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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

(A, B) Intracellular ROS levels were significantly higher in the H2O2 group, as compared with the control. Intracellular ROS levels in the cyanidin-H2O2 and the delphinidin-H2O2 subgroups were lower than in the H2O2 group. The graph represents the mean ± SD of 3 independent experiments (**p<0.01 compared to control group; ###p<0.001 compared to H2O2 group). (C, D) According to the morphological analyses using a confocal microscope, intracellular ROS levels were higher in the H2O2 group than in the control; however, ROS levels were markedly lower in the cyanidin-H2O2 and the delphinidin-H2O2 subgroups than in the H2O2 group. Cya: Cyanidin, Del: Delphinidin.
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f3-bt-24-426: (A, B) Intracellular ROS levels were significantly higher in the H2O2 group, as compared with the control. Intracellular ROS levels in the cyanidin-H2O2 and the delphinidin-H2O2 subgroups were lower than in the H2O2 group. The graph represents the mean ± SD of 3 independent experiments (**p<0.01 compared to control group; ###p<0.001 compared to H2O2 group). (C, D) According to the morphological analyses using a confocal microscope, intracellular ROS levels were higher in the H2O2 group than in the control; however, ROS levels were markedly lower in the cyanidin-H2O2 and the delphinidin-H2O2 subgroups than in the H2O2 group. Cya: Cyanidin, Del: Delphinidin.

Mentions: Flow cytometry analyses indicated that the levels of intracellular ROS production in the 50 and 100 ug/ml cyanidin-H2O2 (Fig. 3A) and in the 10, 50, and 100 μg/ml delphinidin-H2O2 subgroups (Fig. 3B) were all significantly lower than the level in the H2O2 group. These results demonstrated that both cyanidin and delphinidin have the ability to reduce H2O2-mediated intracellular ROS production. The amounts of intracellular ROS were shown to be lower, in a dose-dependent manner, in the groups pretreated with cyanidin than in the H2O2 group (Fig. 3A). The amounts of intracellular ROS were shown to be significantly lower in the groups pretreated with delphinidin than in the H2O2 group, but no dose-dependent significance was found (Fig. 3B). Specifically, the levels of intracellular ROS were shown to decrease until the dose of delphinidin reached 50 mg/ml. However, the decrease in those ROS levels was reversing once the dose of delphinidin reached 100 mg/ml. That corresponded to the cytotoxicity of delphinidin, as shown in Fig. 1B. Confocal microscope analyses showed that H2O2-induced intracellular ROS production was reduced by pretreatment with 50 and with 100 μg/ml doses of cyanidin and delphinidin. While intracellular ROS levels in all the subgroups treated with delphinidin were significantly lower than in the H2O2 group, the 100 μg/ml delphinidin subgroup showed an increase in ROS production over that of the 50 μg/ml subgroup (Fig. 3C, 3D).


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)

(A, B) Intracellular ROS levels were significantly higher in the H2O2 group, as compared with the control. Intracellular ROS levels in the cyanidin-H2O2 and the delphinidin-H2O2 subgroups were lower than in the H2O2 group. The graph represents the mean ± SD of 3 independent experiments (**p<0.01 compared to control group; ###p<0.001 compared to H2O2 group). (C, D) According to the morphological analyses using a confocal microscope, intracellular ROS levels were higher in the H2O2 group than in the control; however, ROS levels were markedly lower in the cyanidin-H2O2 and the delphinidin-H2O2 subgroups than in the H2O2 group. Cya: Cyanidin, Del: Delphinidin.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f3-bt-24-426: (A, B) Intracellular ROS levels were significantly higher in the H2O2 group, as compared with the control. Intracellular ROS levels in the cyanidin-H2O2 and the delphinidin-H2O2 subgroups were lower than in the H2O2 group. The graph represents the mean ± SD of 3 independent experiments (**p<0.01 compared to control group; ###p<0.001 compared to H2O2 group). (C, D) According to the morphological analyses using a confocal microscope, intracellular ROS levels were higher in the H2O2 group than in the control; however, ROS levels were markedly lower in the cyanidin-H2O2 and the delphinidin-H2O2 subgroups than in the H2O2 group. Cya: Cyanidin, Del: Delphinidin.
Mentions: Flow cytometry analyses indicated that the levels of intracellular ROS production in the 50 and 100 ug/ml cyanidin-H2O2 (Fig. 3A) and in the 10, 50, and 100 μg/ml delphinidin-H2O2 subgroups (Fig. 3B) were all significantly lower than the level in the H2O2 group. These results demonstrated that both cyanidin and delphinidin have the ability to reduce H2O2-mediated intracellular ROS production. The amounts of intracellular ROS were shown to be lower, in a dose-dependent manner, in the groups pretreated with cyanidin than in the H2O2 group (Fig. 3A). The amounts of intracellular ROS were shown to be significantly lower in the groups pretreated with delphinidin than in the H2O2 group, but no dose-dependent significance was found (Fig. 3B). Specifically, the levels of intracellular ROS were shown to decrease until the dose of delphinidin reached 50 mg/ml. However, the decrease in those ROS levels was reversing once the dose of delphinidin reached 100 mg/ml. That corresponded to the cytotoxicity of delphinidin, as shown in Fig. 1B. Confocal microscope analyses showed that H2O2-induced intracellular ROS production was reduced by pretreatment with 50 and with 100 μg/ml doses of cyanidin and delphinidin. While intracellular ROS levels in all the subgroups treated with delphinidin were significantly lower than in the H2O2 group, the 100 μg/ml delphinidin subgroup showed an increase in ROS production over that of the 50 μg/ml subgroup (Fig. 3C, 3D).

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