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Aqueous cinnamon extract protects against oxygen‐glucose deprivation‐induced damage in bEnd.3 cells
Author(s) -
Qin Bolin,
Zhao Aiping,
Liu Chao,
Anderson Richard
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.607.2
Subject(s) - oxidative stress , viability assay , apoptosis , pharmacology , chemistry , reactive oxygen species , tumor necrosis factor alpha , inflammation , vasodilation , cell damage , endothelial stem cell , medicine , endocrinology , biochemistry , in vitro
Oxidative stress may contribute to vascular endothelial injury leading to impaired cerebral vascular function following stroke related to diabetes. A cinnamon extract (Cinnulin PF) has been shown to reverse the negative effects of oxidative stress. The aim of this study was to investigate the effects of Cinnulin in an oxygen glucose deprivation (OGD)‐induced injury model, of mouse brain microvascular endothelial (bEnd.3) cells. Cell viability and the expression of the Bcl‐xl; a structural integrity protein, HSP90; and TNFα and phospho‐Nf‐kB p65 were evaluated. A 3h OGD/24h reperfusion insult decreased cell viability and induced Bcl‐xl, HSP90, TNFα, and phospho‐p65 proteins, while the addition of Cinnulin significantly attenuated these effects. A 3h OGD treatment decreased glucose uptake measured by fluorescence microscopy which was also reversed by Cinnulin. PGE2 is an important mediator of many biological functions, including vasodilation, antiinflammatory actions. OGD/24h reperfusion down regulated PGE2 secretion into the media and cellular PGE2 expression. Cinnulin attenuated these effects and also induced SIRT1 protein expression, which is required for the inhibition of apoptosis and inflammatory effects. These effects were inhibited by SIRT1 inhibitor IV. In summary, Cinnulin protects against ischemic injury in bEnd.3 cells and thus cinnamon extract may be beneficial in oxidative stress related chronic diseases.