Swimming exercise stimulates IGF1/ PI3K/Akt and AMPK/SIRT1/PGC1α survival signaling to suppress apoptosis and inflammation in aging hippocampus
Hippocampus is one of the most vulnerable brain regions in terms of age-related pathological change. Exercise is presumed to delay the aging process and promote health because it seems to improve the function of most of the aging mechanisms. The purpose of this study is to evaluate the effects of sw...
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| Veröffentlicht in: | Aging (Albany, NY.) NY.), 2020-04, Vol.12 (8), p.6852-6864 |
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| creator | Lin, Jing-Ying Kuo, Wei-Wen Baskaran, Rathinasamy Kuo, Chia-Hua Chen, Yun-An Chen, William Shao-Tsu Ho, Tsung-Jung Day, Cecilia Hsuan Mahalakshmi, B Huang, Chih-Yang |
| description | Hippocampus is one of the most vulnerable brain regions in terms of age-related pathological change. Exercise is presumed to delay the aging process and promote health because it seems to improve the function of most of the aging mechanisms. The purpose of this study is to evaluate the effects of swimming exercise training on brain inflammation, apoptotic and survival pathways in the hippocampus of D-galactose-induced aging in SD rats. The rats were allocated to the following groups: (1) control; (2) swimming exercise; (3) induced-aging by injecting D-galactose; (4) induced-aging rats with swimming exercise. The longevity-related AMPK/SIRT1/PGC-1α signaling pathway and brain IGF1/PI3K/Akt survival pathway were significantly reduced in D-galactose-induced aging group compared to non-aging control group and increased after exercise training. The inflammation pathway markers were over-expressed in induced-aging hippocampus, exercise significantly inhibited the inflammatory signaling activity. Fas-dependent and mitochondrial-dependent apoptotic pathways were significantly increased in the induced-aging group relative to the control group whereas they were decreased in the aging-exercise group. This study demonstrated that swimming exercise not only reduced aging-induced brain apoptosis and inflammatory signaling activity, but also enhanced the survival pathways in the hippocampus, which provides one of the new beneficial effects for exercise training in aging brain. |
| doi_str_mv | 10.18632/aging.103046 |
| format | Article |
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Exercise is presumed to delay the aging process and promote health because it seems to improve the function of most of the aging mechanisms. The purpose of this study is to evaluate the effects of swimming exercise training on brain inflammation, apoptotic and survival pathways in the hippocampus of D-galactose-induced aging in SD rats. The rats were allocated to the following groups: (1) control; (2) swimming exercise; (3) induced-aging by injecting D-galactose; (4) induced-aging rats with swimming exercise. The longevity-related AMPK/SIRT1/PGC-1α signaling pathway and brain IGF1/PI3K/Akt survival pathway were significantly reduced in D-galactose-induced aging group compared to non-aging control group and increased after exercise training. The inflammation pathway markers were over-expressed in induced-aging hippocampus, exercise significantly inhibited the inflammatory signaling activity. Fas-dependent and mitochondrial-dependent apoptotic pathways were significantly increased in the induced-aging group relative to the control group whereas they were decreased in the aging-exercise group. This study demonstrated that swimming exercise not only reduced aging-induced brain apoptosis and inflammatory signaling activity, but also enhanced the survival pathways in the hippocampus, which provides one of the new beneficial effects for exercise training in aging brain.</description><identifier>ISSN: 1945-4589</identifier><identifier>EISSN: 1945-4589</identifier><identifier>DOI: 10.18632/aging.103046</identifier><identifier>PMID: 32320382</identifier><language>eng</language><publisher>United States: Impact Journals</publisher><subject>Adenylate Kinase - genetics ; Adenylate Kinase - metabolism ; Aging - pathology ; Aging - physiology ; Animals ; Apoptosis ; bcl-X Protein - metabolism ; Caspases - metabolism ; Cyclooxygenase 2 - metabolism ; Fas Ligand Protein - metabolism ; Fas-Associated Death Domain Protein - metabolism ; Gene Expression ; Hippocampus - pathology ; Hippocampus - physiology ; Inflammation - metabolism ; Insulin-Like Growth Factor I - genetics ; Insulin-Like Growth Factor I - metabolism ; Male ; Neurons - pathology ; NF-kappa B - metabolism ; Nitric Oxide Synthase Type II - metabolism ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - genetics ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism ; Phosphatidylinositol 3-Kinase - genetics ; Phosphatidylinositol 3-Kinase - metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-akt - genetics ; Proto-Oncogene Proteins c-akt - metabolism ; Rats ; Receptor, IGF Type 1 - metabolism ; Research Paper ; Signal Transduction ; Sirtuin 1 - genetics ; Sirtuin 1 - metabolism ; Swimming - physiology ; Tumor Necrosis Factor-alpha - metabolism</subject><ispartof>Aging (Albany, NY.), 2020-04, Vol.12 (8), p.6852-6864</ispartof><rights>Copyright © 2020 Lin et al.</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c387t-b853a889172b48e9770e1501c01d19909ffd4152a8a79ae7b365832ae52de1473</citedby><cites>FETCH-LOGICAL-c387t-b853a889172b48e9770e1501c01d19909ffd4152a8a79ae7b365832ae52de1473</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/PMC7202519/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7202519/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32320382$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lin, Jing-Ying</creatorcontrib><creatorcontrib>Kuo, Wei-Wen</creatorcontrib><creatorcontrib>Baskaran, Rathinasamy</creatorcontrib><creatorcontrib>Kuo, Chia-Hua</creatorcontrib><creatorcontrib>Chen, Yun-An</creatorcontrib><creatorcontrib>Chen, William Shao-Tsu</creatorcontrib><creatorcontrib>Ho, Tsung-Jung</creatorcontrib><creatorcontrib>Day, Cecilia Hsuan</creatorcontrib><creatorcontrib>Mahalakshmi, B</creatorcontrib><creatorcontrib>Huang, Chih-Yang</creatorcontrib><title>Swimming exercise stimulates IGF1/ PI3K/Akt and AMPK/SIRT1/PGC1α survival signaling to suppress apoptosis and inflammation in aging hippocampus</title><title>Aging (Albany, NY.)</title><addtitle>Aging (Albany NY)</addtitle><description>Hippocampus is one of the most vulnerable brain regions in terms of age-related pathological change. Exercise is presumed to delay the aging process and promote health because it seems to improve the function of most of the aging mechanisms. The purpose of this study is to evaluate the effects of swimming exercise training on brain inflammation, apoptotic and survival pathways in the hippocampus of D-galactose-induced aging in SD rats. The rats were allocated to the following groups: (1) control; (2) swimming exercise; (3) induced-aging by injecting D-galactose; (4) induced-aging rats with swimming exercise. The longevity-related AMPK/SIRT1/PGC-1α signaling pathway and brain IGF1/PI3K/Akt survival pathway were significantly reduced in D-galactose-induced aging group compared to non-aging control group and increased after exercise training. The inflammation pathway markers were over-expressed in induced-aging hippocampus, exercise significantly inhibited the inflammatory signaling activity. Fas-dependent and mitochondrial-dependent apoptotic pathways were significantly increased in the induced-aging group relative to the control group whereas they were decreased in the aging-exercise group. This study demonstrated that swimming exercise not only reduced aging-induced brain apoptosis and inflammatory signaling activity, but also enhanced the survival pathways in the hippocampus, which provides one of the new beneficial effects for exercise training in aging brain.</description><subject>Adenylate Kinase - genetics</subject><subject>Adenylate Kinase - metabolism</subject><subject>Aging - pathology</subject><subject>Aging - physiology</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>bcl-X Protein - metabolism</subject><subject>Caspases - metabolism</subject><subject>Cyclooxygenase 2 - metabolism</subject><subject>Fas Ligand Protein - metabolism</subject><subject>Fas-Associated Death Domain Protein - metabolism</subject><subject>Gene Expression</subject><subject>Hippocampus - pathology</subject><subject>Hippocampus - physiology</subject><subject>Inflammation - metabolism</subject><subject>Insulin-Like Growth Factor I - genetics</subject><subject>Insulin-Like Growth Factor I - metabolism</subject><subject>Male</subject><subject>Neurons - pathology</subject><subject>NF-kappa B - metabolism</subject><subject>Nitric Oxide Synthase Type II - metabolism</subject><subject>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - genetics</subject><subject>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism</subject><subject>Phosphatidylinositol 3-Kinase - genetics</subject><subject>Phosphatidylinositol 3-Kinase - metabolism</subject><subject>Phosphorylation</subject><subject>Proto-Oncogene Proteins c-akt - genetics</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Rats</subject><subject>Receptor, IGF Type 1 - metabolism</subject><subject>Research Paper</subject><subject>Signal Transduction</subject><subject>Sirtuin 1 - genetics</subject><subject>Sirtuin 1 - metabolism</subject><subject>Swimming - physiology</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><issn>1945-4589</issn><issn>1945-4589</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkc9u1DAQxiMEoqVw5Ip85JLGf-LYviCtVnRZtYgVLWdrNnG2hjg2trPAW_AqvAjPRNgtVTl5PPPNb0bzFcVLgs-JbBitYGfH3TnBDNfNo-KUqJqXNZfq8YP4pHiW0meMG87r5mlxwiijmEl6Wvy8_madmwnIfDextcmglK2bBsgmofXqglRos2aX1eJLRjB2aPF-c1ldrz_ekGqzWpLfv1Ca4t7uYUDJ7kYY_rKyn7MhRJMSguBD9smmQ7sd-wGcg2z9OH_QYXt0a0PwLbgwpefFkx6GZF7cvWfFp4u3N8t35dWH1Xq5uCpbJkUut5IzkFIRQbe1NEoIbAjHpMWkI0ph1fddTTgFCUKBEVvWcMkoGE47Q2rBzoo3R26Yts50rRlzhEGHaB3EH9qD1f9XRnurd36vBcWUEzUDXt8Bov86mZS1s6k1wwCj8VPSlKmaNkKwZpaWR2kbfUrR9PdjCNYHF_XhDvro4qx_9XC3e_U_29gfxp6bFw</recordid><startdate>20200422</startdate><enddate>20200422</enddate><creator>Lin, Jing-Ying</creator><creator>Kuo, Wei-Wen</creator><creator>Baskaran, Rathinasamy</creator><creator>Kuo, Chia-Hua</creator><creator>Chen, Yun-An</creator><creator>Chen, William Shao-Tsu</creator><creator>Ho, Tsung-Jung</creator><creator>Day, Cecilia Hsuan</creator><creator>Mahalakshmi, B</creator><creator>Huang, Chih-Yang</creator><general>Impact Journals</general><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>20200422</creationdate><title>Swimming exercise stimulates IGF1/ PI3K/Akt and AMPK/SIRT1/PGC1α survival signaling to suppress apoptosis and inflammation in aging hippocampus</title><author>Lin, Jing-Ying ; Kuo, Wei-Wen ; Baskaran, Rathinasamy ; Kuo, Chia-Hua ; Chen, Yun-An ; Chen, William Shao-Tsu ; Ho, Tsung-Jung ; Day, Cecilia Hsuan ; Mahalakshmi, B ; Huang, Chih-Yang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c387t-b853a889172b48e9770e1501c01d19909ffd4152a8a79ae7b365832ae52de1473</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Adenylate Kinase - genetics</topic><topic>Adenylate Kinase - metabolism</topic><topic>Aging - pathology</topic><topic>Aging - physiology</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>bcl-X Protein - metabolism</topic><topic>Caspases - metabolism</topic><topic>Cyclooxygenase 2 - metabolism</topic><topic>Fas Ligand Protein - metabolism</topic><topic>Fas-Associated Death Domain Protein - metabolism</topic><topic>Gene Expression</topic><topic>Hippocampus - pathology</topic><topic>Hippocampus - physiology</topic><topic>Inflammation - metabolism</topic><topic>Insulin-Like Growth Factor I - genetics</topic><topic>Insulin-Like Growth Factor I - metabolism</topic><topic>Male</topic><topic>Neurons - pathology</topic><topic>NF-kappa B - metabolism</topic><topic>Nitric Oxide Synthase Type II - metabolism</topic><topic>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - genetics</topic><topic>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism</topic><topic>Phosphatidylinositol 3-Kinase - genetics</topic><topic>Phosphatidylinositol 3-Kinase - metabolism</topic><topic>Phosphorylation</topic><topic>Proto-Oncogene Proteins c-akt - genetics</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Rats</topic><topic>Receptor, IGF Type 1 - metabolism</topic><topic>Research Paper</topic><topic>Signal Transduction</topic><topic>Sirtuin 1 - genetics</topic><topic>Sirtuin 1 - metabolism</topic><topic>Swimming - physiology</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><toplevel>online_resources</toplevel><creatorcontrib>Lin, Jing-Ying</creatorcontrib><creatorcontrib>Kuo, Wei-Wen</creatorcontrib><creatorcontrib>Baskaran, Rathinasamy</creatorcontrib><creatorcontrib>Kuo, Chia-Hua</creatorcontrib><creatorcontrib>Chen, Yun-An</creatorcontrib><creatorcontrib>Chen, William Shao-Tsu</creatorcontrib><creatorcontrib>Ho, Tsung-Jung</creatorcontrib><creatorcontrib>Day, Cecilia Hsuan</creatorcontrib><creatorcontrib>Mahalakshmi, B</creatorcontrib><creatorcontrib>Huang, Chih-Yang</creatorcontrib><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>Aging (Albany, NY.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lin, Jing-Ying</au><au>Kuo, Wei-Wen</au><au>Baskaran, Rathinasamy</au><au>Kuo, Chia-Hua</au><au>Chen, Yun-An</au><au>Chen, William Shao-Tsu</au><au>Ho, Tsung-Jung</au><au>Day, Cecilia Hsuan</au><au>Mahalakshmi, B</au><au>Huang, Chih-Yang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Swimming exercise stimulates IGF1/ PI3K/Akt and AMPK/SIRT1/PGC1α survival signaling to suppress apoptosis and inflammation in aging hippocampus</atitle><jtitle>Aging (Albany, NY.)</jtitle><addtitle>Aging (Albany NY)</addtitle><date>2020-04-22</date><risdate>2020</risdate><volume>12</volume><issue>8</issue><spage>6852</spage><epage>6864</epage><pages>6852-6864</pages><issn>1945-4589</issn><eissn>1945-4589</eissn><abstract>Hippocampus is one of the most vulnerable brain regions in terms of age-related pathological change. Exercise is presumed to delay the aging process and promote health because it seems to improve the function of most of the aging mechanisms. The purpose of this study is to evaluate the effects of swimming exercise training on brain inflammation, apoptotic and survival pathways in the hippocampus of D-galactose-induced aging in SD rats. The rats were allocated to the following groups: (1) control; (2) swimming exercise; (3) induced-aging by injecting D-galactose; (4) induced-aging rats with swimming exercise. The longevity-related AMPK/SIRT1/PGC-1α signaling pathway and brain IGF1/PI3K/Akt survival pathway were significantly reduced in D-galactose-induced aging group compared to non-aging control group and increased after exercise training. The inflammation pathway markers were over-expressed in induced-aging hippocampus, exercise significantly inhibited the inflammatory signaling activity. Fas-dependent and mitochondrial-dependent apoptotic pathways were significantly increased in the induced-aging group relative to the control group whereas they were decreased in the aging-exercise group. This study demonstrated that swimming exercise not only reduced aging-induced brain apoptosis and inflammatory signaling activity, but also enhanced the survival pathways in the hippocampus, which provides one of the new beneficial effects for exercise training in aging brain.</abstract><cop>United States</cop><pub>Impact Journals</pub><pmid>32320382</pmid><doi>10.18632/aging.103046</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adenylate Kinase - genetics Adenylate Kinase - metabolism Aging - pathology Aging - physiology Animals Apoptosis bcl-X Protein - metabolism Caspases - metabolism Cyclooxygenase 2 - metabolism Fas Ligand Protein - metabolism Fas-Associated Death Domain Protein - metabolism Gene Expression Hippocampus - pathology Hippocampus - physiology Inflammation - metabolism Insulin-Like Growth Factor I - genetics Insulin-Like Growth Factor I - metabolism Male Neurons - pathology NF-kappa B - metabolism Nitric Oxide Synthase Type II - metabolism Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - genetics Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism Phosphatidylinositol 3-Kinase - genetics Phosphatidylinositol 3-Kinase - metabolism Phosphorylation Proto-Oncogene Proteins c-akt - genetics Proto-Oncogene Proteins c-akt - metabolism Rats Receptor, IGF Type 1 - metabolism Research Paper Signal Transduction Sirtuin 1 - genetics Sirtuin 1 - metabolism Swimming - physiology Tumor Necrosis Factor-alpha - metabolism |
| title | Swimming exercise stimulates IGF1/ PI3K/Akt and AMPK/SIRT1/PGC1α survival signaling to suppress apoptosis and inflammation in aging hippocampus |
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