Abstract

Biodynes, tocotrienol-rich fraction (TRF), and tocopherol have shown antiaging properties. However, the combined effects of these compounds on skin aging are yet to be investigated. This study aimed to elucidate the skin aging effects of biodynes, TRF, and tocopherol on stress-induced premature senescence (SIPS) model of human diploid fibroblasts (HDFs) by determining the expression of collagen and MMPs at gene and protein levels. Primary HDFs were treated with biodynes, TRF, and tocopherol prior to hydrogen peroxide (H2O2) exposure. The expression of COL1A1, COL3A1, MMP1, MMP2, MMP3, and MMP9 genes was determined by qRT-PCR. Type I and type III procollagen proteins were measured by Western blotting while the activities of MMPs were quantified by fluorometric Sensolyte MMP Kit. Our results showed that biodynes, TRF, and tocopherol upregulated collagen genes and downregulated MMP genes (P < 0.05). Type I procollagen and type III procollagen protein levels were significantly increased in response to biodynes, TRF, and tocopherol treatment (P < 0.05) with reduction in MMP-1, MMP-2, MMP-3, and MMP-9 activities (P < 0.05). These findings indicated that biodynes, TRF, and tocopherol effectively enhanced collagen synthesis and inhibited collagen degradation and therefore may protect the skin from aging.

Highlights

  • Human skin which consists of epidermis, dermis, and subcutaneous tissues provides a shielding layer for internal organs

  • The significant elevation was only found in human diploid fibroblasts (HDFs) treated with tocotrienol-rich fraction (TRF), tocopherol, and BTT (P < 0.05) but not in biodynes-treated cells when the levels of type I procollagen protein were analyzed (Figure 1(b))

  • This study evaluated the effects of biodynes, tocotrienol-rich fraction, and tocopherol in modulating collagen synthesis and degradation, in order to elucidate their underlying mechanism in preventing skin aging

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Summary

Introduction

Human skin which consists of epidermis, dermis, and subcutaneous tissues provides a shielding layer for internal organs. Oxidative stress is one of the factors that contribute to skin aging [1, 2]. Fibroblasts which are the crucial collagen-producing cells provide flatten appearance and elasticity to the skin in cooperation with collagen. Evaluating the loss of collagen, either decreased synthesis or increased degradation, is important in analyzing the factors that may contribute to skin aging [5]. Matrix metalloproteinases (MMPs) play an important role in regulating the turnover of collagen. The elevated level of MMPs caused increased collagen degradation and deterioration of skin structure [6]. Previous study which used stress induced premature senescence (SIPS) model of human diploid fibroblasts has shown the role of MMPs in regulating collagen degradation [7, 8]

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