Antiaging effect of pine pollen in human diploid fibroblasts and in a mouse model induced by D-galactose

Oxid Med Cell Longev. 2012;2012:750963. doi: 10.1155/2012/750963. Epub 2012 Apr 17.

Abstract

The present paper was designed to investigate the effect of pine pollen against aging in human diploid fibroblast 2BS cells and in an accelerated aging model, which was established by subcutaneous injections with D-galactose daily for 8 weeks in C57BL/6J mice. Pine pollen (1 mg/mL and 2 mg/mL) is proved to delay the replicative senescence of 2BS cells as evidenced by enhanced cell proliferation, decreased SA-β-Gal activity, and reversed expression of senescence-associated molecular markers, such as p53, p21(Waf1), p16(INK4a), PTEN, and p27(Kip1) in late PD cells. Besides, pine pollen reversed D-galactose-induced aging effects in neural activity and inflammatory cytokine levels, as indicated by improved memory latency time and reduced error rate in step-down test and decreased concentrations of IL-6 and TNF-α in model mice. Similar to the role of AGEs (advanced glycation endproducts) formation inhibitor aminoguanidine (AG), pine pollen inhibited D-galactose-induced increment of AGEs levels thus reversed the aging phenotypes in model mice. Furthermore, the declined antioxidant activity was obviously reversed upon pine pollen treatment, which may account for its inhibitory effect on nonenzymatic glycation (NEG) in vivo. Our finding presents pine pollen as an attractive agent with potential to retard aging and attenuate age-related diseases in humans.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aging / drug effects*
  • Animals
  • Antioxidants / metabolism
  • Body Weight / drug effects
  • Cell Line
  • Cell Proliferation / drug effects
  • Cellular Senescence / drug effects
  • Cytokines / metabolism
  • Diploidy*
  • Female
  • Fibroblasts / cytology*
  • Fibroblasts / drug effects*
  • Fibroblasts / enzymology
  • Galactose / pharmacology*
  • Glycation End Products, Advanced / metabolism
  • Humans
  • Inflammation Mediators / metabolism
  • Lipid Peroxidation / drug effects
  • Malondialdehyde / metabolism
  • Mice
  • Mice, Inbred C57BL
  • Models, Animal
  • Nervous System / drug effects
  • Pinus / chemistry*
  • Pollen / metabolism*
  • Staining and Labeling
  • Superoxide Dismutase / metabolism
  • beta-Galactosidase / metabolism

Substances

  • Antioxidants
  • Cytokines
  • Glycation End Products, Advanced
  • Inflammation Mediators
  • Malondialdehyde
  • Superoxide Dismutase
  • beta-Galactosidase
  • Galactose