PMID- 29704511
OWN - NLM
STAT- MEDLINE
DCOM- 20180604
LR  - 20220331
IS  - 1872-7786 (Electronic)
IS  - 0009-2797 (Linking)
VI  - 289
DP  - 2018 Jun 1
TI  - NGAL attenuates renal ischemia/reperfusion injury through autophagy activation 
      and apoptosis inhibition in rats.
PG  - 40-46
LID - S0009-2797(17)30396-4 [pii]
LID - 10.1016/j.cbi.2018.04.018 [doi]
AB  - Ischemia/reperfusion (I/R) injury is a main cause of acute kidney injury (AKI), 
      and currently lacks effective therapies. This study is to investigate the level 
      of Neutrophil gelatinase-associated lipocalin (NGAL) and autophagy status during 
      renal I/R injury, so as to determine whether the exogenous NGAL protein could 
      exert a protective effect for I/R injury and explore the potential mechanisms. 
      Forty male Wistar rats were randomly divided into the following four groups: 
      Sham, I/R, pre-treated with NGAL before I/R (I/R + pre-N), treated with NGAL 
      after I/R (I/R + post-N). All rats were subjected to clamping the left renal 
      pedicle for 45 min after right nephrectomy, followed by 24 h of reperfusion. 
      Serum creatinine (SCr) and blood urea nitrogen (BUN) were used for renal 
      function, tubular cell apoptosis and autophagy were measured by terminal 
      deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) method, 
      histological examination and electron microscope, respectively. The tubular cell 
      proliferation was assessed by the protein expression of proliferating cell 
      nuclear antigen (PCNA). Western blotting was used to quantitate the levels of 
      LC3, Beclin-1, Bcl-2 and Bax in kidney tissues. Exogenous NGAL protein 
      intervention significantly improved renal function, reduced tubular cell 
      apoptosis, increased tubular cell proliferation and promoted autophagy activation 
      after renal I/R injury. Further, the efficacy in pre-N was significantly better 
      than post-N. The mechanisms were involved in the regulation of several autophagy 
      and apoptosis-related genes. Our study demonstrated that exogenous NGAL protein 
      play a protective role during I/R injury, which may offer a novel may for 
      prevention and treatment of renal I/R injury.
CI  - Copyright (c) 2018. Published by Elsevier B.V.
FAU - Zhang, Ya-Li
AU  - Zhang YL
AD  - Department of General Practice, The Second Hospital of Hebei Medical University, 
      Shijiazhuang, Hebei, 050000, China.
FAU - Qiao, Shu-Kai
AU  - Qiao SK
AD  - Department of Hematology, The Second Hospital of Hebei Medical University, 
      Shijiazhuang, Hebei, 050000, China.
FAU - Wang, Rong-Ying
AU  - Wang RY
AD  - Department of General Practice, The Second Hospital of Hebei Medical University, 
      Shijiazhuang, Hebei, 050000, China. Electronic address: 
      wangrongying2017@sina.com.
FAU - Guo, Xiao-Nan
AU  - Guo XN
AD  - Department of Hematology, The Second Hospital of Hebei Medical University, 
      Shijiazhuang, Hebei, 050000, China.
LA  - eng
PT  - Journal Article
DEP - 20180425
PL  - Ireland
TA  - Chem Biol Interact
JT  - Chemico-biological interactions
JID - 0227276
RN  - 0 (Lipocalin-2)
RN  - 0 (Proliferating Cell Nuclear Antigen)
RN  - AYI8EX34EU (Creatinine)
SB  - IM
MH  - Animals
MH  - *Apoptosis
MH  - *Autophagy
MH  - Blood Urea Nitrogen
MH  - Cell Proliferation
MH  - Creatinine/blood
MH  - Epithelium/metabolism/pathology
MH  - In Situ Nick-End Labeling
MH  - Kidney Function Tests
MH  - Kidney Tubules/metabolism/pathology
MH  - Lipocalin-2/*metabolism
MH  - Male
MH  - Proliferating Cell Nuclear Antigen/metabolism
MH  - Rats, Wistar
MH  - Reperfusion Injury/*metabolism/*pathology/physiopathology
MH  - Vacuoles/metabolism/ultrastructure
OTO - NOTNLM
OT  - Apoptosis
OT  - Autophagy
OT  - Ischemia-reperfusion
OT  - Neutrophil gelatinase-associated lipocalin
OT  - Proliferation
EDAT- 2018/04/29 06:00
MHDA- 2018/06/05 06:00
CRDT- 2018/04/29 06:00
PHST- 2017/04/21 00:00 [received]
PHST- 2018/04/11 00:00 [revised]
PHST- 2018/04/13 00:00 [accepted]
PHST- 2018/04/29 06:00 [pubmed]
PHST- 2018/06/05 06:00 [medline]
PHST- 2018/04/29 06:00 [entrez]
AID - S0009-2797(17)30396-4 [pii]
AID - 10.1016/j.cbi.2018.04.018 [doi]
PST - ppublish
SO  - Chem Biol Interact. 2018 Jun 1;289:40-46. doi: 10.1016/j.cbi.2018.04.018. Epub 
      2018 Apr 25.