Epigallocatechin-3-gallate Attenuates Renal Damage by Suppressing Oxidative Stress in Diabetic db/db Mice
Epigallocatechin-3-gallate (EGCG), extracted from green tea, has been shown to have antioxidative activity. In the present study, we evaluated the effect of EGCG on the kidney function in db/db mice and also tried to investigate the underlying mechanism of the renoprotective effects of EGCG in both...
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description | Epigallocatechin-3-gallate (EGCG), extracted from green tea, has been shown to have antioxidative activity. In the present study, we evaluated the effect of EGCG on the kidney function in db/db mice and also tried to investigate the underlying mechanism of the renoprotective effects of EGCG in both animals and cells. EGCG treatment could decrease the level of urinary protein, 8-iso-PGF2a, and Ang II. Moreover, EGCG could also change the level of several parameters associated with oxidative stress. In addition, the protein expression levels of AT-1R, p22-phox, p47-phox, p-ERK1/2, p-p38 MAPK, TGF-β1, and α-SMA in diabetic db/db mice were upregulated, and all of these symptoms were downregulated with the treatment of EGCG at 50 and 100 mg/kg/d. Furthermore, the pathological changes were ameliorated in db/db mice after EGCG treatment. HK-2 cell-based experiments indicated that EGCG could inhibit the expression of MAPK pathways, which is the downstream effector of Ang II mediated oxidative stress. All these results indicated that EGCG treatment could ameliorate changes of renal pathology and delay the progression of DKD by suppressing hyperglycemia-induced oxidative stress in diabetic db/db mice. |
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In the present study, we evaluated the effect of EGCG on the kidney function in db/db mice and also tried to investigate the underlying mechanism of the renoprotective effects of EGCG in both animals and cells. EGCG treatment could decrease the level of urinary protein, 8-iso-PGF2a, and Ang II. Moreover, EGCG could also change the level of several parameters associated with oxidative stress. In addition, the protein expression levels of AT-1R, p22-phox, p47-phox, p-ERK1/2, p-p38 MAPK, TGF-β1, and α-SMA in diabetic db/db mice were upregulated, and all of these symptoms were downregulated with the treatment of EGCG at 50 and 100 mg/kg/d. Furthermore, the pathological changes were ameliorated in db/db mice after EGCG treatment. HK-2 cell-based experiments indicated that EGCG could inhibit the expression of MAPK pathways, which is the downstream effector of Ang II mediated oxidative stress. All these results indicated that EGCG treatment could ameliorate changes of renal pathology and delay the progression of DKD by suppressing hyperglycemia-induced oxidative stress in diabetic db/db mice.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2016/2968462</identifier><identifier>PMID: 27698952</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Animals ; Bone morphogenetic proteins ; Catechin ; Catechin - analogs & derivatives ; Catechin - metabolism ; Cytokines ; Diabetes ; Diabetes Insipidus, Nephrogenic - metabolism ; Diabetes Insipidus, Nephrogenic - pathology ; Disease Models, Animal ; Fasting ; Glucose ; Green tea ; Hospitals ; Kidney - pathology ; Kinases ; Metabolism ; Mice ; Mice, Inbred C57BL ; Nephrology ; Oxidative Stress ; Proteins ; Rodents ; Science ; Studies ; Transforming growth factors ; Urine</subject><ispartof>Oxidative medicine and cellular longevity, 2016-01, Vol.2016 (2016), p.1-14</ispartof><rights>Copyright © 2016 Xiu Hong Yang et al.</rights><rights>COPYRIGHT 2016 John Wiley & Sons, Inc.</rights><rights>Copyright © 2016 Xiu Hong Yang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2016 Xiu Hong Yang et al. 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c565t-b8c1ac62cdaea0e9a4679a5bac67598e0f0547d4dbbae16128dec1f80478d1e93</citedby><cites>FETCH-LOGICAL-c565t-b8c1ac62cdaea0e9a4679a5bac67598e0f0547d4dbbae16128dec1f80478d1e93</cites><orcidid>0000-0003-4255-4901 ; 0000-0001-9290-1401</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5028863/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5028863/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27698952$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Cabello-Verrugio, Claudio</contributor><creatorcontrib>Guo, Li Li</creatorcontrib><creatorcontrib>Zhang, Bao Long</creatorcontrib><creatorcontrib>Zhan, Xiao Li</creatorcontrib><creatorcontrib>Pan, Yu</creatorcontrib><creatorcontrib>Yang, Xiu Hong</creatorcontrib><creatorcontrib>Jin, Hui Min</creatorcontrib><title>Epigallocatechin-3-gallate Attenuates Renal Damage by Suppressing Oxidative Stress in Diabetic db/db Mice</title><title>Oxidative medicine and cellular longevity</title><addtitle>Oxid Med Cell Longev</addtitle><description>Epigallocatechin-3-gallate (EGCG), extracted from green tea, has been shown to have antioxidative activity. In the present study, we evaluated the effect of EGCG on the kidney function in db/db mice and also tried to investigate the underlying mechanism of the renoprotective effects of EGCG in both animals and cells. EGCG treatment could decrease the level of urinary protein, 8-iso-PGF2a, and Ang II. Moreover, EGCG could also change the level of several parameters associated with oxidative stress. In addition, the protein expression levels of AT-1R, p22-phox, p47-phox, p-ERK1/2, p-p38 MAPK, TGF-β1, and α-SMA in diabetic db/db mice were upregulated, and all of these symptoms were downregulated with the treatment of EGCG at 50 and 100 mg/kg/d. Furthermore, the pathological changes were ameliorated in db/db mice after EGCG treatment. HK-2 cell-based experiments indicated that EGCG could inhibit the expression of MAPK pathways, which is the downstream effector of Ang II mediated oxidative stress. All these results indicated that EGCG treatment could ameliorate changes of renal pathology and delay the progression of DKD by suppressing hyperglycemia-induced oxidative stress in diabetic db/db mice.</description><subject>Animals</subject><subject>Bone morphogenetic proteins</subject><subject>Catechin</subject><subject>Catechin - analogs & derivatives</subject><subject>Catechin - metabolism</subject><subject>Cytokines</subject><subject>Diabetes</subject><subject>Diabetes Insipidus, Nephrogenic - metabolism</subject><subject>Diabetes Insipidus, Nephrogenic - pathology</subject><subject>Disease Models, Animal</subject><subject>Fasting</subject><subject>Glucose</subject><subject>Green tea</subject><subject>Hospitals</subject><subject>Kidney - pathology</subject><subject>Kinases</subject><subject>Metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Nephrology</subject><subject>Oxidative Stress</subject><subject>Proteins</subject><subject>Rodents</subject><subject>Science</subject><subject>Studies</subject><subject>Transforming growth factors</subject><subject>Urine</subject><issn>1942-0900</issn><issn>1942-0994</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqNkc1v1DAQxSMEoqVw44wscUGCsP6OfUFateVDKqpE4WxN7MnWVTYJcVLof4-jXbbAiZNnxj-9sd8riueMvmVMqRWnTK-41UZq_qA4ZlbyklorHx5qSo-KJyndUKoFl-xxccQrbY1V_LiI50PcQNv2Hib017ErRbn0uSPracJuzlUiX7CDlpzBFjZI6jtyNQ_DiCnFbkMuf8YAU7xFcjUtMxI7chahxil6EupVqMnn6PFp8aiBNuGz_XlSfHt__vX0Y3lx-eHT6fqi9EqrqayNZ-A19wEQKFqQurKg6jyrlDVIG6pkFWSoa0CmGTcBPWsMlZUJDK04Kd7tdIe53mLw2E0jtG4Y4xbGO9dDdH_fdPHabfpbpyg3Ross8GovMPbfZ0yT28bkMXvSYT8nx4xQQmuraUZf_oPe9POYrVooTjXXXIp7KhuLLnZNn_f6RdStFVOML3KZerOj_NinNGJzeDKjbknaLUm7fdIZf_HnNw_w72gz8HoH5FAD_Ij_KYeZwQbuacZENl78AugRuns</recordid><startdate>20160101</startdate><enddate>20160101</enddate><creator>Guo, Li Li</creator><creator>Zhang, Bao Long</creator><creator>Zhan, Xiao Li</creator><creator>Pan, Yu</creator><creator>Yang, Xiu Hong</creator><creator>Jin, Hui Min</creator><general>Hindawi Publishing Corporation</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><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>8G5</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>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-4255-4901</orcidid><orcidid>https://orcid.org/0000-0001-9290-1401</orcidid></search><sort><creationdate>20160101</creationdate><title>Epigallocatechin-3-gallate Attenuates Renal Damage by Suppressing Oxidative Stress in Diabetic db/db Mice</title><author>Guo, Li Li ; 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In the present study, we evaluated the effect of EGCG on the kidney function in db/db mice and also tried to investigate the underlying mechanism of the renoprotective effects of EGCG in both animals and cells. EGCG treatment could decrease the level of urinary protein, 8-iso-PGF2a, and Ang II. Moreover, EGCG could also change the level of several parameters associated with oxidative stress. In addition, the protein expression levels of AT-1R, p22-phox, p47-phox, p-ERK1/2, p-p38 MAPK, TGF-β1, and α-SMA in diabetic db/db mice were upregulated, and all of these symptoms were downregulated with the treatment of EGCG at 50 and 100 mg/kg/d. Furthermore, the pathological changes were ameliorated in db/db mice after EGCG treatment. HK-2 cell-based experiments indicated that EGCG could inhibit the expression of MAPK pathways, which is the downstream effector of Ang II mediated oxidative stress. All these results indicated that EGCG treatment could ameliorate changes of renal pathology and delay the progression of DKD by suppressing hyperglycemia-induced oxidative stress in diabetic db/db mice.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>27698952</pmid><doi>10.1155/2016/2968462</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0003-4255-4901</orcidid><orcidid>https://orcid.org/0000-0001-9290-1401</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Animals Bone morphogenetic proteins Catechin Catechin - analogs & derivatives Catechin - metabolism Cytokines Diabetes Diabetes Insipidus, Nephrogenic - metabolism Diabetes Insipidus, Nephrogenic - pathology Disease Models, Animal Fasting Glucose Green tea Hospitals Kidney - pathology Kinases Metabolism Mice Mice, Inbred C57BL Nephrology Oxidative Stress Proteins Rodents Science Studies Transforming growth factors Urine |
title | Epigallocatechin-3-gallate Attenuates Renal Damage by Suppressing Oxidative Stress in Diabetic db/db Mice |
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