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

BMC Complementary and Alternative Medicine

Ko Hosokawa²  Kenji Yano²  Masaya Tohyama³  Tateki Kubo²  Ken Matsuda⁴  Koichi Tomita²  Yuki Hata²  Shingo Miyata¹  Kenta Shingaki³  Takuya Magome⁵  Takashi Fujiwara²  Ryoko Ichibori²  Shigeyuki Kanazawa²  Tomoko Tanigawa² 

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

[2]Department of Plastic Surgery, Osaka University Graduate School of Medicine, Suita-shi, Osaka, Japan

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

[4]Division of Plastic and Reconstructive Surgery, Niigata University Graduate School of Medicine, Niigata-shi, Niigata, Japan

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

关键词: Oxidative stress;    Apoptosis;    Fibroblast;    Catechin;   

Others  :  1220190
DOI  :  10.1186/1472-6882-14-133

 received in 2013-09-24, accepted in 2014-03-24,  发布年份 2014

【 摘 要 】

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.

【 授权许可】

   
2014 Tanigawa et al.; licensee BioMed Central Ltd.

【 图 表 】

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