TABLE 1.
Studies | Study design | Changes with tocotrienol treatment |
---|---|---|
Makpol et al. (2013) | Cells: Primary human diploid fibroblasts (HDFs) from foreskins of subjects, aged between 9–12 years | ↑ COL1A1, COL3A1 genes |
Model: Oxidative stress induced by H2O2 for 2 weeks | ↓ MMP-1, MMP-2, MMP-3, andMMP-9 genes | |
Treatment: Pretreatment with TRF/Tocopherol (500 μg/ml; 100 μg/ml) at passage 4 | ||
Makpol et al. (2010) | Cells: Normal skin fibroblast cell lines derived from young (21-year-old, YF) and middle-aged (40-year-old, MF) humans | ↑ Telomerase activity (middle fibroblast), telomere length (young & old fibroblast) |
Treatment: γ-tocotrienol for 24 h before or after incubation with IC50 dose of H2O2 for 2 h | ↓ Telomerase activity (young & old fibroblast) | |
↔ telomere length (middle fibroblast) | ||
Nakagawa et al. (2010) | Cells: Human keratinocytes (HaCaT) cells were incubated for 3 and 24 h in either SQ-OOH or γ-T3 | ↓ ROS generation, NF-kB activation, COX-2 mRNA expression, PGE2 production, interleukins |
Treatment: incubation for 3 and 24 h in either SQ-OOH or γ-T3. Various inflammatory markers were studied, such as interleukins, tumor necrosis factor-a, COX-2 and B-actin | ||
Makpol et al. (2012) | Cells: Primary human diploid fibroblast (HDFs) derived from foreskins of three 9- to 12-year-old boys after circumcision after consent was obtained | ↑ BCL2AI mRNA |
Treatment: Young HDFs were exposed to prolonged low doses of H2O2, which mimics the oxidative stress in vivo to induce premature senescence state instead of acute induction with sublethal doses of H2O2 | ↓ Annexin V-FITC positive cells, cytochrome C, caspase-9 and caspase-3, BAX mRNA | |
Makpol et al. (2011) | Cells: derived from human skin fibroblast Treatment: cells were divided into groups of untreated control, hydrogen peroxide (H2O2)-induced oxidative stress (20 μM H2O2 exposure for 2 weeks), TRF treatment, and pre- and posttreatment of TRF to H2O2-induced oxidative stress | ↑ COL I, COL III, collagen synthesis |
↔ COL IV |
Abbreviation: ↓ decrease, inhibit or downregulate; ↑ increase, upregulate; ↔ no change; TRF, tocotrienol-rich fraction; COL, collagen; MMP, matrix metalloproteinases; ROS, reactive oxygen species; NF-κB, nuclear factor kappa B; COX-2, cyclooxygenase 2; PGE2, prostaglandin E2; SQ-OOH, squalene hydroperoxide; BCL2AI, B-cell lymphoma 2 AI; BAX, BCL2 associated X.