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Tocotrienol-rich fraction prevents cellular aging by modulating cell proliferation signaling pathways

S C Khor1, Y A Mohd Yusof1, W Z Wan Ngah1

  • 1Department of Biochemistry, Level 17, Pre-Clinical Building, Universiti Kebangsaan Malaysia Medical Center, Jalan Yaacob Latif, Bandar Tun Razak, Cheras, 56000 Kuala Lumpur, Malaysia.

La Clinica Terapeutica
|May 7, 2015
PubMed
Abstract

Insights

Tocotrienol-rich fraction (TRF) may delay cellular aging by modulating gene expression in human diploid fibroblasts. TRF treatment decreased pro-aging genes and increased anti-aging genes, promoting cell cycle progression.

Area of Science:

  • Cellular and Molecular Biology
  • Gerontology
  • Nutritional Science

Background:

  • Vitamin E is explored for preventing age-related diseases.
  • Tocotrienol-rich fraction (TRF) mechanism in delaying cellular aging needs elucidation.
  • Proliferation signaling pathways are key targets in cellular aging.

Purpose of the Study:

  • To investigate the mechanism of TRF in delaying cellular aging.
  • To target proliferation signaling pathways in human diploid fibroblasts (HDFs).

Main Methods:

  • TRF treatment applied to young, pre-senescent, and senescent HDFs.
  • Analysis of gene and protein expression in PI3K/AKT and RAF/MEK/ERK pathways.
  • Comparison of transcriptional profiles at different cellular aging stages.

Main Results:

  • Cellular aging altered mRNA levels of AKT, FOXO3, CDKN1A, RSK1, ELK1, FOS, and SIRT1.
  • TRF decreased AKT, FOXO3, ERK, and RSK1 mRNA in senescent cells.
  • TRF increased ELK1, FOS, and SIRT1 mRNA, and decreased P21Cip1 protein in senescent cells.

Conclusions:

  • TRF exhibits gene-modulating properties.
  • TRF may promote cell cycle progression during cellular aging.
  • TRF's effects on proliferation signaling pathways are crucial for its anti-aging potential.
Keywords:
Cellular agingGene expressionHuman diploid fibroblastsTocotrienol-rich fractionVitamin E

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