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Myrciaria cauliflora extract improves diabetic nephropathy via suppression of oxidative stress and inflammation in streptozotocin-nicotinamide mice
Myrciaria cauliflora is a functional food rich in anthocyanins, possessing antioxidative and anti-inflammatory properties. Our previous results demonstrated M. cauliflora extract (MCE) had beneficial effects in diabetic nephropathy (DN) and via the inhibition of Ras/PI3K/Akt and kidney fibrosis-rela...
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Published in: | Yàowu shi͡p︡in fenxi 2016-10, Vol.24 (4), p.730-737 |
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description | Myrciaria cauliflora is a functional food rich in anthocyanins, possessing antioxidative and anti-inflammatory properties. Our previous results demonstrated M. cauliflora extract (MCE) had beneficial effects in diabetic nephropathy (DN) and via the inhibition of Ras/PI3K/Akt and kidney fibrosis-related proteins. The purpose of this study was to assess the benefit of MCE in diabetes associated with kidney inflammation and glycemic regulation in streptozotocin–nicotinamide (STZ/NA)-induced diabetic mice. Compared with the untreated diabetic group, MCE significantly improved blood glucose and serum biochemical characteristic levels. Exposure to MCE increased antioxidative enzyme activity and diminished reactive oxygen synthesis. Mice receiving MCE supplementation had reduced intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), monocyte chemoattractant protein 1 (MCP-1), colony stimulating factor 1 (CSF-1), interleukin-1β (IL-1β), IL-6 and tumor necrosis factor α (TNF-α) levels compared to the untreated diabetic mice. Inflammatory and fibrotic related proteins such as collagen IV, fibronectin, Janus kinase (JAK), phosphorylated signal transducer and activator of transcription 3 (STAT3), protein kinase C beta (PKC-β), and nuclear factor kappa B (NF-κB) were also inhibited by MCE treatment in STZ/NA mice. These results suggest that MCE may be used as a hypoglycemic agent and antioxidant in Type 2 diabetic mice.
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doi_str_mv | 10.1016/j.jfda.2016.03.009 |
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[Display omitted]</description><identifier>ISSN: 1021-9498</identifier><identifier>EISSN: 2224-6614</identifier><identifier>DOI: 10.1016/j.jfda.2016.03.009</identifier><identifier>PMID: 28911610</identifier><language>eng</language><publisher>China (Republic : 1949- ): Elsevier B.V</publisher><subject>1-Phosphatidylinositol 3-kinase ; Adhesion ; AKT protein ; Animals ; Anthocyanins ; Anti-inflammatory agents ; Antioxidants ; Cell adhesion ; Cell adhesion molecules ; Chemical synthesis ; Collagen (type IV) ; Colony-stimulating factor ; Cytokines ; Diabetes ; Diabetes mellitus ; Diabetes Mellitus, Experimental ; Diabetic Nephropathies ; Diabetic nephropathy ; Diabetic retinopathy ; Diet ; Dietary supplements ; Enzymatic activity ; Enzyme activity ; Fibronectin ; Fibrosis ; Functional foods & nutraceuticals ; Hyperglycemia ; Inflammation ; Insulin resistance ; Intercellular adhesion molecule 1 ; Interleukin 6 ; Janus kinase ; Kidney diseases ; Kidneys ; Macrophage colony-stimulating factor ; Metabolism ; Mice ; Molecular chains ; Monocyte chemoattractant protein ; Monocyte chemoattractant protein 1 ; Monocytes ; Myrciaria cauliflora ; Myrciaria cauliflora extract (MCE) ; Myrtaceae ; Nephropathy ; Niacinamide ; Nicotinamide ; Obesity ; Original ; Oxidative Stress ; Phosphatidylinositol 3-Kinases ; Phytochemicals ; Plant Extracts ; Proteins ; Rodents ; Streptozocin ; Transcription ; Tumor necrosis factor-TNF ; Urine</subject><ispartof>Yàowu shi͡p︡in fenxi, 2016-10, Vol.24 (4), p.730-737</ispartof><rights>2016</rights><rights>Copyright © 2016. Published by Elsevier B.V.</rights><rights>Copyright Elsevier Limited Oct 2016</rights><rights>2016 Taiwan Food and Drug Administration 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c483t-c029b2d12e9f59dca3d33c7011a4a66ca3fa894f89078f23237221e82fce61cf3</citedby><cites>FETCH-LOGICAL-c483t-c029b2d12e9f59dca3d33c7011a4a66ca3fa894f89078f23237221e82fce61cf3</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/PMC9337277/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1021949816300503$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,3536,27901,27902,45756,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28911610$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hsu, Jeng-Dong</creatorcontrib><creatorcontrib>Wu, Chia-Chun</creatorcontrib><creatorcontrib>Hung, Chi-Nan</creatorcontrib><creatorcontrib>Wang, Chau-Jong</creatorcontrib><creatorcontrib>Huang, Hui-Pei</creatorcontrib><title>Myrciaria cauliflora extract improves diabetic nephropathy via suppression of oxidative stress and inflammation in streptozotocin-nicotinamide mice</title><title>Yàowu shi͡p︡in fenxi</title><addtitle>J Food Drug Anal</addtitle><description>Myrciaria cauliflora is a functional food rich in anthocyanins, possessing antioxidative and anti-inflammatory properties. Our previous results demonstrated M. cauliflora extract (MCE) had beneficial effects in diabetic nephropathy (DN) and via the inhibition of Ras/PI3K/Akt and kidney fibrosis-related proteins. The purpose of this study was to assess the benefit of MCE in diabetes associated with kidney inflammation and glycemic regulation in streptozotocin–nicotinamide (STZ/NA)-induced diabetic mice. Compared with the untreated diabetic group, MCE significantly improved blood glucose and serum biochemical characteristic levels. Exposure to MCE increased antioxidative enzyme activity and diminished reactive oxygen synthesis. Mice receiving MCE supplementation had reduced intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), monocyte chemoattractant protein 1 (MCP-1), colony stimulating factor 1 (CSF-1), interleukin-1β (IL-1β), IL-6 and tumor necrosis factor α (TNF-α) levels compared to the untreated diabetic mice. Inflammatory and fibrotic related proteins such as collagen IV, fibronectin, Janus kinase (JAK), phosphorylated signal transducer and activator of transcription 3 (STAT3), protein kinase C beta (PKC-β), and nuclear factor kappa B (NF-κB) were also inhibited by MCE treatment in STZ/NA mice. These results suggest that MCE may be used as a hypoglycemic agent and antioxidant in Type 2 diabetic mice.
[Display omitted]</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>Adhesion</subject><subject>AKT protein</subject><subject>Animals</subject><subject>Anthocyanins</subject><subject>Anti-inflammatory agents</subject><subject>Antioxidants</subject><subject>Cell adhesion</subject><subject>Cell adhesion molecules</subject><subject>Chemical synthesis</subject><subject>Collagen (type IV)</subject><subject>Colony-stimulating factor</subject><subject>Cytokines</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus, Experimental</subject><subject>Diabetic Nephropathies</subject><subject>Diabetic nephropathy</subject><subject>Diabetic retinopathy</subject><subject>Diet</subject><subject>Dietary supplements</subject><subject>Enzymatic activity</subject><subject>Enzyme activity</subject><subject>Fibronectin</subject><subject>Fibrosis</subject><subject>Functional foods & nutraceuticals</subject><subject>Hyperglycemia</subject><subject>Inflammation</subject><subject>Insulin resistance</subject><subject>Intercellular adhesion molecule 1</subject><subject>Interleukin 6</subject><subject>Janus kinase</subject><subject>Kidney diseases</subject><subject>Kidneys</subject><subject>Macrophage colony-stimulating factor</subject><subject>Metabolism</subject><subject>Mice</subject><subject>Molecular chains</subject><subject>Monocyte chemoattractant protein</subject><subject>Monocyte chemoattractant protein 1</subject><subject>Monocytes</subject><subject>Myrciaria cauliflora</subject><subject>Myrciaria cauliflora extract (MCE)</subject><subject>Myrtaceae</subject><subject>Nephropathy</subject><subject>Niacinamide</subject><subject>Nicotinamide</subject><subject>Obesity</subject><subject>Original</subject><subject>Oxidative Stress</subject><subject>Phosphatidylinositol 3-Kinases</subject><subject>Phytochemicals</subject><subject>Plant Extracts</subject><subject>Proteins</subject><subject>Rodents</subject><subject>Streptozocin</subject><subject>Transcription</subject><subject>Tumor necrosis factor-TNF</subject><subject>Urine</subject><issn>1021-9498</issn><issn>2224-6614</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><recordid>eNp9UU1v1DAQjRCIbgt_gAOyxDnBH2kSSwgJVVCQirjA2fLaY3aixA62N-r2b_CH8bKlggsHazwz770Z-1XVC0YbRln3emxGZ3XDy72hoqFUPqo2nPO27jrWPq42jHJWy1YOZ9V5SiOl3aWQ_Gl1xgfJWMfopvr5-RAN6oiaGL2f0E0hagK3OWqTCc5LDCskYlFvIaMhHpZdDIvOuwNZCyntlyVCShg8CY6EW7Q64wok5WOZaG8JejfpeS71AkL_u7XkcBdyMOhrjyZk9HpGC2RGA8-qJ05PCZ7fx4vq24f3X68-1jdfrj9dvbupTTuIXBvK5ZZbxkG6S2mNFlYI01PGdKu7ruROD7J1g6T94LjgouecwcCdgY4ZJy6qtyfdZb-dwRrw5dWTWiLOOh5U0Kj-7Xjcqe9hVVIUqb4vAq_uBWL4sYeU1Rj20ZedFaetlOW0bUHxE8rEkFIE9zCBUXU0Uo3qaKQ6GqmoUMXIQnr5924PlD_OFcCbEwDKD60IUSWD4A1YjGCysgH_p_8Lw5e1Kw</recordid><startdate>20161001</startdate><enddate>20161001</enddate><creator>Hsu, 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improves diabetic nephropathy via suppression of oxidative stress and inflammation in streptozotocin-nicotinamide mice</title><author>Hsu, Jeng-Dong ; Wu, Chia-Chun ; Hung, Chi-Nan ; Wang, Chau-Jong ; Huang, Hui-Pei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c483t-c029b2d12e9f59dca3d33c7011a4a66ca3fa894f89078f23237221e82fce61cf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>Adhesion</topic><topic>AKT protein</topic><topic>Animals</topic><topic>Anthocyanins</topic><topic>Anti-inflammatory agents</topic><topic>Antioxidants</topic><topic>Cell adhesion</topic><topic>Cell adhesion molecules</topic><topic>Chemical synthesis</topic><topic>Collagen (type IV)</topic><topic>Colony-stimulating factor</topic><topic>Cytokines</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes Mellitus, Experimental</topic><topic>Diabetic Nephropathies</topic><topic>Diabetic nephropathy</topic><topic>Diabetic retinopathy</topic><topic>Diet</topic><topic>Dietary supplements</topic><topic>Enzymatic activity</topic><topic>Enzyme activity</topic><topic>Fibronectin</topic><topic>Fibrosis</topic><topic>Functional foods & nutraceuticals</topic><topic>Hyperglycemia</topic><topic>Inflammation</topic><topic>Insulin resistance</topic><topic>Intercellular adhesion molecule 1</topic><topic>Interleukin 6</topic><topic>Janus kinase</topic><topic>Kidney diseases</topic><topic>Kidneys</topic><topic>Macrophage colony-stimulating factor</topic><topic>Metabolism</topic><topic>Mice</topic><topic>Molecular chains</topic><topic>Monocyte chemoattractant protein</topic><topic>Monocyte chemoattractant protein 1</topic><topic>Monocytes</topic><topic>Myrciaria cauliflora</topic><topic>Myrciaria cauliflora extract (MCE)</topic><topic>Myrtaceae</topic><topic>Nephropathy</topic><topic>Niacinamide</topic><topic>Nicotinamide</topic><topic>Obesity</topic><topic>Original</topic><topic>Oxidative Stress</topic><topic>Phosphatidylinositol 3-Kinases</topic><topic>Phytochemicals</topic><topic>Plant Extracts</topic><topic>Proteins</topic><topic>Rodents</topic><topic>Streptozocin</topic><topic>Transcription</topic><topic>Tumor necrosis factor-TNF</topic><topic>Urine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hsu, Jeng-Dong</creatorcontrib><creatorcontrib>Wu, Chia-Chun</creatorcontrib><creatorcontrib>Hung, Chi-Nan</creatorcontrib><creatorcontrib>Wang, Chau-Jong</creatorcontrib><creatorcontrib>Huang, Hui-Pei</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE 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Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Engineering collection</collection><collection>ProQuest Central Basic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Yàowu shi͡p︡in fenxi</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hsu, Jeng-Dong</au><au>Wu, Chia-Chun</au><au>Hung, Chi-Nan</au><au>Wang, Chau-Jong</au><au>Huang, Hui-Pei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Myrciaria cauliflora extract improves diabetic nephropathy via suppression of oxidative stress and inflammation in streptozotocin-nicotinamide mice</atitle><jtitle>Yàowu shi͡p︡in fenxi</jtitle><addtitle>J Food Drug Anal</addtitle><date>2016-10-01</date><risdate>2016</risdate><volume>24</volume><issue>4</issue><spage>730</spage><epage>737</epage><pages>730-737</pages><issn>1021-9498</issn><eissn>2224-6614</eissn><abstract>Myrciaria cauliflora is a functional food rich in anthocyanins, possessing antioxidative and anti-inflammatory properties. Our previous results demonstrated M. cauliflora extract (MCE) had beneficial effects in diabetic nephropathy (DN) and via the inhibition of Ras/PI3K/Akt and kidney fibrosis-related proteins. The purpose of this study was to assess the benefit of MCE in diabetes associated with kidney inflammation and glycemic regulation in streptozotocin–nicotinamide (STZ/NA)-induced diabetic mice. Compared with the untreated diabetic group, MCE significantly improved blood glucose and serum biochemical characteristic levels. Exposure to MCE increased antioxidative enzyme activity and diminished reactive oxygen synthesis. Mice receiving MCE supplementation had reduced intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), monocyte chemoattractant protein 1 (MCP-1), colony stimulating factor 1 (CSF-1), interleukin-1β (IL-1β), IL-6 and tumor necrosis factor α (TNF-α) levels compared to the untreated diabetic mice. Inflammatory and fibrotic related proteins such as collagen IV, fibronectin, Janus kinase (JAK), phosphorylated signal transducer and activator of transcription 3 (STAT3), protein kinase C beta (PKC-β), and nuclear factor kappa B (NF-κB) were also inhibited by MCE treatment in STZ/NA mice. These results suggest that MCE may be used as a hypoglycemic agent and antioxidant in Type 2 diabetic mice.
[Display omitted]</abstract><cop>China (Republic : 1949- )</cop><pub>Elsevier B.V</pub><pmid>28911610</pmid><doi>10.1016/j.jfda.2016.03.009</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 1-Phosphatidylinositol 3-kinase Adhesion AKT protein Animals Anthocyanins Anti-inflammatory agents Antioxidants Cell adhesion Cell adhesion molecules Chemical synthesis Collagen (type IV) Colony-stimulating factor Cytokines Diabetes Diabetes mellitus Diabetes Mellitus, Experimental Diabetic Nephropathies Diabetic nephropathy Diabetic retinopathy Diet Dietary supplements Enzymatic activity Enzyme activity Fibronectin Fibrosis Functional foods & nutraceuticals Hyperglycemia Inflammation Insulin resistance Intercellular adhesion molecule 1 Interleukin 6 Janus kinase Kidney diseases Kidneys Macrophage colony-stimulating factor Metabolism Mice Molecular chains Monocyte chemoattractant protein Monocyte chemoattractant protein 1 Monocytes Myrciaria cauliflora Myrciaria cauliflora extract (MCE) Myrtaceae Nephropathy Niacinamide Nicotinamide Obesity Original Oxidative Stress Phosphatidylinositol 3-Kinases Phytochemicals Plant Extracts Proteins Rodents Streptozocin Transcription Tumor necrosis factor-TNF Urine |
title | Myrciaria cauliflora extract improves diabetic nephropathy via suppression of oxidative stress and inflammation in streptozotocin-nicotinamide mice |
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