Journal
FREE RADICAL BIOLOGY AND MEDICINE
Volume 53, Issue 2, Pages 357-365Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2012.04.030
Keywords
Advanced glycation end products; Apoptosis; Iso-flavones; NADPH oxidase; Oxidative stress; Retinal pericyte; Puerarin
Funding
- Korea Institute of Oriental Medicine (KIOM) [K10040, K11040]
- National Research Council of Science & Technology (NST), Republic of Korea [K11040] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Retinal pericyte loss is one of the histopathological hallmarks of early diabetic retinopathy. Puerarin (4'-7-dihydroxy-8-beta-D-glucosylisoflavone), which is an isoflavone-C-glucoside, causes various pharmacological effects that include antihyperglycemic and anti-inflammatory activities. In the present study, we determined the efficacy and possible mechanism of puerarin on the advanced glycation end product (AGE)-modified bovine serum albumin (BSA)-induced apoptosis of cultured bovine retinal pericytes and rat retinal pericytes in intravitreally AGE-modified rat serum albumin (RSA)-injected eyes. Puerarin significantly inhibited pericyte apoptosis, the generation of reactive oxygen species (ROS), and NADPH oxidase activity by inhibiting the phosphorylation of p47phox and Rac1 which were induced by the AGE-BSA treatment. The puerarin treatment markedly suppressed the activation of nuclear factor-kappaB (NF-kappa B). In addition, the in vivo apoptosis of the retinal pericyte of rats that was stimulated by the intravitreal injection of AGE-RSA was evidently attenuated by the puerarin treatment. These results demonstrate that puerarin may exert inhibitory effects on AGE-induced pericyte apoptosis by interfering with the NADPH oxidase-related ROS pathways and blocking NF-kappa B activation, thereby ameliorating retinal microvascular dysfunction. (C) 2012 Elsevier Inc. All rights reserved.
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