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Open Access Research article

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

Tomoko Tanigawa1, Shigeyuki Kanazawa1*, Ryoko Ichibori1, Takashi Fujiwara1, Takuya Magome2, Kenta Shingaki3, Shingo Miyata4, Yuki Hata1, Koichi Tomita1, Ken Matsuda5, Tateki Kubo1, Masaya Tohyama3, Kenji Yano1 and Ko Hosokawa1

Author Affiliations

1 Department of Plastic Surgery, Osaka University Graduate School of Medicine, Suita-shi, Osaka, Japan

2 Department of Child Development and Molecular Brain Science, United Graduate School of Child Development, Osaka University, Suita-shi, Osaka, Japan

3 Department of Research & Development Noevir Co., Ltd. Higashiomi, Shiga, Japan

4 Division of Molecular Brain Science, Research Institute of Traditional Asian Medicine, Kinki University, Osakasayama, Osaka, Japan

5 Division of Plastic and Reconstructive Surgery, Niigata University Graduate School of Medicine, Niigata-shi, Niigata, Japan

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BMC Complementary and Alternative Medicine 2014, 14:133  doi:10.1186/1472-6882-14-133

Published: 8 April 2014

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.

Keywords:
Catechin; Fibroblast; Apoptosis; Oxidative stress