Modulation of collagen synthesis and its gene expression in human skin fibroblasts by tocotrienol-rich fraction.

INTRODUCTION

Skin aging may occur as a result of increased free radicals in the body. Vitamin E, the major chain-breaking antioxidant, prevents propagation of oxidative stress, especially in biological membranes. In this study, the molecular mechanism of tocotrienol-rich fraction (TRF) in preventing oxidative stress-induced skin aging was evaluated by determining the rate of total collagen synthesis and its gene expression in human skin fibroblasts.

MATERIAL AND METHODS

Primary culture of human skin fibroblasts was derived from circumcision foreskin of 9 to 12 year-old boys. Fibroblast cells were divided into 5 different treatment groups: untreated control, hydrogen peroxide (H(2)O(2))-induced oxidative stress (20 µM H(2)O(2) exposure for 2 weeks), TRF treatment, and pre- and post-treatment of TRF to H(2)O(2)-induced oxidative stress.

RESULTS

Our results showed that H(2)O(2)-induced oxidative stress decreased the rate of total collagen synthesis and down-regulated COL I and COL III in skin fibroblasts. Pre-treatment of TRF protected against H(2)O(2)-induced oxidative stress as shown by increase in total collagen synthesis and up-regulation of COL I and COL III (p<0.05) genes. However, similar protective effects against H(2)O(2)-induced oxidative stress were not observed in the post-treated fibroblasts.

CONCLUSIONS

Tocotrienol-rich fraction protects against H(2)O(2)-induced oxidative stress in human skin fibroblast culture by modulating the expression of COL I and COL III genes with concomitant increase in the rate of total collagen synthesis. These findings may indicate TRF protection against oxidative stress-induced skin aging.