beheshti University of Medical Sciences, School of Advanced Technologies in Medicine, Biotechnology Department, Tehran, Iran
245    10
$a 14-3-3ζ protein protects against brain ischemia/reperfusion injury and induces BDNF transcription after MCAO in rat / $c Naeemeh Khalesi, Mojgan Bandehpour, Mohammad Reza Bigdeli, Hassan Niknejad, Ali Dabbagh, Bahram Kazemi
504    __
$a Literatura
520    9_
$a Brain ischemia is a leading cause of death and disability worldwide that occurs when blood supply of the brain is disrupted. Brain-derived neurotrophic factor (BDNF) is a protective factor in neurodegenerative conditions. Nevertheless, there are some problems when exogenous BDNF is to be used in the clinic. 14-3-3ζ is a pro-survival highly-expressed protein in the brain that protects neurons against death. This study evaluates 14-3-3ζ effects on BDNF transcription at early time point after ischemia and its possible protective effects against ischemia damage. Human 14-3-3ζ protein was purified after expression. Rats were assigned into four groups, including sham, ischemia, and two treatment groups. Stereotaxic cannula implantation was carried out in the right cerebral ventricle. After one week, rats underwent middle cerebral artery occlusion (MCAO) surgery and received 14-3-3ζ (produced in our laboratory or standard form as control) in the middle of ischemia time. At 6 h of reperfusion after ischemia, brain parts containing the hippocampus, the cortex, the piriform cortex-amygdala and the striatum were collected for real time PCR analysis. At 24 h of reperfusion after ischemia, neurological function evaluation and infarction volume measurement were performed. The present study showed that 14-3-3ζ could up-regulate BDNF mRNA at early time point after ischemia in the hippocampus, in the cortex and in the piriform cortex-amygdala and could also improve neurological outcome and reduce infarct volume. It seems that 14-3-3ζ could be a candidate factor for increasing endogenous BDNF in the brain and a potential therapeutic factor against brain ischemia.
650    12
$a ischemie mozku $x metabolismus $7 D002545
650    _2
$a receptor trkB $x metabolismus $x účinky léků $7 D020813
650    _2
$a vazba proteinů $7 D011485
650    _2
$a proteiny 14-3-3 $x farmakologie $x terapeutické užití $7 D048948
650    _2
$a neuroprotektivní látky $7 D018696
650    _2
$a modely nemocí na zvířatech $7 D004195
650    _2
$a infarkt arteria cerebri media $x farmakoterapie $x metabolismus $x patologie $7 D020244
650    _2
$a izoformy RNA $x metabolismus $x účinky léků $7 D059368
650    _2
$a laboratorní zvířata $7 D000830
650    _2
$a potkani Wistar $7 D017208
650    _2
$a mužské pohlaví $7 D008297
650    _2
$a dospělí $7 D000328
655    _2
$a práce podpořená grantem $7 D013485
700    1_
$a Bandehpour, Mojgan $u Shahid Beheshti University of Medical Sciences, Cellular and Molecular Biology Research Center, Tehran, Iran
700    1_
$a Bigdeli, Mohammad Reza $u Shahid Beheshti University, Faculty of Life Sciences and Biotechnology, Department of Animal Sciences and Biotechnology, Tehran, Iran; Shahid Beheshti University, Institute for Cognitive and Brain Science, Tehran, Iran
700    1_
$a Niknejad, Hassan $u Shahid Beheshti University of Medical Sciences, School of Medicine, Department of Pharmacology, Tehran, Iran
700    1_
$a Dabbagh, Ali $u Shahid Beheshti University of Medical Sciences, Anesthesiology Research Center, Tehran, Iran
700    1_
$a Kazemi, Bahram $u Shahid Beheshti University of Medical Sciences, School of Advanced Technologies in Medicine, Biotechnology Department, Tehran, Iran; Shahid Beheshti University of Medical Sciences, Cellular and Molecular Biology Research Center, Tehran, Iran
773    0_
$t Journal of applied biomedicine $x 1214-021X $g Roč. 17, č. 2 (2019), s. 99-106 $w MED00012667
856    41
$u https://jab.zsf.jcu.cz/pdfs/jab/2019/02/02.pdf $y plný text volně přístupný
910    __
$a ABA008 $b B 2301 $c 1249 $y p $z 0
990    __
$a 20190923112237 $b ABA008
991    __
$a 20200420112711 $b ABA008
999    __
$a ok $b bmc $g 1446012 $s 1071036
BAS    __
$a 3
BMC    __
$a 2019 $b 17 $c 2 $d 99-106 $i 1214-021X $m Journal of Applied Biomedicine $x MED00012667
LZP    __
$c NLK125 $d 20200420 $a NLK 2019-36/dk

Najít záznam

Citační ukazatele

Možnosti archivace