Punicalagin Attenuates Neuronal Apoptosis by Upregulating 5‑Hydroxymethylcytosine in the Diabetic Mouse Brain
Punicalagin exerts neuroprotective activity by improving AMP-activated kinase (AMPK) and mitochondrial Krebs cycle. AMPK and Krebs cycle metabolites regulate 5-hydroxymethylcytosine (5hmC) via acting on ten-eleven translocation (TET) enzymes. Therefore, we hypothesized that punicalagin inhibits diab...
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Veröffentlicht in: | Journal of agricultural and food chemistry 2022-04, Vol.70 (16), p.4995-5004 |
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creator | He, Xin Pei, Shengjie Meng, Xiangyuan Hua, Qinglian Zhang, Tianyu Wang, Yan Zhang, Zhizhao Zhu, Xinyu Liu, Run Guo, Yurong Chen, Lei Li, Duo |
description | Punicalagin exerts neuroprotective activity by improving AMP-activated kinase (AMPK) and mitochondrial Krebs cycle. AMPK and Krebs cycle metabolites regulate 5-hydroxymethylcytosine (5hmC) via acting on ten-eleven translocation (TET) enzymes. Therefore, we hypothesized that punicalagin inhibits diabetes-related neuronal apoptosis by upregulating 5hmC in the diabetic mouse brain. C57BL/6J mice aged 8 weeks were randomly separated into five groups (n = 10), normal control (NC), diabetes mellitus (DM), resveratrol (RES), low-dose punicalagin (LPU), and high-dose punicalagin (HPU). Compared with other groups, the neuronal apoptosis rate was significantly higher and the 5hmC level of the cerebral cortex was significantly lower in the DM group. The levels of TET2 and P-AMPKα/AMPKα were significantly lower in the DM group than in both LPU and HPU groups. The ratio of (succinic acid + fumaric acid)/α-ketoglutarate was significantly higher in the DM group than in other groups. The present results suggest that punicalagin upregulates 5hmC via activating AMPK and maintaining Krebs cycle homeostasis, thus inhibiting neuronal apoptosis in the diabetic mouse brain. |
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AMPK and Krebs cycle metabolites regulate 5-hydroxymethylcytosine (5hmC) via acting on ten-eleven translocation (TET) enzymes. Therefore, we hypothesized that punicalagin inhibits diabetes-related neuronal apoptosis by upregulating 5hmC in the diabetic mouse brain. C57BL/6J mice aged 8 weeks were randomly separated into five groups (n = 10), normal control (NC), diabetes mellitus (DM), resveratrol (RES), low-dose punicalagin (LPU), and high-dose punicalagin (HPU). Compared with other groups, the neuronal apoptosis rate was significantly higher and the 5hmC level of the cerebral cortex was significantly lower in the DM group. The levels of TET2 and P-AMPKα/AMPKα were significantly lower in the DM group than in both LPU and HPU groups. The ratio of (succinic acid + fumaric acid)/α-ketoglutarate was significantly higher in the DM group than in other groups. The present results suggest that punicalagin upregulates 5hmC via activating AMPK and maintaining Krebs cycle homeostasis, thus inhibiting neuronal apoptosis in the diabetic mouse brain.</description><identifier>ISSN: 0021-8561</identifier><identifier>EISSN: 1520-5118</identifier><identifier>DOI: 10.1021/acs.jafc.2c00863</identifier><identifier>PMID: 35412829</identifier><language>eng</language><publisher>United States: American Chemical Society</publisher><subject>5-Methylcytosine - analogs & derivatives ; AMP-Activated Protein Kinases - genetics ; AMP-Activated Protein Kinases - metabolism ; Animals ; Apoptosis ; Bioactive Constituents, Metabolites, and Functions ; Brain - metabolism ; Diabetes Mellitus - metabolism ; Hydrolyzable Tannins ; Mice ; Mice, Inbred C57BL</subject><ispartof>Journal of agricultural and food chemistry, 2022-04, Vol.70 (16), p.4995-5004</ispartof><rights>2022 American Chemical Society</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-a336t-b5b6d561f46508957496046fdf3704b16773ca750a488c7a978dd85092aa69833</citedby><cites>FETCH-LOGICAL-a336t-b5b6d561f46508957496046fdf3704b16773ca750a488c7a978dd85092aa69833</cites><orcidid>0000-0002-6407-5293 ; 0000-0001-5227-5565</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://pubs.acs.org/doi/pdf/10.1021/acs.jafc.2c00863$$EPDF$$P50$$Gacs$$H</linktopdf><linktohtml>$$Uhttps://pubs.acs.org/doi/10.1021/acs.jafc.2c00863$$EHTML$$P50$$Gacs$$H</linktohtml><link.rule.ids>315,781,785,2766,27078,27926,27927,56740,56790</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35412829$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>He, Xin</creatorcontrib><creatorcontrib>Pei, Shengjie</creatorcontrib><creatorcontrib>Meng, Xiangyuan</creatorcontrib><creatorcontrib>Hua, Qinglian</creatorcontrib><creatorcontrib>Zhang, Tianyu</creatorcontrib><creatorcontrib>Wang, Yan</creatorcontrib><creatorcontrib>Zhang, Zhizhao</creatorcontrib><creatorcontrib>Zhu, Xinyu</creatorcontrib><creatorcontrib>Liu, Run</creatorcontrib><creatorcontrib>Guo, Yurong</creatorcontrib><creatorcontrib>Chen, Lei</creatorcontrib><creatorcontrib>Li, Duo</creatorcontrib><title>Punicalagin Attenuates Neuronal Apoptosis by Upregulating 5‑Hydroxymethylcytosine in the Diabetic Mouse Brain</title><title>Journal of agricultural and food chemistry</title><addtitle>J. Agric. Food Chem</addtitle><description>Punicalagin exerts neuroprotective activity by improving AMP-activated kinase (AMPK) and mitochondrial Krebs cycle. AMPK and Krebs cycle metabolites regulate 5-hydroxymethylcytosine (5hmC) via acting on ten-eleven translocation (TET) enzymes. Therefore, we hypothesized that punicalagin inhibits diabetes-related neuronal apoptosis by upregulating 5hmC in the diabetic mouse brain. C57BL/6J mice aged 8 weeks were randomly separated into five groups (n = 10), normal control (NC), diabetes mellitus (DM), resveratrol (RES), low-dose punicalagin (LPU), and high-dose punicalagin (HPU). Compared with other groups, the neuronal apoptosis rate was significantly higher and the 5hmC level of the cerebral cortex was significantly lower in the DM group. The levels of TET2 and P-AMPKα/AMPKα were significantly lower in the DM group than in both LPU and HPU groups. The ratio of (succinic acid + fumaric acid)/α-ketoglutarate was significantly higher in the DM group than in other groups. The present results suggest that punicalagin upregulates 5hmC via activating AMPK and maintaining Krebs cycle homeostasis, thus inhibiting neuronal apoptosis in the diabetic mouse brain.</description><subject>5-Methylcytosine - analogs & derivatives</subject><subject>AMP-Activated Protein Kinases - genetics</subject><subject>AMP-Activated Protein Kinases - metabolism</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Bioactive Constituents, Metabolites, and Functions</subject><subject>Brain - metabolism</subject><subject>Diabetes Mellitus - metabolism</subject><subject>Hydrolyzable Tannins</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><issn>0021-8561</issn><issn>1520-5118</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kLtO7DAURS10EQyPngq5pCCDncSPlMMbiVcBdXTiOINRJg62I5GOX-AX-RI8zEB3T3Oatbe2FkIHlEwpSekJKD99hUZNU0WI5NkGmlCWkoRRKv-hCYlMIhmn22jH-1cSGSbIFtrOWE5TmRYTZB-HzihoYW46PAtBdwME7fG9HpztoMWz3vbBeuNxNeLn3un50EIw3Ryzr4_P67F29n1c6PAytmpcgp3GsSq8aHxuoNLBKHxnB6_xqQPT7aHNBlqv99d_Fz1fXjydXSe3D1c3Z7PbBLKMh6RiFa_j8CbnjMiCibzgJOdN3WSC5BXlQmQKBCOQS6kEFELWtWSkSAF4IbNsFx2tentn3wbtQ7kwXum2hU7HNWXK8yKeSJcoWaHKWe-dbsremQW4saSkXGouo-Zyqblca46Rw3X7UC10_Rf49RqB4xXwE7WDiyr9__u-AW21iqU</recordid><startdate>20220427</startdate><enddate>20220427</enddate><creator>He, Xin</creator><creator>Pei, Shengjie</creator><creator>Meng, Xiangyuan</creator><creator>Hua, Qinglian</creator><creator>Zhang, Tianyu</creator><creator>Wang, Yan</creator><creator>Zhang, Zhizhao</creator><creator>Zhu, Xinyu</creator><creator>Liu, Run</creator><creator>Guo, Yurong</creator><creator>Chen, Lei</creator><creator>Li, Duo</creator><general>American Chemical Society</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><orcidid>https://orcid.org/0000-0002-6407-5293</orcidid><orcidid>https://orcid.org/0000-0001-5227-5565</orcidid></search><sort><creationdate>20220427</creationdate><title>Punicalagin Attenuates Neuronal Apoptosis by Upregulating 5‑Hydroxymethylcytosine in the Diabetic Mouse Brain</title><author>He, Xin ; Pei, Shengjie ; Meng, Xiangyuan ; Hua, Qinglian ; Zhang, Tianyu ; Wang, Yan ; Zhang, Zhizhao ; Zhu, Xinyu ; Liu, Run ; Guo, Yurong ; Chen, Lei ; Li, Duo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-a336t-b5b6d561f46508957496046fdf3704b16773ca750a488c7a978dd85092aa69833</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>5-Methylcytosine - analogs & derivatives</topic><topic>AMP-Activated Protein Kinases - genetics</topic><topic>AMP-Activated Protein Kinases - metabolism</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Bioactive Constituents, Metabolites, and Functions</topic><topic>Brain - metabolism</topic><topic>Diabetes Mellitus - metabolism</topic><topic>Hydrolyzable Tannins</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>He, Xin</creatorcontrib><creatorcontrib>Pei, Shengjie</creatorcontrib><creatorcontrib>Meng, Xiangyuan</creatorcontrib><creatorcontrib>Hua, Qinglian</creatorcontrib><creatorcontrib>Zhang, Tianyu</creatorcontrib><creatorcontrib>Wang, Yan</creatorcontrib><creatorcontrib>Zhang, Zhizhao</creatorcontrib><creatorcontrib>Zhu, Xinyu</creatorcontrib><creatorcontrib>Liu, Run</creatorcontrib><creatorcontrib>Guo, Yurong</creatorcontrib><creatorcontrib>Chen, Lei</creatorcontrib><creatorcontrib>Li, Duo</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><jtitle>Journal of agricultural and food chemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>He, Xin</au><au>Pei, Shengjie</au><au>Meng, Xiangyuan</au><au>Hua, Qinglian</au><au>Zhang, Tianyu</au><au>Wang, Yan</au><au>Zhang, Zhizhao</au><au>Zhu, Xinyu</au><au>Liu, Run</au><au>Guo, Yurong</au><au>Chen, Lei</au><au>Li, Duo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Punicalagin Attenuates Neuronal Apoptosis by Upregulating 5‑Hydroxymethylcytosine in the Diabetic Mouse Brain</atitle><jtitle>Journal of agricultural and food chemistry</jtitle><addtitle>J. Agric. Food Chem</addtitle><date>2022-04-27</date><risdate>2022</risdate><volume>70</volume><issue>16</issue><spage>4995</spage><epage>5004</epage><pages>4995-5004</pages><issn>0021-8561</issn><eissn>1520-5118</eissn><abstract>Punicalagin exerts neuroprotective activity by improving AMP-activated kinase (AMPK) and mitochondrial Krebs cycle. AMPK and Krebs cycle metabolites regulate 5-hydroxymethylcytosine (5hmC) via acting on ten-eleven translocation (TET) enzymes. Therefore, we hypothesized that punicalagin inhibits diabetes-related neuronal apoptosis by upregulating 5hmC in the diabetic mouse brain. C57BL/6J mice aged 8 weeks were randomly separated into five groups (n = 10), normal control (NC), diabetes mellitus (DM), resveratrol (RES), low-dose punicalagin (LPU), and high-dose punicalagin (HPU). Compared with other groups, the neuronal apoptosis rate was significantly higher and the 5hmC level of the cerebral cortex was significantly lower in the DM group. The levels of TET2 and P-AMPKα/AMPKα were significantly lower in the DM group than in both LPU and HPU groups. The ratio of (succinic acid + fumaric acid)/α-ketoglutarate was significantly higher in the DM group than in other groups. The present results suggest that punicalagin upregulates 5hmC via activating AMPK and maintaining Krebs cycle homeostasis, thus inhibiting neuronal apoptosis in the diabetic mouse brain.</abstract><cop>United States</cop><pub>American Chemical Society</pub><pmid>35412829</pmid><doi>10.1021/acs.jafc.2c00863</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-6407-5293</orcidid><orcidid>https://orcid.org/0000-0001-5227-5565</orcidid></addata></record> |
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subjects | 5-Methylcytosine - analogs & derivatives AMP-Activated Protein Kinases - genetics AMP-Activated Protein Kinases - metabolism Animals Apoptosis Bioactive Constituents, Metabolites, and Functions Brain - metabolism Diabetes Mellitus - metabolism Hydrolyzable Tannins Mice Mice, Inbred C57BL |
title | Punicalagin Attenuates Neuronal Apoptosis by Upregulating 5‑Hydroxymethylcytosine in the Diabetic Mouse Brain |
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