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3'- O -β-d-glucopyranosyl-α,4,2',4',6'-pentahydroxy-dihydrochalcone, from Bark of Eysenhardtia polystachya Prevents Diabetic Nephropathy via Inhibiting Protein Glycation in STZ-Nicotinamide Induced Diabetic Mice
Previous studies have shown that accumulation of advanced glycation end products (AGEs) can be the cause of diabetic nephropathy (DN) in diabetic patients. Dihydrochalcone 3'- -β-d-glucopyranosyl α,4,2',4',6'-pentahydroxy⁻dihydrochalcone ( ) is a powerful antiglycation compound p...
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| Published in: | Molecules (Basel, Switzerland) Switzerland), 2019-03, Vol.24 (7), p.1214 |
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| creator | Pérez Gutierrez, Rosa Martha García Campoy, Abraham Heriberto Paredes Carrera, Silvia Patricia Muñiz Ramirez, Alethia Mota Flores, José Maria Flores Valle, Sergio Odin |
| description | Previous studies have shown that accumulation of advanced glycation end products (AGEs) can be the cause of diabetic nephropathy (DN) in diabetic patients. Dihydrochalcone 3'-
-β-d-glucopyranosyl α,4,2',4',6'-pentahydroxy⁻dihydrochalcone (
) is a powerful antiglycation compound previously isolated from
. The aim was to investigate whether (
) was able to protect against diabetic nephropathy in streptozotocin (STZ)-induced diabetic mice, which displayed renal dysfunction markers such as body weight, creatinine, uric acid, serum urea, total urinary protein, and urea nitrogen in the blood (BUN). In addition, pathological changes were evaluated including glycated hemoglobin (HbA1c), advanced glycation end products (AGEs) in the kidney, as well as in circulation level and pro-inflammatory markers ICAM-1 levels in diabetic mice. After 5 weeks, these elevated markers of dihydrochalcone treatment (25, 50 and 100 mg/kg) were significantly (
< 0.05) attenuated. In addition, they ameliorate the indices of renal inflammation as indicated by ICAM-1 markers. The kidney and circulatory AGEs levels in diabetic mice were significantly (
< 0.05) attenuated by (
) treatment. Histological analysis of kidney tissues showed an important recovery in its structure compared with the diabetic group. It was found that the compound (
) attenuated the renal damage in diabetic mice by inhibiting AGEs formation. |
| doi_str_mv | 10.3390/molecules24071214 |
| format | article |
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-β-d-glucopyranosyl α,4,2',4',6'-pentahydroxy⁻dihydrochalcone (
) is a powerful antiglycation compound previously isolated from
. The aim was to investigate whether (
) was able to protect against diabetic nephropathy in streptozotocin (STZ)-induced diabetic mice, which displayed renal dysfunction markers such as body weight, creatinine, uric acid, serum urea, total urinary protein, and urea nitrogen in the blood (BUN). In addition, pathological changes were evaluated including glycated hemoglobin (HbA1c), advanced glycation end products (AGEs) in the kidney, as well as in circulation level and pro-inflammatory markers ICAM-1 levels in diabetic mice. After 5 weeks, these elevated markers of dihydrochalcone treatment (25, 50 and 100 mg/kg) were significantly (
< 0.05) attenuated. In addition, they ameliorate the indices of renal inflammation as indicated by ICAM-1 markers. The kidney and circulatory AGEs levels in diabetic mice were significantly (
< 0.05) attenuated by (
) treatment. Histological analysis of kidney tissues showed an important recovery in its structure compared with the diabetic group. It was found that the compound (
) attenuated the renal damage in diabetic mice by inhibiting AGEs formation.</description><identifier>ISSN: 1420-3049</identifier><identifier>EISSN: 1420-3049</identifier><identifier>DOI: 10.3390/molecules24071214</identifier><identifier>PMID: 30925713</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>advanced glycation end-product ; Advanced glycosylation end products ; Animals ; Attenuation ; Bark ; Biomarkers - metabolism ; Body weight ; Body Weight - drug effects ; Chalcones - chemical synthesis ; Chalcones - chemistry ; Chalcones - pharmacology ; Chalcones - therapeutic use ; Creatinine ; Creatinine - blood ; Diabetes ; Diabetes mellitus ; Diabetes Mellitus, Experimental - blood ; Diabetes Mellitus, Experimental - drug therapy ; diabetic mice ; Diabetic Nephropathies - blood ; Diabetic Nephropathies - drug therapy ; Diabetic Nephropathies - pathology ; Diabetic nephropathy ; dihydrochalcone ; Drinking ; Eysenhardtia polystachya ; Fabaceae - chemistry ; Feeding Behavior ; Food ; Glucose ; Glucose - metabolism ; Glycated Hemoglobin A - metabolism ; Glycation End Products, Advanced - blood ; Glycosylation ; Hemoglobin ; Hyperglycemia ; Inflammation ; Inflammation Mediators - metabolism ; Intercellular adhesion molecule 1 ; Kidney - drug effects ; Kidney - pathology ; Kidneys ; Male ; Markers ; Mice, Inbred C57BL ; Nephropathy ; Niacinamide ; Nicotinamide ; Nitrogen ; Organ Size - drug effects ; Oxidative stress ; Plant Bark - chemistry ; Proteins ; Rats ; Renal function ; renoprotective ; Streptozocin ; Tissue analysis ; Urea ; Urea - blood ; Uric acid ; Uric Acid - blood ; Urine</subject><ispartof>Molecules (Basel, Switzerland), 2019-03, Vol.24 (7), p.1214</ispartof><rights>2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2019 by the authors. 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c563t-f5b89698d8b6f9997926e8344ed45402c813c2e3eb526ef3d3fea17f51989b7c3</citedby><cites>FETCH-LOGICAL-c563t-f5b89698d8b6f9997926e8344ed45402c813c2e3eb526ef3d3fea17f51989b7c3</cites><orcidid>0000-0002-5499-9169 ; 0000-0002-5441-3690</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2548949598/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2548949598?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,74998</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30925713$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pérez Gutierrez, Rosa Martha</creatorcontrib><creatorcontrib>García Campoy, Abraham Heriberto</creatorcontrib><creatorcontrib>Paredes Carrera, Silvia Patricia</creatorcontrib><creatorcontrib>Muñiz Ramirez, Alethia</creatorcontrib><creatorcontrib>Mota Flores, José Maria</creatorcontrib><creatorcontrib>Flores Valle, Sergio Odin</creatorcontrib><title>3'- O -β-d-glucopyranosyl-α,4,2',4',6'-pentahydroxy-dihydrochalcone, from Bark of Eysenhardtia polystachya Prevents Diabetic Nephropathy via Inhibiting Protein Glycation in STZ-Nicotinamide Induced Diabetic Mice</title><title>Molecules (Basel, Switzerland)</title><addtitle>Molecules</addtitle><description>Previous studies have shown that accumulation of advanced glycation end products (AGEs) can be the cause of diabetic nephropathy (DN) in diabetic patients. Dihydrochalcone 3'-
-β-d-glucopyranosyl α,4,2',4',6'-pentahydroxy⁻dihydrochalcone (
) is a powerful antiglycation compound previously isolated from
. The aim was to investigate whether (
) was able to protect against diabetic nephropathy in streptozotocin (STZ)-induced diabetic mice, which displayed renal dysfunction markers such as body weight, creatinine, uric acid, serum urea, total urinary protein, and urea nitrogen in the blood (BUN). In addition, pathological changes were evaluated including glycated hemoglobin (HbA1c), advanced glycation end products (AGEs) in the kidney, as well as in circulation level and pro-inflammatory markers ICAM-1 levels in diabetic mice. After 5 weeks, these elevated markers of dihydrochalcone treatment (25, 50 and 100 mg/kg) were significantly (
< 0.05) attenuated. In addition, they ameliorate the indices of renal inflammation as indicated by ICAM-1 markers. The kidney and circulatory AGEs levels in diabetic mice were significantly (
< 0.05) attenuated by (
) treatment. Histological analysis of kidney tissues showed an important recovery in its structure compared with the diabetic group. It was found that the compound (
) attenuated the renal damage in diabetic mice by inhibiting AGEs formation.</description><subject>advanced glycation end-product</subject><subject>Advanced glycosylation end products</subject><subject>Animals</subject><subject>Attenuation</subject><subject>Bark</subject><subject>Biomarkers - metabolism</subject><subject>Body weight</subject><subject>Body Weight - drug effects</subject><subject>Chalcones - chemical synthesis</subject><subject>Chalcones - chemistry</subject><subject>Chalcones - pharmacology</subject><subject>Chalcones - therapeutic use</subject><subject>Creatinine</subject><subject>Creatinine - blood</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus, Experimental - blood</subject><subject>Diabetes Mellitus, Experimental - drug therapy</subject><subject>diabetic mice</subject><subject>Diabetic Nephropathies - blood</subject><subject>Diabetic Nephropathies - drug therapy</subject><subject>Diabetic Nephropathies - pathology</subject><subject>Diabetic nephropathy</subject><subject>dihydrochalcone</subject><subject>Drinking</subject><subject>Eysenhardtia polystachya</subject><subject>Fabaceae - chemistry</subject><subject>Feeding Behavior</subject><subject>Food</subject><subject>Glucose</subject><subject>Glucose - metabolism</subject><subject>Glycated Hemoglobin A - metabolism</subject><subject>Glycation End Products, Advanced - blood</subject><subject>Glycosylation</subject><subject>Hemoglobin</subject><subject>Hyperglycemia</subject><subject>Inflammation</subject><subject>Inflammation Mediators - metabolism</subject><subject>Intercellular adhesion molecule 1</subject><subject>Kidney - drug effects</subject><subject>Kidney - pathology</subject><subject>Kidneys</subject><subject>Male</subject><subject>Markers</subject><subject>Mice, Inbred C57BL</subject><subject>Nephropathy</subject><subject>Niacinamide</subject><subject>Nicotinamide</subject><subject>Nitrogen</subject><subject>Organ Size - drug effects</subject><subject>Oxidative stress</subject><subject>Plant Bark - chemistry</subject><subject>Proteins</subject><subject>Rats</subject><subject>Renal function</subject><subject>renoprotective</subject><subject>Streptozocin</subject><subject>Tissue analysis</subject><subject>Urea</subject><subject>Urea - blood</subject><subject>Uric acid</subject><subject>Uric Acid - blood</subject><subject>Urine</subject><issn>1420-3049</issn><issn>1420-3049</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNplks1u1DAQgCMEoqXwAFyQJQ7LYQ2O7fz4ggSllJVKi0S5cIkce7zxksTBTlbkseBBeuN9MN1SWjh57Pnm03g0SfI4Jc8ZE-RF51pQUwuBclKkNOV3kv2UU4IZ4eLujXgveRDChpCIpNn9ZI8RQbMiZfvJT7bA6Azhix9Y43U7KTfMXvYuzC2--L7kS7pY8sUyX-AB-lE2s_bu24y1vYxUI1vlelgi412HXkv_BTmDjuYAfSO9Hq1Eg2vnMErVzBJ98LCNmoDeWFnDaBU6haHxbpBjM6NtpFd9Y2s72n4dYTeC7dFxOys5WtejePl4_hmfWuUiITurIRboSYH-a3xvFTxM7hnZBnh0dR4kn94enR--wydnx6vDVydYZTkbscnqUuSi1GWdGyFEIWgOJeMcNM84oapMmaLAoM5iwjDNDMi0MFkqSlEXih0kq51XO7mpBm876efKSVtdPji_rqSPTbVQCWJYYUqaF1EtQZWFNLkxutBABKMiul7uXMNUd6BVnJOX7S3p7Uxvm2rttlXOS5ITEgXPrgTefZ0gjFVng4K2lT24KVSUElKUGeMsok__QTdu8n0cVUUzXgouMlFGKt1RyrsQPJjrZlJS_V7A6r8FjDVPbv7iuuLPxrFfle7dJg</recordid><startdate>20190328</startdate><enddate>20190328</enddate><creator>Pérez Gutierrez, Rosa Martha</creator><creator>García Campoy, Abraham Heriberto</creator><creator>Paredes Carrera, Silvia Patricia</creator><creator>Muñiz Ramirez, Alethia</creator><creator>Mota Flores, José Maria</creator><creator>Flores Valle, Sergio Odin</creator><general>MDPI AG</general><general>MDPI</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-5499-9169</orcidid><orcidid>https://orcid.org/0000-0002-5441-3690</orcidid></search><sort><creationdate>20190328</creationdate><title>3'- O -β-d-glucopyranosyl-α,4,2',4',6'-pentahydroxy-dihydrochalcone, from Bark of Eysenhardtia polystachya Prevents Diabetic Nephropathy via Inhibiting Protein Glycation in STZ-Nicotinamide Induced Diabetic Mice</title><author>Pérez Gutierrez, Rosa Martha ; García Campoy, Abraham Heriberto ; Paredes Carrera, Silvia Patricia ; Muñiz Ramirez, Alethia ; Mota Flores, José Maria ; Flores Valle, Sergio Odin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c563t-f5b89698d8b6f9997926e8344ed45402c813c2e3eb526ef3d3fea17f51989b7c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>advanced glycation end-product</topic><topic>Advanced glycosylation end products</topic><topic>Animals</topic><topic>Attenuation</topic><topic>Bark</topic><topic>Biomarkers - metabolism</topic><topic>Body weight</topic><topic>Body Weight - drug effects</topic><topic>Chalcones - chemical synthesis</topic><topic>Chalcones - chemistry</topic><topic>Chalcones - pharmacology</topic><topic>Chalcones - therapeutic use</topic><topic>Creatinine</topic><topic>Creatinine - blood</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes Mellitus, Experimental - blood</topic><topic>Diabetes Mellitus, Experimental - drug therapy</topic><topic>diabetic mice</topic><topic>Diabetic Nephropathies - blood</topic><topic>Diabetic Nephropathies - drug therapy</topic><topic>Diabetic Nephropathies - pathology</topic><topic>Diabetic nephropathy</topic><topic>dihydrochalcone</topic><topic>Drinking</topic><topic>Eysenhardtia polystachya</topic><topic>Fabaceae - chemistry</topic><topic>Feeding Behavior</topic><topic>Food</topic><topic>Glucose</topic><topic>Glucose - metabolism</topic><topic>Glycated Hemoglobin A - metabolism</topic><topic>Glycation End Products, Advanced - blood</topic><topic>Glycosylation</topic><topic>Hemoglobin</topic><topic>Hyperglycemia</topic><topic>Inflammation</topic><topic>Inflammation Mediators - metabolism</topic><topic>Intercellular adhesion molecule 1</topic><topic>Kidney - drug effects</topic><topic>Kidney - pathology</topic><topic>Kidneys</topic><topic>Male</topic><topic>Markers</topic><topic>Mice, Inbred C57BL</topic><topic>Nephropathy</topic><topic>Niacinamide</topic><topic>Nicotinamide</topic><topic>Nitrogen</topic><topic>Organ Size - drug effects</topic><topic>Oxidative stress</topic><topic>Plant Bark - chemistry</topic><topic>Proteins</topic><topic>Rats</topic><topic>Renal function</topic><topic>renoprotective</topic><topic>Streptozocin</topic><topic>Tissue analysis</topic><topic>Urea</topic><topic>Urea - blood</topic><topic>Uric acid</topic><topic>Uric Acid - blood</topic><topic>Urine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pérez Gutierrez, Rosa Martha</creatorcontrib><creatorcontrib>García Campoy, Abraham Heriberto</creatorcontrib><creatorcontrib>Paredes Carrera, Silvia Patricia</creatorcontrib><creatorcontrib>Muñiz Ramirez, Alethia</creatorcontrib><creatorcontrib>Mota Flores, José Maria</creatorcontrib><creatorcontrib>Flores Valle, Sergio Odin</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Proquest Health & Medical Complete</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Molecules (Basel, Switzerland)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pérez Gutierrez, Rosa Martha</au><au>García Campoy, Abraham Heriberto</au><au>Paredes Carrera, Silvia Patricia</au><au>Muñiz Ramirez, Alethia</au><au>Mota Flores, José Maria</au><au>Flores Valle, Sergio Odin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>3'- O -β-d-glucopyranosyl-α,4,2',4',6'-pentahydroxy-dihydrochalcone, from Bark of Eysenhardtia polystachya Prevents Diabetic Nephropathy via Inhibiting Protein Glycation in STZ-Nicotinamide Induced Diabetic Mice</atitle><jtitle>Molecules (Basel, Switzerland)</jtitle><addtitle>Molecules</addtitle><date>2019-03-28</date><risdate>2019</risdate><volume>24</volume><issue>7</issue><spage>1214</spage><pages>1214-</pages><issn>1420-3049</issn><eissn>1420-3049</eissn><abstract>Previous studies have shown that accumulation of advanced glycation end products (AGEs) can be the cause of diabetic nephropathy (DN) in diabetic patients. Dihydrochalcone 3'-
-β-d-glucopyranosyl α,4,2',4',6'-pentahydroxy⁻dihydrochalcone (
) is a powerful antiglycation compound previously isolated from
. The aim was to investigate whether (
) was able to protect against diabetic nephropathy in streptozotocin (STZ)-induced diabetic mice, which displayed renal dysfunction markers such as body weight, creatinine, uric acid, serum urea, total urinary protein, and urea nitrogen in the blood (BUN). In addition, pathological changes were evaluated including glycated hemoglobin (HbA1c), advanced glycation end products (AGEs) in the kidney, as well as in circulation level and pro-inflammatory markers ICAM-1 levels in diabetic mice. After 5 weeks, these elevated markers of dihydrochalcone treatment (25, 50 and 100 mg/kg) were significantly (
< 0.05) attenuated. In addition, they ameliorate the indices of renal inflammation as indicated by ICAM-1 markers. The kidney and circulatory AGEs levels in diabetic mice were significantly (
< 0.05) attenuated by (
) treatment. Histological analysis of kidney tissues showed an important recovery in its structure compared with the diabetic group. It was found that the compound (
) attenuated the renal damage in diabetic mice by inhibiting AGEs formation.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>30925713</pmid><doi>10.3390/molecules24071214</doi><orcidid>https://orcid.org/0000-0002-5499-9169</orcidid><orcidid>https://orcid.org/0000-0002-5441-3690</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1420-3049 |
| ispartof | Molecules (Basel, Switzerland), 2019-03, Vol.24 (7), p.1214 |
| issn | 1420-3049 1420-3049 |
| language | eng |
| recordid | cdi_doaj_primary_oai_doaj_org_article_90f37f8267454aec87af6ffd7de09329 |
| source | Publicly Available Content Database; PubMed Central |
| subjects | advanced glycation end-product Advanced glycosylation end products Animals Attenuation Bark Biomarkers - metabolism Body weight Body Weight - drug effects Chalcones - chemical synthesis Chalcones - chemistry Chalcones - pharmacology Chalcones - therapeutic use Creatinine Creatinine - blood Diabetes Diabetes mellitus Diabetes Mellitus, Experimental - blood Diabetes Mellitus, Experimental - drug therapy diabetic mice Diabetic Nephropathies - blood Diabetic Nephropathies - drug therapy Diabetic Nephropathies - pathology Diabetic nephropathy dihydrochalcone Drinking Eysenhardtia polystachya Fabaceae - chemistry Feeding Behavior Food Glucose Glucose - metabolism Glycated Hemoglobin A - metabolism Glycation End Products, Advanced - blood Glycosylation Hemoglobin Hyperglycemia Inflammation Inflammation Mediators - metabolism Intercellular adhesion molecule 1 Kidney - drug effects Kidney - pathology Kidneys Male Markers Mice, Inbred C57BL Nephropathy Niacinamide Nicotinamide Nitrogen Organ Size - drug effects Oxidative stress Plant Bark - chemistry Proteins Rats Renal function renoprotective Streptozocin Tissue analysis Urea Urea - blood Uric acid Uric Acid - blood Urine |
| title | 3'- O -β-d-glucopyranosyl-α,4,2',4',6'-pentahydroxy-dihydrochalcone, from Bark of Eysenhardtia polystachya Prevents Diabetic Nephropathy via Inhibiting Protein Glycation in STZ-Nicotinamide Induced Diabetic Mice |
| url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-07T21%3A53%3A43IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_doaj_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=3'-%20O%20-%CE%B2-d-glucopyranosyl-%CE%B1,4,2',4',6'-pentahydroxy-dihydrochalcone,%20from%20Bark%20of%20Eysenhardtia%20polystachya%20Prevents%20Diabetic%20Nephropathy%20via%20Inhibiting%20Protein%20Glycation%20in%20STZ-Nicotinamide%20Induced%20Diabetic%20Mice&rft.jtitle=Molecules%20(Basel,%20Switzerland)&rft.au=P%C3%A9rez%20Gutierrez,%20Rosa%20Martha&rft.date=2019-03-28&rft.volume=24&rft.issue=7&rft.spage=1214&rft.pages=1214-&rft.issn=1420-3049&rft.eissn=1420-3049&rft_id=info:doi/10.3390/molecules24071214&rft_dat=%3Cproquest_doaj_%3E2548949598%3C/proquest_doaj_%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c563t-f5b89698d8b6f9997926e8344ed45402c813c2e3eb526ef3d3fea17f51989b7c3%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=2548949598&rft_id=info:pmid/30925713&rfr_iscdi=true |