PMID- 23064522
OWN - NLM
STAT- MEDLINE
DCOM- 20130403
LR  - 20190727
IS  - 1349-3329 (Electronic)
IS  - 0040-8727 (Linking)
VI  - 228
IP  - 3
DP  - 2012 Nov
TI  - D-allose ameliorates cisplatin-induced nephrotoxicity in mice.
PG  - 215-21
AB  - Cisplatin (cis-diamminedichloroplatinum II) is a potent antineoplastic agent 
      widely used to treat various forms of cancer. However, its therapeutic use is 
      limited because of dose-dependent nephrotoxicity. Inflammatory mechanisms may 
      play an important role in the pathogenesis of cisplatin nephrotoxicity. D-allose 
      is an aldo-hexose present in nature that recently has been demonstrated to 
      inhibit production of inflammatory mediators in septic kidneys. The purpose of 
      this study was to determine the protective effects of D-allose on 
      cisplatin-induced nephrotoxicity. Cisplatin (20 mg/kg) was administered by 
      intraperitoneal injection to mice in the cisplatin group and the cisplatin plus 
      D-allose group, as was normal saline to control group mice. D-allose was 
      intraperitoneally administered immediately after cisplatin injection. Serum and 
      renal tumor necrosis factor (TNF)-alpha concentrations, renal monocyte 
      chemoattractant protein-1 (MCP-1; a chemotactic factor for monocytes), renal 
      function, histological changes and renal cortex neutrophil infiltration were 
      determined 72 h after cisplatin injection. The serum TNF-alpha concentration in 
      the cisplatin plus D-allose (400 mg/kg body weight) group significantly decreased 
      in comparison with that in the cisplatin group. The renal TNF-alpha and MCP-1 
      concentrations in the cisplatin plus D-allose group significantly decreased in 
      comparison with those in the cisplatin group. Neutrophil infiltration in the 
      cisplatin plus D-allose group was significantly lower than that in the cisplatin 
      group. Cisplatin-induced renal dysfunction and renal tubular injury scores were 
      attenuated by D-allose treatment. These results reveal that D-allose attenuates 
      cisplatin-induced nephrotoxicity by suppressing renal inflammation. Hence, 
      D-allose may become a new therapeutic candidate for treatment of 
      cisplatin-induced nephrotoxicity.
FAU - Miyawaki, Yuki
AU  - Miyawaki Y
AD  - Department of Anesthesiology, Faculty of Medicine, Kagawa University, Kagawa, 
      Japan. yukiyuki@med.kagawa-u.ac.jp
FAU - Ueki, Masaaki
AU  - Ueki M
FAU - Ueno, Masaki
AU  - Ueno M
FAU - Asaga, Takehiko
AU  - Asaga T
FAU - Tokuda, Masaaki
AU  - Tokuda M
FAU - Shirakami, Gotaro
AU  - Shirakami G
LA  - eng
PT  - Journal Article
PL  - Japan
TA  - Tohoku J Exp Med
JT  - The Tohoku journal of experimental medicine
JID - 0417355
RN  - 0 (Chemokine CCL2)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 6038-51-3 (allose)
RN  - IY9XDZ35W2 (Glucose)
RN  - Q20Q21Q62J (Cisplatin)
SB  - IM
MH  - Animals
MH  - Chemokine CCL2/metabolism
MH  - Cisplatin
MH  - Glucose/pharmacology/*therapeutic use
MH  - Inflammation/complications/drug therapy/pathology
MH  - Kidney/drug effects/metabolism/pathology
MH  - Kidney Diseases/blood/*chemically induced/*drug therapy/prevention & control
MH  - Kidney Function Tests
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Neutrophil Infiltration/drug effects
MH  - Tumor Necrosis Factor-alpha/blood
EDAT- 2012/10/16 06:00
MHDA- 2013/04/04 06:00
CRDT- 2012/10/16 06:00
PHST- 2012/10/16 06:00 [entrez]
PHST- 2012/10/16 06:00 [pubmed]
PHST- 2013/04/04 06:00 [medline]
AID - DN/JST.JSTAGE/tjem/228.215 [pii]
AID - 10.1620/tjem.228.215 [doi]
PST - ppublish
SO  - Tohoku J Exp Med. 2012 Nov;228(3):215-21. doi: 10.1620/tjem.228.215.