PMID- 15892182
OWN - NLM
STAT- MEDLINE
DCOM- 20060223
LR  - 20171116
IS  - 1520-7552 (Print)
IS  - 1520-7552 (Linking)
VI  - 22
IP  - 1
DP  - 2006 Jan-Feb
TI  - Antioxidants and an inhibitor of advanced glycation ameliorate death of retinal 
      microvascular cells in diabetic retinopathy.
PG  - 38-45
AB  - BACKGROUND: Pericyte ghosts and acellular capillaries are well known as early 
      histological changes resulting from diabetic retinopathy. These histological 
      changes mean that the cell death of retinal microvessels has accelerated. It was 
      reported that apoptosis of retinal microvascular cells (RMCs) was increased in 
      diabetic patients. Therefore, we investigated apoptosis of RMCs in Goto-Kakizaki 
      (GK) rats, a type 2 diabetic model, and involvement with antioxidants (a 
      combination of vitamins C and E) or a novel inhibitor of advanced glycation, 
      OPB-9195. METHODS: GK rats were treated with the antioxidants combination or 
      OPB-9195 for 36 weeks. We obtained isolated preparations of the vascular network 
      from their retinas by trypsin digestion. Apoptosis of retinal vascular cells was 
      detected with terminal deoxynucleotidyl transferase-mediated dUTP nick end 
      labeling (TUNEL) assay. RESULTS: We found that apoptosis of RMCs was increased in 
      the diabetic GK rats. Furthermore, a combination of vitamins C and E and an 
      advanced glycation end-products inhibitor mostly inhibited this increased 
      apoptosis. CONCLUSIONS: We concluded that apoptosis of RMCs was a good marker 
      that indicates the progression of diabetic retinopathy in GK rats. Both oxidative 
      stress and the accumulation of advanced glycation end-products appears to promote 
      the apoptosis of retinal microvascular cells, and antioxidants or advanced 
      glycation end-products inhibitors might ameliorate diabetic retinopathy.
CI  - Copyright (c) 2005 John Wiley & Sons, Ltd.
FAU - Yatoh, Shigeru
AU  - Yatoh S
AD  - Division of Endocrinology and Metabolism, Department of Internal Medicine, 
      Institute of Clinical Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan. 
      s-yatoh@yf6.so-net.ne.jp
FAU - Mizutani, Masakazu
AU  - Mizutani M
FAU - Yokoo, Tomotaka
AU  - Yokoo T
FAU - Kozawa, Tadahiko
AU  - Kozawa T
FAU - Sone, Hirohito
AU  - Sone H
FAU - Toyoshima, Hideo
AU  - Toyoshima H
FAU - Suzuki, Seiji
AU  - Suzuki S
FAU - Shimano, Hitoshi
AU  - Shimano H
FAU - Kawakami, Yasushi
AU  - Kawakami Y
FAU - Okuda, Yukichi
AU  - Okuda Y
FAU - Yamada, Nobuhiro
AU  - Yamada N
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Diabetes Metab Res Rev
JT  - Diabetes/metabolism research and reviews
JID - 100883450
RN  - 0 (Antioxidants)
RN  - 0 (Glycation End Products, Advanced)
RN  - 0 (OPB 9195)
RN  - 0 (Thiadiazoles)
RN  - 0 (Thiazolidines)
RN  - 1406-18-4 (Vitamin E)
RN  - PQ6CK8PD0R (Ascorbic Acid)
SB  - IM
MH  - Animals
MH  - Antioxidants/*therapeutic use
MH  - Apoptosis/*drug effects
MH  - Ascorbic Acid/therapeutic use
MH  - Diabetes Mellitus, Type 2/metabolism/pathology/*prevention & control
MH  - Diabetic Retinopathy/metabolism/pathology/*prevention & control
MH  - Disease Models, Animal
MH  - Glycation End Products, Advanced/*antagonists & inhibitors/metabolism
MH  - In Situ Nick-End Labeling
MH  - Male
MH  - Oxidative Stress
MH  - Rats
MH  - Rats, Wistar
MH  - Retinal Vessels/*drug effects/metabolism/pathology
MH  - Thiadiazoles/*therapeutic use
MH  - Thiazolidines
MH  - Vitamin E/therapeutic use
EDAT- 2005/05/14 09:00
MHDA- 2006/02/24 09:00
CRDT- 2005/05/14 09:00
PHST- 2005/05/14 09:00 [pubmed]
PHST- 2006/02/24 09:00 [medline]
PHST- 2005/05/14 09:00 [entrez]
AID - 10.1002/dmrr.562 [doi]
PST - ppublish
SO  - Diabetes Metab Res Rev. 2006 Jan-Feb;22(1):38-45. doi: 10.1002/dmrr.562.