• Biomolecules & Therapeutics
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• v.24 no.4
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• pp.426-432
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• 2016

Age-related rotator cuff tendon degeneration is related to tenofibroblast apoptosis. Anthocyanins reduce oxidative stress-induced apoptotic cell death in tenofibroblasts. The current study investigated the presence of cell protective effects in cyanidin and delphinidin, the most common aglycon forms of anthocyanins. We determined whether these anthocyanidins have antiapoptotic and antinecrotic effects in tenofibroblasts exposed to $H_2O_2$, and evaluated their biomolecular mechanisms. Both cyanidin and delphinidin inhibited $H_2O_2$-induced apoptosis in a dose-dependent manner. However, at concentrations of $100{\mu}g/ml$ or greater, delphinidin showed cytotoxicity against tenofibroblasts and a decreased antinecrotic effect. Cyanidin and delphinidin both showed inhibitory effects on the $H_2O_2$-induced increase in intracellular ROS formation and the activation of ERK1/2 and JNK. In conclusion, both cyanidin and delphinidin have cytoprotective effects on cultured tenofibroblasts exposed to $H_2O_2$. These results suggest that cyanidin and delphinidin are both beneficial for the treatment of oxidative stress-mediated tenofibroblast cell death, but their working concentrations are different.

• Journal of the Korean Wood Science and Technology
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• v.42 no.5
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• pp.523-532
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• 2014

This study was done to evaluate the antioxidant effect of oak hot water extracts on the oxidative stress induced by reactive oxygen species (ROS). The cytotoxicity of $H_2O_2$-induced oxidative stress was performed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay for the cell viability according to the dose-dependent treatment. Oak extracts demonstrated a dose-dependent ability to inhibit $H_2O_2$-induced apoptosis in cultured tenofibroblasts, as assessed by MTT assay and FACS analysis. $H_2O_2$ increased the phosphorylation of extracellular regulated kinase1/2 (ERK1/2) and of c-Jun N-terminal kinase (JNK) and the production of reactive oxygen species (ROS). In contrast, treatment with oak extracts was decreased this activation of ERK1/2 and JNK, as confirmed by western blot analysis, and reduced the production of ROS, as verified by fluorescent microscopic and flow cytometry (FACS) analyses. These findings suggest that oak extracts, by suppressing JNK, ERK1/2, and intracellular ROS production, have a concentration-dependent antiapoptotic effect on achilles tenofibroblasts exposed to an oxidative stressor, and may have therapeutic potential.