Detail
Article
Online article
FT
Medvik - BMC
  • Something wrong with this record ?

Ulinastatin alleviates neurological deficiencies evoked by transient cerebral ischemia via improving autophagy, Nrf-2-ARE and apoptosis signals in hippocampus

X. M. Jiang, J. H. Hu, L. L. Wang, C. Ma, X. Wang, X. L. Liu

. 2018 ; 67 (4) : 637-646. [pub] 20180510

Language English Country Czech Republic

Document type Journal Article

Persistent link   https://www.medvik.cz/link/bmc19004014

Ulinastatin [or called as urinary trypsin inhibitor (UTI)] plays a role in regulating neurological deficits evoked by transient cerebral ischemia. However, the underlying mechanisms still need to be determined. The present study was to examine the effects of UTI on autophagy, Nrf2-ARE and apoptosis signal pathway in the hippocampus in the process of neurological functions after cerebral ischemia using a rat model of cardiac arrest (CA). CA was induced by asphyxia followed by cardiopulmonary resuscitation (CPR) in rats. Western blot analysis was employed to determine the expression of representative autophagy (namely, Atg5, LC3, Beclin 1), p62 protein (a maker of autophagic flux), and Nrf2-ARE pathways. Neuronal apoptosis was assessed by determining expression levels of Caspase-3 and Caspase-9, and by examining terminal deoxynucleotide transferase-mediated dUTP nick-end labeling (TUNEL). The modified neurological severity score (mNSS) and spatial working memory performance were used to assess neurological deficiencies in CA rats. Our results show that CA amplified autophagy and apoptotic Caspase-3/Caspase-9, and downregulated Nrf2-ARE pathway in the hippocampus CA1 region. Systemic administration of UTI attenuated autophagy and apoptosis, and largely restored Nrf2-ARE signal pathway following cerebral ischemia and thereby alleviated neurological deficits with increasing survival of CA rats. Our data suggest that UTI improves the worsened protein expression of autophagy and apoptosis, and restores Nrf2-ARE signals in the hippocampus and this is linked to inhibition of neurological deficiencies in transient cerebral ischemia. UTI plays a beneficial role in modulating neurological deficits induced by transient cerebral ischemia via central autophagy, apoptosis and Nrf2-ARE mechanisms.

References provided by Crossref.org

000      
00000naa a2200000 a 4500
001      
bmc19004014
003      
CZ-PrNML
005      
20190208091450.0
007      
ta
008      
190124s2018 xr ad f 000 0|eng||
009      
AR
024    7_
$a 10.33549/physiolres.933780 $2 doi
035    __
$a (PubMed)29750875
040    __
$a ABA008 $b cze $d ABA008 $e AACR2
041    0_
$a eng
044    __
$a xr
100    1_
$a Jiang, Xiao-Ming $u Department of Emergency Medicine, The First Hospital of Jilin University, Changchun, Jilin, China
245    10
$a Ulinastatin alleviates neurological deficiencies evoked by transient cerebral ischemia via improving autophagy, Nrf-2-ARE and apoptosis signals in hippocampus / $c X. M. Jiang, J. H. Hu, L. L. Wang, C. Ma, X. Wang, X. L. Liu
520    9_
$a Ulinastatin [or called as urinary trypsin inhibitor (UTI)] plays a role in regulating neurological deficits evoked by transient cerebral ischemia. However, the underlying mechanisms still need to be determined. The present study was to examine the effects of UTI on autophagy, Nrf2-ARE and apoptosis signal pathway in the hippocampus in the process of neurological functions after cerebral ischemia using a rat model of cardiac arrest (CA). CA was induced by asphyxia followed by cardiopulmonary resuscitation (CPR) in rats. Western blot analysis was employed to determine the expression of representative autophagy (namely, Atg5, LC3, Beclin 1), p62 protein (a maker of autophagic flux), and Nrf2-ARE pathways. Neuronal apoptosis was assessed by determining expression levels of Caspase-3 and Caspase-9, and by examining terminal deoxynucleotide transferase-mediated dUTP nick-end labeling (TUNEL). The modified neurological severity score (mNSS) and spatial working memory performance were used to assess neurological deficiencies in CA rats. Our results show that CA amplified autophagy and apoptotic Caspase-3/Caspase-9, and downregulated Nrf2-ARE pathway in the hippocampus CA1 region. Systemic administration of UTI attenuated autophagy and apoptosis, and largely restored Nrf2-ARE signal pathway following cerebral ischemia and thereby alleviated neurological deficits with increasing survival of CA rats. Our data suggest that UTI improves the worsened protein expression of autophagy and apoptosis, and restores Nrf2-ARE signals in the hippocampus and this is linked to inhibition of neurological deficiencies in transient cerebral ischemia. UTI plays a beneficial role in modulating neurological deficits induced by transient cerebral ischemia via central autophagy, apoptosis and Nrf2-ARE mechanisms.
650    _2
$a zvířata $7 D000818
650    _2
$a antioxidační responzivní elementy $x účinky léků $x fyziologie $7 D061745
650    _2
$a apoptóza $x účinky léků $x fyziologie $7 D017209
650    _2
$a autofagie $x účinky léků $x fyziologie $7 D001343
650    _2
$a glykoproteiny $x farmakologie $x terapeutické užití $7 D006023
650    _2
$a hipokampus $x účinky léků $x metabolismus $x patologie $7 D006624
650    _2
$a tranzitorní ischemická ataka $x farmakoterapie $x metabolismus $x patologie $7 D002546
650    _2
$a mužské pohlaví $7 D008297
650    _2
$a faktor 2 související s NF-E2 $x metabolismus $7 D051267
650    _2
$a neuroprotektivní látky $x farmakologie $x terapeutické užití $7 D018696
650    _2
$a náhodné rozdělení $7 D011897
650    _2
$a krysa rodu Rattus $7 D051381
650    _2
$a potkani Sprague-Dawley $7 D017207
650    _2
$a signální transdukce $x účinky léků $x fyziologie $7 D015398
650    _2
$a inhibitory trypsinu $x farmakologie $x terapeutické užití $7 D014361
655    _2
$a časopisecké články $7 D016428
700    1_
$a Hu, Jing-Hai $u Department of Urology, The First Hospital of Jilin University, Changchun, Jilin, China
700    1_
$a Wang, Lu-Lu $u Cardiovascular Center for Diagnostics and Treatment, The First Hospital of Jilin University, Changchun, Jilin, China
700    1_
$a Ma, Chi $u Department of Brain Tumor Surgery, The First Hospital of Jilin University, Changchun, Jilin, China
700    1_
$a Wang, Xu $u Department of Neurology and Neuroscience Center, The First Hospital of Jilin University, Changchun, Jilin, China
700    1_
$a Liu, Xiao-Liang $u Department of Emergency Medicine, The First Hospital of Jilin University, Changchun, Jilin, China
773    0_
$w MED00003824 $t Physiological research $x 1802-9973 $g Roč. 67, č. 4 (2018), s. 637-646
856    41
$u https://pubmed.ncbi.nlm.nih.gov/29750875 $y Pubmed
910    __
$a ABA008 $b A 4120 $c 266 $y 4 $z 0
990    __
$a 20190124 $b ABA008
991    __
$a 20190208082151 $b ABA008
999    __
$a ok $b bmc $g 1374803 $s 1042192
BAS    __
$a 3
BAS    __
$a PreBMC
BMC    __
$a 2018 $b 67 $c 4 $d 637-646 $e 20180510 $i 1802-9973 $m Physiological research $n Physiol. Res. (Print) $x MED00003824
LZP    __
$b NLK118 $a Pubmed-20190124

Find record

Citation metrics

Archiving options