Phlorotannin protects against streptozotocin-induced pancreatic β cell damage by reducing oxidative stress and apoptosis

Title
Phlorotannin protects against streptozotocin-induced pancreatic β cell damage by reducing oxidative stress and apoptosis
Author(s)
허수진; 예보람; 장지이; 김민선; 이승홍; 전유진
KIOST Author(s)
Heo, Soo Jin(허수진)
Publication Year
2014-10-27
Abstract
Pancreatic β cells are extremely sensitive to oxidative stress, which probably has an important role in β cell damage in diabetes. The protective effect of octaphlorethol A (OPA), a novel phenolic compound isolated from Ishige foliacea, against streptozotocin (STZ)-induced pancreatic β cell damage was investigated using a rat insulinoma cell line (RINm5F pancreatic β cells). Pretreatment with OPA decreased the death of STZ-treated pancreatic β cells at concentrations of 12.5 μg/ml or 50 μg/ml, and reduced the generation of thiobarbituric acid reactive substances and intracellular reactive oxygen species in a dose-dependent manner in STZ-treated pancreatic β cells. In addition, the OPA pretreatment increased the activities of antioxidant enzymes such as catalase, superoxide dismutase, and glutathione peroxidase in STZ-treated pancreatic β cells. Moreover, OPA treatment elevated the level of insulin, which was reduced by STZ treatment, and protected pancreatic b cells against damage under STZ-treated conditions. These effects were mediated by suppressing apoptosis and were associated with increased anti-apoptotic Bcl-xL expression and reduced pro-apoptotic Bax and cleaved caspase-3 expression. These findings indicate that OPA may be useful as a potential pharmaceutical agent to protect against pancreatic β cell damage caused by oxidative stress associated with diabetes.gainst streptozotocin (STZ)-induced pancreatic β cell damage was investigated using a rat insulinoma cell line (RINm5F pancreatic β cells). Pretreatment with OPA decreased the death of STZ-treated pancreatic β cells at concentrations of 12.5 μg/ml or 50 μg/ml, and reduced the generation of thiobarbituric acid reactive substances and intracellular reactive oxygen species in a dose-dependent manner in STZ-treated pancreatic β cells. In addition, the OPA pretreatment increased the activities of antioxidant enzymes such as catalase, superoxide dismutase, and glutathione peroxidase in STZ-treated pancreatic β cells. Moreover, OPA treatment elevated the level of insulin, which was reduced by STZ treatment, and protected pancreatic b cells against damage under STZ-treated conditions. These effects were mediated by suppressing apoptosis and were associated with increased anti-apoptotic Bcl-xL expression and reduced pro-apoptotic Bax and cleaved caspase-3 expression. These findings indicate that OPA may be useful as a potential pharmaceutical agent to protect against pancreatic β cell damage caused by oxidative stress associated with diabetes.
URI
https://sciwatch.kiost.ac.kr/handle/2020.kiost/25898
Bibliographic Citation
The 10th KSMB Annual Meeting & Symposium, pp.92, 2014
Publisher
한국해양바이오학회
Type
Conference
Language
English
Publisher
한국해양바이오학회
Related Researcher
Research Interests

Marine Biotechnology,Marine Natural Products,Bioactivities,해양생물공학,해양천연물학,생리활성

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