Antiaging Effect of Pine Pollen in Human Diploid Fibroblasts and in a Mouse Model Induced by D-Galactose
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 pr...
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| Veröffentlicht in: | Oxidative medicine and cellular longevity 2012-01, Vol.2012 (2012), p.1-10 |
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| container_title | Oxidative medicine and cellular longevity |
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| creator | Mao, Gen-Xiang Zheng, Ling-Di Cao, Yong-Bao Chen, Zhuo-Mei Lv, Yuan-Dong Wang, Ya-Zhen Hu, Xi-Lian Wang, Guo-Fu Yan, Jing |
| description | 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, p21Waf1, p16INK4a, PTEN, and p27Kip1 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. |
| doi_str_mv | 10.1155/2012/750963 |
| format | Article |
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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, p21Waf1, p16INK4a, PTEN, and p27Kip1 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.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2012/750963</identifier><identifier>PMID: 22577492</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Puplishing Corporation</publisher><subject>Aging - drug effects ; Animals ; Antioxidants - metabolism ; beta-Galactosidase - 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</subject><ispartof>Oxidative medicine and cellular longevity, 2012-01, Vol.2012 (2012), p.1-10</ispartof><rights>Copyright © 2012 Gen-Xiang Mao et al.</rights><rights>Copyright © 2012 Gen-Xiang Mao et al. 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c438t-71979a75c795301f77f0761c393f11645cce897bc4dc7dc9824f819dbd520f6d3</citedby><cites>FETCH-LOGICAL-c438t-71979a75c795301f77f0761c393f11645cce897bc4dc7dc9824f819dbd520f6d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3345248/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3345248/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22577492$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Antonio Behr, Guilherme</contributor><creatorcontrib>Mao, Gen-Xiang</creatorcontrib><creatorcontrib>Zheng, Ling-Di</creatorcontrib><creatorcontrib>Cao, Yong-Bao</creatorcontrib><creatorcontrib>Chen, Zhuo-Mei</creatorcontrib><creatorcontrib>Lv, Yuan-Dong</creatorcontrib><creatorcontrib>Wang, Ya-Zhen</creatorcontrib><creatorcontrib>Hu, Xi-Lian</creatorcontrib><creatorcontrib>Wang, Guo-Fu</creatorcontrib><creatorcontrib>Yan, Jing</creatorcontrib><title>Antiaging Effect of Pine Pollen in Human Diploid Fibroblasts and in a Mouse Model Induced by D-Galactose</title><title>Oxidative medicine and cellular longevity</title><addtitle>Oxid Med Cell Longev</addtitle><description>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, p21Waf1, p16INK4a, PTEN, and p27Kip1 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.</description><subject>Aging - drug effects</subject><subject>Animals</subject><subject>Antioxidants - metabolism</subject><subject>beta-Galactosidase - metabolism</subject><subject>Body Weight - drug effects</subject><subject>Cell Line</subject><subject>Cell Proliferation - drug effects</subject><subject>Cellular Senescence - drug effects</subject><subject>Cytokines - metabolism</subject><subject>Diploidy</subject><subject>Female</subject><subject>Fibroblasts - cytology</subject><subject>Fibroblasts - drug effects</subject><subject>Fibroblasts - enzymology</subject><subject>Galactose - pharmacology</subject><subject>Glycation End Products, Advanced - metabolism</subject><subject>Humans</subject><subject>Inflammation Mediators - metabolism</subject><subject>Lipid Peroxidation - drug effects</subject><subject>Malondialdehyde - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Models, Animal</subject><subject>Nervous System - drug effects</subject><subject>Pinus - chemistry</subject><subject>Pollen - metabolism</subject><subject>Staining and Labeling</subject><subject>Superoxide Dismutase - metabolism</subject><issn>1942-0900</issn><issn>1942-0994</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><recordid>eNqF0c1rFDEYBvAgFlurJ89KjqJMm8_J5CKUfkPFHvQcMsmb3Ug2WSczSv97Z5m62FMvSSA_nnw8CL2j5IRSKU8ZoexUSaJb_gIdUS1YQ7QWL_drQg7R61p_EtJyJugrdMiYVEpodoTWZ3mMdhXzCl-GAG7EJeD7mAHfl5Qg45jxzbSxGV_EbSrR46vYD6VPto4V2-x3wOKvZaowjx4Svs1-cuBx_4AvmmubrBtLhTfoINhU4e3jfIx-XF1-P79p7r5d356f3TVO8G5sFNVKWyWd0pITGpQKRLXUcc0Dpa2QzkGnVe-Ed8o73TEROqp97yUjofX8GH1ZcrdTvwHvII-DTWY7xI0dHkyx0TzdyXFtVuW34VxIJro54ONjwFB-TVBHs4nVQUo2w_xKQ-fvVkLoTsz080LdUGodIOyPocTsujG7bszSzaw__H-zvf1Xxgw-LWAds7d_4jNp7xcMM4Fg91ho2bGO_wVYJJ9-</recordid><startdate>20120101</startdate><enddate>20120101</enddate><creator>Mao, Gen-Xiang</creator><creator>Zheng, Ling-Di</creator><creator>Cao, Yong-Bao</creator><creator>Chen, Zhuo-Mei</creator><creator>Lv, Yuan-Dong</creator><creator>Wang, Ya-Zhen</creator><creator>Hu, Xi-Lian</creator><creator>Wang, Guo-Fu</creator><creator>Yan, Jing</creator><general>Hindawi Puplishing Corporation</general><general>Hindawi Publishing Corporation</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20120101</creationdate><title>Antiaging Effect of Pine Pollen in Human Diploid Fibroblasts and in a Mouse Model Induced by D-Galactose</title><author>Mao, Gen-Xiang ; Zheng, Ling-Di ; Cao, Yong-Bao ; Chen, Zhuo-Mei ; Lv, Yuan-Dong ; Wang, Ya-Zhen ; Hu, Xi-Lian ; Wang, Guo-Fu ; Yan, Jing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c438t-71979a75c795301f77f0761c393f11645cce897bc4dc7dc9824f819dbd520f6d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Aging - drug effects</topic><topic>Animals</topic><topic>Antioxidants - metabolism</topic><topic>beta-Galactosidase - metabolism</topic><topic>Body Weight - drug effects</topic><topic>Cell Line</topic><topic>Cell Proliferation - drug effects</topic><topic>Cellular Senescence - drug effects</topic><topic>Cytokines - metabolism</topic><topic>Diploidy</topic><topic>Female</topic><topic>Fibroblasts - cytology</topic><topic>Fibroblasts - drug effects</topic><topic>Fibroblasts - enzymology</topic><topic>Galactose - pharmacology</topic><topic>Glycation End Products, Advanced - metabolism</topic><topic>Humans</topic><topic>Inflammation Mediators - metabolism</topic><topic>Lipid Peroxidation - drug effects</topic><topic>Malondialdehyde - metabolism</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Models, Animal</topic><topic>Nervous System - drug effects</topic><topic>Pinus - chemistry</topic><topic>Pollen - metabolism</topic><topic>Staining and Labeling</topic><topic>Superoxide Dismutase - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mao, Gen-Xiang</creatorcontrib><creatorcontrib>Zheng, Ling-Di</creatorcontrib><creatorcontrib>Cao, Yong-Bao</creatorcontrib><creatorcontrib>Chen, Zhuo-Mei</creatorcontrib><creatorcontrib>Lv, Yuan-Dong</creatorcontrib><creatorcontrib>Wang, Ya-Zhen</creatorcontrib><creatorcontrib>Hu, Xi-Lian</creatorcontrib><creatorcontrib>Wang, Guo-Fu</creatorcontrib><creatorcontrib>Yan, Jing</creatorcontrib><collection>الدوريات العلمية والإحصائية - e-Marefa Academic and Statistical Periodicals</collection><collection>معرفة - المحتوى العربي الأكاديمي المتكامل - e-Marefa Academic Complete</collection><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oxidative medicine and cellular longevity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mao, Gen-Xiang</au><au>Zheng, Ling-Di</au><au>Cao, Yong-Bao</au><au>Chen, Zhuo-Mei</au><au>Lv, Yuan-Dong</au><au>Wang, Ya-Zhen</au><au>Hu, Xi-Lian</au><au>Wang, Guo-Fu</au><au>Yan, Jing</au><au>Antonio Behr, Guilherme</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Antiaging Effect of Pine Pollen in Human Diploid Fibroblasts and in a Mouse Model Induced by D-Galactose</atitle><jtitle>Oxidative medicine and cellular longevity</jtitle><addtitle>Oxid Med Cell Longev</addtitle><date>2012-01-01</date><risdate>2012</risdate><volume>2012</volume><issue>2012</issue><spage>1</spage><epage>10</epage><pages>1-10</pages><issn>1942-0900</issn><eissn>1942-0994</eissn><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, p21Waf1, p16INK4a, PTEN, and p27Kip1 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.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Puplishing Corporation</pub><pmid>22577492</pmid><doi>10.1155/2012/750963</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; PubMed Central Open Access; EZB-FREE-00999 freely available EZB journals; Wiley Online Library (Open Access Collection); PubMed Central; Alma/SFX Local Collection |
| subjects | Aging - drug effects Animals Antioxidants - metabolism beta-Galactosidase - 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 |
| title | Antiaging Effect of Pine Pollen in Human Diploid Fibroblasts and in a Mouse Model Induced by D-Galactose |
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