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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

Proinflammatory cytokines levels of young control (I), D-galactose alone (100 mg/kg) treated (II), D-galactose combined with pine pollen (500, 1000, 1500 mg/kg) treated (III, IV, V), and D-galactose combined with AG (100 mg/mg) treated (VI) mice. IL-6 and TNF-α in sera and brains were determined by quantitative ELISA kits. Data were results of ten animals for each group and expressed as mean ± SEM. Statistical significant difference: *P < 0.05, versus I; #P < 0.05, versus II.
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fig6: Proinflammatory cytokines levels of young control (I), D-galactose alone (100 mg/kg) treated (II), D-galactose combined with pine pollen (500, 1000, 1500 mg/kg) treated (III, IV, V), and D-galactose combined with AG (100 mg/mg) treated (VI) mice. IL-6 and TNF-α in sera and brains were determined by quantitative ELISA kits. Data were results of ten animals for each group and expressed as mean ± SEM. Statistical significant difference: *P < 0.05, versus I; #P < 0.05, versus II.

Mentions: It is well documented that aging is associated with increased circulating levels of proinflammatory cytokines. Increased levels of inflammatory serum markers in the elderly are associated with neurodegenerative diseases, such as dementia, Parkinson's disease [26]. As shown in Figure 6, the TNF-α and IL-6 levels in serum and cerebral were significantly elevated in D-galactose-treated mice in comparison to those in control group. Notably, pine pollen treatment significantly prevented the increment of cerebral IL-6 which was comparable to that of AG treatment. A decreased trend of TNF-α level in sera and brains was also observed upon pine pollen treatment in model mice, though the difference was not statistically significant.


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)

Proinflammatory cytokines levels of young control (I), D-galactose alone (100 mg/kg) treated (II), D-galactose combined with pine pollen (500, 1000, 1500 mg/kg) treated (III, IV, V), and D-galactose combined with AG (100 mg/mg) treated (VI) mice. IL-6 and TNF-α in sera and brains were determined by quantitative ELISA kits. Data were results of ten animals for each group and expressed as mean ± SEM. Statistical significant difference: *P < 0.05, versus I; #P < 0.05, versus II.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig6: Proinflammatory cytokines levels of young control (I), D-galactose alone (100 mg/kg) treated (II), D-galactose combined with pine pollen (500, 1000, 1500 mg/kg) treated (III, IV, V), and D-galactose combined with AG (100 mg/mg) treated (VI) mice. IL-6 and TNF-α in sera and brains were determined by quantitative ELISA kits. Data were results of ten animals for each group and expressed as mean ± SEM. Statistical significant difference: *P < 0.05, versus I; #P < 0.05, versus II.
Mentions: It is well documented that aging is associated with increased circulating levels of proinflammatory cytokines. Increased levels of inflammatory serum markers in the elderly are associated with neurodegenerative diseases, such as dementia, Parkinson's disease [26]. As shown in Figure 6, the TNF-α and IL-6 levels in serum and cerebral were significantly elevated in D-galactose-treated mice in comparison to those in control group. Notably, pine pollen treatment significantly prevented the increment of cerebral IL-6 which was comparable to that of AG treatment. A decreased trend of TNF-α level in sera and brains was also observed upon pine pollen treatment in model mice, though the difference was not statistically significant.

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