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Cytoprotective effects of catechin 7‐ O ‐β‐ D glucopyranoside against mitochondrial dysfunction damaged by streptozotocin in RINm5F cells
Author(s) -
Kim Ki Cheon,
Kim Jin Sook,
Ah Kang Kyoung,
Kim Jong Min,
Won Hyun Jin
Publication year - 2010
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.1703
Subject(s) - xanthine oxidase , reactive oxygen species , streptozotocin , chemistry , catalase , mitochondrion , superoxide dismutase , xanthine , lipid peroxidation , biochemistry , oxidative stress , mitochondrial ros , pharmacology , superoxide , biology , endocrinology , enzyme , diabetes mellitus
The protective effects of catechin 7‐ O ‐β‐ D glucopyranoside (C7G) against streptozotocin (STZ)‐induced mitochondrial damage in rat pancreatic β‐cells (RINm5F) were investigated. A marked increase in mitochondrial reactive oxygen species (ROS) was observed in STZ‐treated cells; this increase was restricted by C7G treatment. C7G also scavenged superoxide anions and hydroxyl radicals generated by xanthine/xanthine oxidase (xanthine/XO) and the Fenton reaction (FeSO 4 + H 2 O 2 ), respectively. C7G restored activity and expression of both mitochondrial manganese superoxide dismutase (MnSOD) and catalase (CAT), which were suppressed by STZ treatment. In addition, C7G prevented STZ‐induced mitochondrial lipid peroxidation, protein carbonyl, and DNA base modification. C7G restored the loss of mitochondrial membrane potential (Δ ψ ) that was disrupted by STZ treatment, and prevented cell death via inhibition of apoptosis. These results suggest that C7G has a protective effect against STZ‐induced cell damage by its antioxidant effects and the attenuation of mitochondrial dysfunction. Copyright © 2010 John Wiley & Sons, Ltd.