PMID- 31814566
OWN - NLM
STAT- MEDLINE
DCOM- 20191212
LR  - 20200108
IS  - 1007-8738 (Print)
IS  - 1007-8738 (Linking)
VI  - 35
IP  - 10
DP  - 2019 Oct
TI  - [LIGHT/ TNFSF14 alleviates cisplatin-induced acute kidney injury in mice and its 
      mechanism].
PG  - 897-902
AB  - Objective To investigate the role of LIGHT/TNFSF14 (TNF superfamily protein 14) 
      in cisplatin-induced acute kidney injury (Cis-AKI) in mice and explore the 
      underlying mechanism. Methods Male wild-type (WT) and LIGHT gene knockout 
      (LIGHT(-/-)) C57BL/6 mice were selected and divided into four groups: saline- and 
      cisplatin-treated WT mice, saline- and cisplatin-treated LIGHT(-/-) mice. The 
      cisplatin groups were given a single intraperitoneal injection of cisplatin (20 
      mg/kg, 200 muL), and the saline groups were injected with equal volume of normal 
      saline (9 g/L). After 72 hours, the mice were sacrificed, blood was taken from 
      the eyeball, and kidney tissues were collected. Blood urea nitrogen (BUN) and 
      serum creatinine (Scr) were measured by automatic biochemical analyzer. HE 
      staining was used to detect the histopathological changes of kidney tissues, The 
      mRNA levels of LIGHT, kidney injury molecule 1 (KIM-1), interleukin-6 (IL-6), 
      monocyte chemotactic protein 1 (MCP-1), and tumor necrosis factor (TNF-alpha) were 
      detected by real-time quantitative PCR. The protein levels of LIGHT, Bcl2, BAX 
      and cytochrome C were detected by Western blot analysis or immunohistochemical 
      staining. Results Compared with saline-treated WT mice, the expression of LIGHT 
      in renal tissue of cisplatin-treated WT mice significantly increased. Compared 
      with cisplatin-treated WT mice, the kidney injury in cisplatin-treated LIGHT(-/-) 
      mice was more serious; BUN and Scr increased; and the pathological damage of 
      kidney tissue was more obvious. Moreover, the mRNA levels of IL-6, MCP-1 and 
      TNF-alpha, as well as the protein levels of BAX and cytochrome C increased, while the 
      protein levels of Bcl2 decreased. Conclusion LIGHT plays a protective role in 
      Cis-AKI, which may be related to down-regulated secretion of inflammatory factors 
      and decreased apoptosis.
FAU - Yang, Yan
AU  - Yang Y
AD  - Department of Kidney Diseases, Southwest Hospital, Army medical university, 
      Chongqing 400038, China.
FAU - Zhong, Yu
AU  - Zhong Y
AD  - Department of Kidney Diseases, Southwest Hospital, Army medical university, 
      Chongqing 400038, China.
FAU - Meng, Li
AU  - Meng L
AD  - Department of Kidney Diseases, Southwest Hospital, Army medical university, 
      Chongqing 400038, China.
FAU - Xie, Pan
AU  - Xie P
AD  - Department of Kidney Diseases, Southwest Hospital, Army medical university, 
      Chongqing 400038, China.
FAU - Xu, Guilian
AU  - Xu G
AD  - Department of Immunology, School of Basic Medicine, Army medical university, 
      Chongqing 400038, China.
FAU - Peng, Kanfu
AU  - Peng K
AD  - Department of Immunology, School of Basic Medicine, Army medical university, 
      Chongqing 400038, China. *Corresponding author, E-mail: 392906786@qq.com.
LA  - chi
PT  - Journal Article
PL  - China
TA  - Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi
JT  - Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular 
      immunology
JID - 101139110
RN  - 0 (Tnfsf14 protein, mouse)
RN  - 0 (Tumor Necrosis Factor Ligand Superfamily Member 14)
RN  - AYI8EX34EU (Creatinine)
RN  - Q20Q21Q62J (Cisplatin)
SB  - IM
MH  - Acute Kidney Injury/*chemically induced
MH  - Animals
MH  - Apoptosis
MH  - Blood Urea Nitrogen
MH  - Cisplatin/*toxicity
MH  - Creatinine/blood
MH  - Kidney/pathology
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Tumor Necrosis Factor Ligand Superfamily Member 14/*metabolism
EDAT- 2019/12/10 06:00
MHDA- 2019/12/18 06:00
CRDT- 2019/12/10 06:00
PHST- 2019/12/10 06:00 [entrez]
PHST- 2019/12/10 06:00 [pubmed]
PHST- 2019/12/18 06:00 [medline]
PST - ppublish
SO  - Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2019 Oct;35(10):897-902.