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A novel polysaccharide from Lentinus edodes mycelia protects MIN6 cells against high glucose-induced damage via the MAPKs and Nrf2 pathways
Diabetes mellitus is one of the most widespread diseases in the world, high glucose can damage islet cells, it is important to discover new natural products to inhibit high glucose damage. The protective effects and mechanisms of a novel Lentinus edodes mycelia polysaccharide (LMP) against damage in...
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Published in: | Food & nutrition research 2019-06, Vol.63, p.1-9 |
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description | Diabetes mellitus is one of the most widespread diseases in the world, high glucose can damage islet cells, it is important to discover new natural products to inhibit high glucose damage. The protective effects and mechanisms of a novel Lentinus edodes mycelia polysaccharide (LMP) against damage induced by high glucose in MIN6 cells were explored.
Cell viability, malondialdehyde (MDA) inhibition, lactate dehydrogenase (LDH) release and the activity of superoxide dismutase (SOD) were evaluated under 40 mM glucose with or without LMP for 48 h. Cell signaling pathway analysis was performed to investigate the possible mechanisms of the protective effects of LMP in MIN6 cells.
The results showed that LMP could increase cell viability and the activity of SOD, decrease the reactive oxygen species ( ROS) production, and reduce the MDA content and LDH release in high glucose-induced MIN6 cells. Moreover, LMP prevented high glucose-induced apoptosis by decreasing the expression of Bax and the activation of caspase-1 and caspase-3. Cell signaling pathway analysis showed that p38 mitogen-activated protein kinase (MAPK) and JNK pathways were inhibited and the Nrf2 pathway was activated after treated with LMP.
The protective effects of LMP against MIN6 cells damage induced by high glucose might rely on the regulation of the MAPK and Nrf2 pathways. These results indicated that LMP had great potential as a therapeutic agent for the treatment of diabetes mellitus. |
doi_str_mv | 10.29219/fnr.v63.1598 |
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Cell viability, malondialdehyde (MDA) inhibition, lactate dehydrogenase (LDH) release and the activity of superoxide dismutase (SOD) were evaluated under 40 mM glucose with or without LMP for 48 h. Cell signaling pathway analysis was performed to investigate the possible mechanisms of the protective effects of LMP in MIN6 cells.
The results showed that LMP could increase cell viability and the activity of SOD, decrease the reactive oxygen species ( ROS) production, and reduce the MDA content and LDH release in high glucose-induced MIN6 cells. Moreover, LMP prevented high glucose-induced apoptosis by decreasing the expression of Bax and the activation of caspase-1 and caspase-3. Cell signaling pathway analysis showed that p38 mitogen-activated protein kinase (MAPK) and JNK pathways were inhibited and the Nrf2 pathway was activated after treated with LMP.
The protective effects of LMP against MIN6 cells damage induced by high glucose might rely on the regulation of the MAPK and Nrf2 pathways. These results indicated that LMP had great potential as a therapeutic agent for the treatment of diabetes mellitus.</description><identifier>ISSN: 1654-661X</identifier><identifier>EISSN: 1654-661X</identifier><identifier>DOI: 10.29219/fnr.v63.1598</identifier><identifier>PMID: 31217790</identifier><language>eng</language><publisher>Sweden: Open Academia</publisher><subject>LMP ; MAPK ; MIN6 cells ; Nrf2 ; Original ; Oxidative stress ; ROS</subject><ispartof>Food & nutrition research, 2019-06, Vol.63, p.1-9</ispartof><rights>2019 Xiangyu Cao et al. 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c414t-c0966f29cc2e5a23e00b51007a370a581ab817952dedca983be2512e22fd273b3</citedby><cites>FETCH-LOGICAL-c414t-c0966f29cc2e5a23e00b51007a370a581ab817952dedca983be2512e22fd273b3</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/PMC6560380/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6560380/$$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/31217790$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cao, Xiangyu</creatorcontrib><creatorcontrib>Liu, Dan</creatorcontrib><creatorcontrib>Xia, Ying</creatorcontrib><creatorcontrib>Cai, Tiange</creatorcontrib><creatorcontrib>He, Yin</creatorcontrib><creatorcontrib>Liu, Jianli</creatorcontrib><title>A novel polysaccharide from Lentinus edodes mycelia protects MIN6 cells against high glucose-induced damage via the MAPKs and Nrf2 pathways</title><title>Food & nutrition research</title><addtitle>Food Nutr Res</addtitle><description>Diabetes mellitus is one of the most widespread diseases in the world, high glucose can damage islet cells, it is important to discover new natural products to inhibit high glucose damage. The protective effects and mechanisms of a novel Lentinus edodes mycelia polysaccharide (LMP) against damage induced by high glucose in MIN6 cells were explored.
Cell viability, malondialdehyde (MDA) inhibition, lactate dehydrogenase (LDH) release and the activity of superoxide dismutase (SOD) were evaluated under 40 mM glucose with or without LMP for 48 h. Cell signaling pathway analysis was performed to investigate the possible mechanisms of the protective effects of LMP in MIN6 cells.
The results showed that LMP could increase cell viability and the activity of SOD, decrease the reactive oxygen species ( ROS) production, and reduce the MDA content and LDH release in high glucose-induced MIN6 cells. Moreover, LMP prevented high glucose-induced apoptosis by decreasing the expression of Bax and the activation of caspase-1 and caspase-3. Cell signaling pathway analysis showed that p38 mitogen-activated protein kinase (MAPK) and JNK pathways were inhibited and the Nrf2 pathway was activated after treated with LMP.
The protective effects of LMP against MIN6 cells damage induced by high glucose might rely on the regulation of the MAPK and Nrf2 pathways. These results indicated that LMP had great potential as a therapeutic agent for the treatment of diabetes mellitus.</description><subject>LMP</subject><subject>MAPK</subject><subject>MIN6 cells</subject><subject>Nrf2</subject><subject>Original</subject><subject>Oxidative stress</subject><subject>ROS</subject><issn>1654-661X</issn><issn>1654-661X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>DOA</sourceid><recordid>eNpVkk1v1DAQhiMEoqVw5Ip85JLFH3ESX5BWVaErtoUDSNysiT1JXCXxYieL9jfwp-t2S9WePBq_84xn_GbZe0ZXXHGmPrVTWO1LsWJS1S-yU1bKIi9L9vvlk_gkexPjDaWloHXxOjsRjLOqUvQ0-7cmk9_jQHZ-OEQwpofgLJI2-JFscZrdtESC1luMZDwYHByQXfAzmjmSq811SVJuiAQ6cFOcSe-6nnTDYnzE3E12MWiJhRE6JPtUO_dIrtY_vqWKyZLr0HKyg7n_C4f4NnvVwhDx3cN5lv36cvHz_DLffv-6OV9vc1OwYs4NVWXZcmUMRwlcIKWNZJRWICoKsmbQ1KxSklu0BlQtGuSSceS8tbwSjTjLNkeu9XCjd8GNEA7ag9P3CR86DWF2ZkDd1kxAYjBZ8KLitZJto6SwApG3QpnE-nxk7ZZmTP3SxgIMz6DPbybX687vdSlLKmqaAB8fAMH_WTDOenTxbqUwoV-i5rwomEjjySTNj1ITfIwB28c2jOp7M-hkBp3MoO_MkPQfnr7tUf3_98Utx8-yYw</recordid><startdate>20190606</startdate><enddate>20190606</enddate><creator>Cao, Xiangyu</creator><creator>Liu, Dan</creator><creator>Xia, Ying</creator><creator>Cai, Tiange</creator><creator>He, Yin</creator><creator>Liu, Jianli</creator><general>Open Academia</general><general>Swedish Nutrition Foundation</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20190606</creationdate><title>A novel polysaccharide from Lentinus edodes mycelia protects MIN6 cells against high glucose-induced damage via the MAPKs and Nrf2 pathways</title><author>Cao, Xiangyu ; Liu, Dan ; Xia, Ying ; Cai, Tiange ; He, Yin ; Liu, Jianli</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c414t-c0966f29cc2e5a23e00b51007a370a581ab817952dedca983be2512e22fd273b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>LMP</topic><topic>MAPK</topic><topic>MIN6 cells</topic><topic>Nrf2</topic><topic>Original</topic><topic>Oxidative stress</topic><topic>ROS</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cao, Xiangyu</creatorcontrib><creatorcontrib>Liu, Dan</creatorcontrib><creatorcontrib>Xia, Ying</creatorcontrib><creatorcontrib>Cai, Tiange</creatorcontrib><creatorcontrib>He, Yin</creatorcontrib><creatorcontrib>Liu, Jianli</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Food & nutrition research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cao, Xiangyu</au><au>Liu, Dan</au><au>Xia, Ying</au><au>Cai, Tiange</au><au>He, Yin</au><au>Liu, Jianli</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A novel polysaccharide from Lentinus edodes mycelia protects MIN6 cells against high glucose-induced damage via the MAPKs and Nrf2 pathways</atitle><jtitle>Food & nutrition research</jtitle><addtitle>Food Nutr Res</addtitle><date>2019-06-06</date><risdate>2019</risdate><volume>63</volume><spage>1</spage><epage>9</epage><pages>1-9</pages><issn>1654-661X</issn><eissn>1654-661X</eissn><abstract>Diabetes mellitus is one of the most widespread diseases in the world, high glucose can damage islet cells, it is important to discover new natural products to inhibit high glucose damage. The protective effects and mechanisms of a novel Lentinus edodes mycelia polysaccharide (LMP) against damage induced by high glucose in MIN6 cells were explored.
Cell viability, malondialdehyde (MDA) inhibition, lactate dehydrogenase (LDH) release and the activity of superoxide dismutase (SOD) were evaluated under 40 mM glucose with or without LMP for 48 h. Cell signaling pathway analysis was performed to investigate the possible mechanisms of the protective effects of LMP in MIN6 cells.
The results showed that LMP could increase cell viability and the activity of SOD, decrease the reactive oxygen species ( ROS) production, and reduce the MDA content and LDH release in high glucose-induced MIN6 cells. Moreover, LMP prevented high glucose-induced apoptosis by decreasing the expression of Bax and the activation of caspase-1 and caspase-3. Cell signaling pathway analysis showed that p38 mitogen-activated protein kinase (MAPK) and JNK pathways were inhibited and the Nrf2 pathway was activated after treated with LMP.
The protective effects of LMP against MIN6 cells damage induced by high glucose might rely on the regulation of the MAPK and Nrf2 pathways. These results indicated that LMP had great potential as a therapeutic agent for the treatment of diabetes mellitus.</abstract><cop>Sweden</cop><pub>Open Academia</pub><pmid>31217790</pmid><doi>10.29219/fnr.v63.1598</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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title | A novel polysaccharide from Lentinus edodes mycelia protects MIN6 cells against high glucose-induced damage via the MAPKs and Nrf2 pathways |
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