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BMC Complement Altern Med. 2014 Apr 8;14:133. doi: 10.1186/1472-6882-14-133.

(+)-Catechin protects dermal fibroblasts against oxidative stress-induced apoptosis.

Author information

1
Department of Plastic Surgery, Osaka University Graduate School of Medicine, Suita-shi, Osaka, Japan. kanazawa@psurg.med.osaka-u.ac.jp.

Abstract

BACKGROUND:

Oxidative stress has been suggested as a mechanism underlying skin aging, as it triggers apoptosis in various cell types, including fibroblasts, which play important roles in the preservation of healthy, youthful skin. Catechins, which are antioxidants contained in green tea, exert various actions such as anti-inflammatory, anti-bacterial, and anti-cancer actions. In this study, we investigated the effect of (+)-catechin on apoptosis induced by oxidative stress in fibroblasts.

METHODS:

Fibroblasts (NIH3T3) under oxidative stress induced by hydrogen peroxide (0.1 mM) were treated with either vehicle or (+)-catechin (0-100 μM). The effect of (+)-catechin on cell viability, apoptosis, phosphorylation of c-Jun terminal kinases (JNK) and p38, and activation of caspase-3 in fibroblasts under oxidative stress were evaluated.

RESULTS:

Hydrogen peroxide induced apoptotic cell death in fibroblasts, accompanied by induction of phosphorylation of JNK and p38 and activation of caspase-3. Pretreatment of the fibroblasts with (+)-catechin inhibited hydrogen peroxide-induced apoptosis and reduced phosphorylation of JNK and p38 and activation of caspase-3.

CONCLUSION:

(+)-Catechin protects against oxidative stress-induced cell death in fibroblasts, possibly by inhibiting phosphorylation of p38 and JNK. These results suggest that (+)-catechin has potential as a therapeutic agent for the prevention of skin aging.

PMID:
24712558
PMCID:
PMC4004505
DOI:
10.1186/1472-6882-14-133
[Indexed for MEDLINE]
Free PMC Article
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