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Cytoprotective Mechanism of Cyanidin and Delphinidin against Oxidative Stress-Induced Tenofibroblast Death.

Nam DC, Hah YS, Nam JB, Kim RJ, Park HB - Biomol Ther (Seoul) (2016)

Bottom Line: Cyanidin and delphinidin both showed inhibitory effects on the H2O2-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 H2O2.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Orthopaedic Surgery, School of Medicine and Hospital, Gyeongsang National University, Jinju 52727, Republic of Korea.

ABSTRACT
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 H2O2, and evaluated their biomolecular mechanisms. Both cyanidin and delphinidin inhibited H2O2-induced apoptosis in a dose-dependent manner. However, at concentrations of 100 μg/ml or greater, delphinidin showed cytotoxicity against tenofibroblasts and a decreased antinecrotic effect. Cyanidin and delphinidin both showed inhibitory effects on the H2O2-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 H2O2. 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.

No MeSH data available.


Related in: MedlinePlus

MAPKs activation was assessed using western blot analyses. Western blot analyses demonstrated that expressions of phosphorylations of p38, JNK, and ERK were higher in the H2O2 group than in the control. Those expressions were lower in the cyanidin-H2O2 and delphinidin-H2O2 subgroups than in the H2O2 group.
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f4-bt-24-426: MAPKs activation was assessed using western blot analyses. Western blot analyses demonstrated that expressions of phosphorylations of p38, JNK, and ERK were higher in the H2O2 group than in the control. Those expressions were lower in the cyanidin-H2O2 and delphinidin-H2O2 subgroups than in the H2O2 group.

Mentions: The western blot analyses indicated that 1 h of exposure to H2O2 induced phosphorylation of ERK1/2, JNK, and p38. Treatment with either cyanidin or delphinidin did not induce phosphorylation of ERK1/2, JNK, or p38. Pretreatment with cyanidin or delphinidin reduced the H2O2-induced phosphorylation of ERK1/2, JNK, and p38 (Fig. 4). Cyanidin inhibited the phosphorylation of ERK1/2 and JNK similarly (Fig. 4A). Delphinidin inhibited the phosphorylation of ERK1/2 more markedly than that of JNK (Fig. 4B).


Cytoprotective Mechanism of Cyanidin and Delphinidin against Oxidative Stress-Induced Tenofibroblast Death.

Nam DC, Hah YS, Nam JB, Kim RJ, Park HB - Biomol Ther (Seoul) (2016)

MAPKs activation was assessed using western blot analyses. Western blot analyses demonstrated that expressions of phosphorylations of p38, JNK, and ERK were higher in the H2O2 group than in the control. Those expressions were lower in the cyanidin-H2O2 and delphinidin-H2O2 subgroups than in the H2O2 group.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4930287&req=5

f4-bt-24-426: MAPKs activation was assessed using western blot analyses. Western blot analyses demonstrated that expressions of phosphorylations of p38, JNK, and ERK were higher in the H2O2 group than in the control. Those expressions were lower in the cyanidin-H2O2 and delphinidin-H2O2 subgroups than in the H2O2 group.
Mentions: The western blot analyses indicated that 1 h of exposure to H2O2 induced phosphorylation of ERK1/2, JNK, and p38. Treatment with either cyanidin or delphinidin did not induce phosphorylation of ERK1/2, JNK, or p38. Pretreatment with cyanidin or delphinidin reduced the H2O2-induced phosphorylation of ERK1/2, JNK, and p38 (Fig. 4). Cyanidin inhibited the phosphorylation of ERK1/2 and JNK similarly (Fig. 4A). Delphinidin inhibited the phosphorylation of ERK1/2 more markedly than that of JNK (Fig. 4B).

Bottom Line: Cyanidin and delphinidin both showed inhibitory effects on the H2O2-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 H2O2.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Orthopaedic Surgery, School of Medicine and Hospital, Gyeongsang National University, Jinju 52727, Republic of Korea.

ABSTRACT
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 H2O2, and evaluated their biomolecular mechanisms. Both cyanidin and delphinidin inhibited H2O2-induced apoptosis in a dose-dependent manner. However, at concentrations of 100 μg/ml or greater, delphinidin showed cytotoxicity against tenofibroblasts and a decreased antinecrotic effect. Cyanidin and delphinidin both showed inhibitory effects on the H2O2-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 H2O2. 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.

No MeSH data available.


Related in: MedlinePlus