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

Mao GX, Zheng LD, Cao YB, Chen ZM, Lv YD, Wang YZ, Hu XL, Wang GF, Yan J - Oxid Med Cell Longev (2012)

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Zhejiang Provincial Key Laboratory of Geriatrics, Zhejiang Hospital, Hangzhou, China.

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.

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Related in: MedlinePlus

Line graph showing result of impedence-based cell proliferation assay (Xcelligence). The cell index (see Section 2) was plotted against time for the 2BS cells. Pine pollen (PP) was added 24 h after cell-seeding, and an approx. 20% elevation compared with the control was observed between 24–48 h under PP (1 mg/mL and 2 mg/mL) incubation.
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fig1: Line graph showing result of impedence-based cell proliferation assay (Xcelligence). The cell index (see Section 2) was plotted against time for the 2BS cells. Pine pollen (PP) was added 24 h after cell-seeding, and an approx. 20% elevation compared with the control was observed between 24–48 h under PP (1 mg/mL and 2 mg/mL) incubation.

Mentions: In this study, we firstly observed the effects of pine pollen on replicative lifespan and biomarkers related to replicative senescence in human fetal lung diploid fibroblasts (2BS). Pine pollen significantly delayed replicative senescence of 2BS cells by at least 7 PDs (see Table 1). The two concentrations of pine pollen (1 mg/mL and 2 mg/mL) showed a similar gain in PDs. The growth rate of pine pollen treatment cells was dramatically increased compared to that of the control cells (Table 1). Meanwhile, pine pollen improved the proliferation of 2BS cells as demonstrated by using the Xcelligence system (Roche Applied Science, Basel, Switzerland), an impedance-based nondestructive assay of cell proliferation. Cells at PD30 incubated with pine pollen at 1 mg/mL and 2 mg/mL for 24–48 h showed a maximum 20% elevation on cell index (CI) compared with that of control (Figure 1).


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

Mao GX, Zheng LD, Cao YB, Chen ZM, Lv YD, Wang YZ, Hu XL, Wang GF, Yan J - Oxid Med Cell Longev (2012)

Line graph showing result of impedence-based cell proliferation assay (Xcelligence). The cell index (see Section 2) was plotted against time for the 2BS cells. Pine pollen (PP) was added 24 h after cell-seeding, and an approx. 20% elevation compared with the control was observed between 24–48 h under PP (1 mg/mL and 2 mg/mL) incubation.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3345248&req=5

fig1: Line graph showing result of impedence-based cell proliferation assay (Xcelligence). The cell index (see Section 2) was plotted against time for the 2BS cells. Pine pollen (PP) was added 24 h after cell-seeding, and an approx. 20% elevation compared with the control was observed between 24–48 h under PP (1 mg/mL and 2 mg/mL) incubation.
Mentions: In this study, we firstly observed the effects of pine pollen on replicative lifespan and biomarkers related to replicative senescence in human fetal lung diploid fibroblasts (2BS). Pine pollen significantly delayed replicative senescence of 2BS cells by at least 7 PDs (see Table 1). The two concentrations of pine pollen (1 mg/mL and 2 mg/mL) showed a similar gain in PDs. The growth rate of pine pollen treatment cells was dramatically increased compared to that of the control cells (Table 1). Meanwhile, pine pollen improved the proliferation of 2BS cells as demonstrated by using the Xcelligence system (Roche Applied Science, Basel, Switzerland), an impedance-based nondestructive assay of cell proliferation. Cells at PD30 incubated with pine pollen at 1 mg/mL and 2 mg/mL for 24–48 h showed a maximum 20% elevation on cell index (CI) compared with that of control (Figure 1).

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Zhejiang Provincial Key Laboratory of Geriatrics, Zhejiang Hospital, Hangzhou, China.

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.

Show MeSH
Related in: MedlinePlus