Protective Effects of Two Safflower Derived Compounds, Kaempferol and Hydroxysafflor Yellow A, on Hyperglycaemic Stress-Induced Podocyte Apoptosis via Modulating of Macrophage M1/M2 Polarization
Objective. The primary initiating mechanism in diabetes nephropathy (DN) is hyperglycemia-induced inflammation in which macrophage and podocyte play important roles. The present research is aimed at exploring the effects of kaempferol (Ka) and hydroxysafflor yellow A (HSYA) on classically activated...
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description | Objective. The primary initiating mechanism in diabetes nephropathy (DN) is hyperglycemia-induced inflammation in which macrophage and podocyte play important roles. The present research is aimed at exploring the effects of kaempferol (Ka) and hydroxysafflor yellow A (HSYA) on classically activated (M1)/alternatively activated (M2) macrophage polarization and podocyte apoptosis under hyperglycaemic conditions in vitro. Methods. (1) RAW264.7 cells were treated with 11.1 mM glucose (NG), 33.3 mM glucose (HG), Ka 4–8 μM, and HSYA 100–200 μM separately. The expressions of inducible nitric oxide synthase (iNOS), tumor necrosis factor- (TNF-) α, mannose receptor (CD206), and arginase- (Arg-) 1 were quantified by Western blotting and real-time quantitative PCR. The collected supernatants from macrophage were named as (NG) MS, (HG) MS, (Ka) MS, and (HSYA) MS. (2) The podocyte survival rate was assessed by Bromodeoxyuridine assay, while TNF-α and interleukin- (IL-) 1β levels were evaluated by Elisa. Results. (1) Compared to the HG group, the Ka and HSYA 100 μM groups decreased iNOS and TNF-α levels and increased Arg-1 and CD206 expressions significantly (protein and mRNA: p |
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The primary initiating mechanism in diabetes nephropathy (DN) is hyperglycemia-induced inflammation in which macrophage and podocyte play important roles. The present research is aimed at exploring the effects of kaempferol (Ka) and hydroxysafflor yellow A (HSYA) on classically activated (M1)/alternatively activated (M2) macrophage polarization and podocyte apoptosis under hyperglycaemic conditions in vitro. Methods. (1) RAW264.7 cells were treated with 11.1 mM glucose (NG), 33.3 mM glucose (HG), Ka 4–8 μM, and HSYA 100–200 μM separately. The expressions of inducible nitric oxide synthase (iNOS), tumor necrosis factor- (TNF-) α, mannose receptor (CD206), and arginase- (Arg-) 1 were quantified by Western blotting and real-time quantitative PCR. The collected supernatants from macrophage were named as (NG) MS, (HG) MS, (Ka) MS, and (HSYA) MS. (2) The podocyte survival rate was assessed by Bromodeoxyuridine assay, while TNF-α and interleukin- (IL-) 1β levels were evaluated by Elisa. Results. (1) Compared to the HG group, the Ka and HSYA 100 μM groups decreased iNOS and TNF-α levels and increased Arg-1 and CD206 expressions significantly (protein and mRNA: p<0.05, respectively). (2) The podocyte survival rate of Ka 8 μM was higher than that of HG, and the rates of (Ka) MS and (HSYA 100 μM) MS were higher than that of (HG) MS significantly (all: p<0.05). (3) TNF-α and IL-1β levels of Ka and HSYA 100 μM were significantly lower than those of the HG group, and both levels in the (Ka) MS and (HSYA) MS were lower than those in the (HG) MS group significantly (p<0.05, respectively). Conclusion. The protective effects of Ka and HSYA on podocyte apoptosis under hyperglycemic stress are related to their modulation on M1/M2 polarization and the lowering effects on TNF-α and IL-1β levels.</description><identifier>ISSN: 2314-8861</identifier><identifier>EISSN: 2314-7156</identifier><identifier>DOI: 10.1155/2020/2462039</identifier><identifier>PMID: 33102606</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Animals ; Antibodies ; Apoptosis ; Arginase ; Bromodeoxyuridine ; Carthamus tinctorius - immunology ; Cell Differentiation ; Cells, Cultured ; Chalcone - analogs & derivatives ; Chalcone - therapeutic use ; Chinese medicine ; Cytokines - metabolism ; Dextrose ; Diabetes ; Diabetes mellitus ; Glucose ; Humans ; Hyperglycemia ; Hyperglycemia - drug therapy ; IL-1β ; Immunology ; Immunomodulation ; Inflammation ; Instrument industry ; Interleukins ; Kaempferol ; Kaempferols - therapeutic use ; Laboratories ; Life Sciences & Biomedicine ; Macrophages ; Macrophages - immunology ; Mannose ; Membranes ; Mice ; mRNA ; Nephropathy ; Nitric oxide ; Nitric-oxide synthase ; Podocytes - physiology ; Polarization ; Proteins ; Quinones - therapeutic use ; RAW 264.7 Cells ; RNA ; Science & Technology ; Stress, Physiological ; Th1 Cells - immunology ; Th2 Cells - immunology ; Tumor necrosis factor ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α ; Western blotting</subject><ispartof>Journal of Immunology Research, 2020-10, Vol.2020 (2020), p.1-11, Article 2462039</ispartof><rights>Copyright © 2020 Yuanping Li et al.</rights><rights>COPYRIGHT 2020 John Wiley & Sons, Inc.</rights><rights>Copyright © 2020 Yuanping Li et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2020 Yuanping Li et al. 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>true</woscitedreferencessubscribed><woscitedreferencescount>18</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wos000582216100001</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c635t-f8464c06a6103fc86e5ef443cff4856e02a806891e5c49dd658bbc119baf60b83</citedby><cites>FETCH-LOGICAL-c635t-f8464c06a6103fc86e5ef443cff4856e02a806891e5c49dd658bbc119baf60b83</cites><orcidid>0000-0002-3631-4015 ; 0000-0002-6940-0788 ; 0000-0001-8095-811X ; 0000-0001-6325-062X ; 0000-0003-2667-1809 ; 0000-0002-5692-5729</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/PMC7569436/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7569436/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,878,886,2103,2115,27929,27930,28253,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33102606$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Wang, Kai</contributor><contributor>Kai Wang</contributor><creatorcontrib>Zhao, Xiaoyun</creatorcontrib><creatorcontrib>Zhang, Xilan</creatorcontrib><creatorcontrib>Shen, Dayue</creatorcontrib><creatorcontrib>Zheng, Dan</creatorcontrib><creatorcontrib>Li, Yuanping</creatorcontrib><creatorcontrib>Liao, Hui</creatorcontrib><title>Protective Effects of Two Safflower Derived Compounds, Kaempferol and Hydroxysafflor Yellow A, on Hyperglycaemic Stress-Induced Podocyte Apoptosis via Modulating of Macrophage M1/M2 Polarization</title><title>Journal of Immunology Research</title><addtitle>J IMMUNOL RES</addtitle><addtitle>J Immunol Res</addtitle><description>Objective. The primary initiating mechanism in diabetes nephropathy (DN) is hyperglycemia-induced inflammation in which macrophage and podocyte play important roles. The present research is aimed at exploring the effects of kaempferol (Ka) and hydroxysafflor yellow A (HSYA) on classically activated (M1)/alternatively activated (M2) macrophage polarization and podocyte apoptosis under hyperglycaemic conditions in vitro. Methods. (1) RAW264.7 cells were treated with 11.1 mM glucose (NG), 33.3 mM glucose (HG), Ka 4–8 μM, and HSYA 100–200 μM separately. The expressions of inducible nitric oxide synthase (iNOS), tumor necrosis factor- (TNF-) α, mannose receptor (CD206), and arginase- (Arg-) 1 were quantified by Western blotting and real-time quantitative PCR. The collected supernatants from macrophage were named as (NG) MS, (HG) MS, (Ka) MS, and (HSYA) MS. (2) The podocyte survival rate was assessed by Bromodeoxyuridine assay, while TNF-α and interleukin- (IL-) 1β levels were evaluated by Elisa. Results. (1) Compared to the HG group, the Ka and HSYA 100 μM groups decreased iNOS and TNF-α levels and increased Arg-1 and CD206 expressions significantly (protein and mRNA: p<0.05, respectively). (2) The podocyte survival rate of Ka 8 μM was higher than that of HG, and the rates of (Ka) MS and (HSYA 100 μM) MS were higher than that of (HG) MS significantly (all: p<0.05). (3) TNF-α and IL-1β levels of Ka and HSYA 100 μM were significantly lower than those of the HG group, and both levels in the (Ka) MS and (HSYA) MS were lower than those in the (HG) MS group significantly (p<0.05, respectively). Conclusion. The protective effects of Ka and HSYA on podocyte apoptosis under hyperglycemic stress are related to their modulation on M1/M2 polarization and the lowering effects on TNF-α and IL-1β levels.</description><subject>Animals</subject><subject>Antibodies</subject><subject>Apoptosis</subject><subject>Arginase</subject><subject>Bromodeoxyuridine</subject><subject>Carthamus tinctorius - immunology</subject><subject>Cell Differentiation</subject><subject>Cells, Cultured</subject><subject>Chalcone - analogs & derivatives</subject><subject>Chalcone - therapeutic use</subject><subject>Chinese medicine</subject><subject>Cytokines - metabolism</subject><subject>Dextrose</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Glucose</subject><subject>Humans</subject><subject>Hyperglycemia</subject><subject>Hyperglycemia - drug therapy</subject><subject>IL-1β</subject><subject>Immunology</subject><subject>Immunomodulation</subject><subject>Inflammation</subject><subject>Instrument industry</subject><subject>Interleukins</subject><subject>Kaempferol</subject><subject>Kaempferols - therapeutic use</subject><subject>Laboratories</subject><subject>Life Sciences & Biomedicine</subject><subject>Macrophages</subject><subject>Macrophages - immunology</subject><subject>Mannose</subject><subject>Membranes</subject><subject>Mice</subject><subject>mRNA</subject><subject>Nephropathy</subject><subject>Nitric oxide</subject><subject>Nitric-oxide synthase</subject><subject>Podocytes - physiology</subject><subject>Polarization</subject><subject>Proteins</subject><subject>Quinones - therapeutic use</subject><subject>RAW 264.7 Cells</subject><subject>RNA</subject><subject>Science & Technology</subject><subject>Stress, Physiological</subject><subject>Th1 Cells - immunology</subject><subject>Th2 Cells - immunology</subject><subject>Tumor necrosis factor</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><subject>Western blotting</subject><issn>2314-8861</issn><issn>2314-7156</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>AOWDO</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNkl1v0zAUhiMEYtPYHdfIEhJCYt38kTjODVJVBptYxaSNC64ixx-tp9QOdrJSfh6_jNO1bCviguQils_zvnbOebPsJcHHhBTFCcUUn9CcU8yqJ9k-ZSQflaTgT7drITjZyw5Tcg0ucMkYF_x5tscYwZRjvp_9uoyhN6p3twadWgurhIJF18uArqS1bViaiD6YCHWNJmHRhcHrdIQ-S7PorImhRdJrdLbSMfxYpTtJRN9MC0o0PkLBQ60zcdauFEicQld9NCmNzr0eFHheBh3Uqjdo3IWuD8kldOskmgY9tLJ3fra-zlSqGLq5nBk0JSdTCqpWRvcTgOBfZM-sbJM53H4Psq8fT68nZ6OLL5_OJ-OLkeKs6EdW5DxXmEtOMLNKcFMYm-dMWZuLghtMpcBcVMQUKq-05oVoGkVI1UjLcSPYQXa-8dVB3tRddAsZV3WQrr7bCHFWy9g71ZraVpXSjbZUWZo3ohEltQwmULKSyFJY8Hq_8eqGZmG0Mr6Pst0x3a14N69n4bYuC17ljIPB261BDN8Hk_p64ZKCtktvwpBqmhd5TiiMGdDXf6E3YYgeWrWmSFlgTtgDNZPwA87bAOeqtWk95lWJK-gHAer4HxS8ej3b4I11sL8jePNIMDey7ecptMN6cGkXPNqAMOmUorH3zSC4Xme9Xme93mYd8FePG3gP_0k2AGIDLE0TbFLOeGXuMYxxISglkAV4yMT1d1GaQLp7kL77f-kDPXdey6X7z3sbYIyVDzQRJSYl-w3wyDHl</recordid><startdate>20201010</startdate><enddate>20201010</enddate><creator>Zhao, Xiaoyun</creator><creator>Zhang, Xilan</creator><creator>Shen, Dayue</creator><creator>Zheng, Dan</creator><creator>Li, Yuanping</creator><creator>Liao, Hui</creator><general>Hindawi Publishing Corporation</general><general>Hindawi</general><general>Hindawi Publishing Group</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>AOWDO</scope><scope>BLEPL</scope><scope>DTL</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>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>CWDGH</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</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/0000-0002-3631-4015</orcidid><orcidid>https://orcid.org/0000-0002-6940-0788</orcidid><orcidid>https://orcid.org/0000-0001-8095-811X</orcidid><orcidid>https://orcid.org/0000-0001-6325-062X</orcidid><orcidid>https://orcid.org/0000-0003-2667-1809</orcidid><orcidid>https://orcid.org/0000-0002-5692-5729</orcidid></search><sort><creationdate>20201010</creationdate><title>Protective Effects of Two Safflower Derived Compounds, Kaempferol and Hydroxysafflor Yellow A, on Hyperglycaemic Stress-Induced Podocyte Apoptosis via Modulating of Macrophage M1/M2 Polarization</title><author>Zhao, Xiaoyun ; Zhang, Xilan ; Shen, Dayue ; Zheng, Dan ; Li, Yuanping ; Liao, Hui</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c635t-f8464c06a6103fc86e5ef443cff4856e02a806891e5c49dd658bbc119baf60b83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Animals</topic><topic>Antibodies</topic><topic>Apoptosis</topic><topic>Arginase</topic><topic>Bromodeoxyuridine</topic><topic>Carthamus tinctorius - immunology</topic><topic>Cell Differentiation</topic><topic>Cells, Cultured</topic><topic>Chalcone - analogs & derivatives</topic><topic>Chalcone - therapeutic use</topic><topic>Chinese medicine</topic><topic>Cytokines - metabolism</topic><topic>Dextrose</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Glucose</topic><topic>Humans</topic><topic>Hyperglycemia</topic><topic>Hyperglycemia - drug therapy</topic><topic>IL-1β</topic><topic>Immunology</topic><topic>Immunomodulation</topic><topic>Inflammation</topic><topic>Instrument industry</topic><topic>Interleukins</topic><topic>Kaempferol</topic><topic>Kaempferols - therapeutic use</topic><topic>Laboratories</topic><topic>Life Sciences & Biomedicine</topic><topic>Macrophages</topic><topic>Macrophages - immunology</topic><topic>Mannose</topic><topic>Membranes</topic><topic>Mice</topic><topic>mRNA</topic><topic>Nephropathy</topic><topic>Nitric oxide</topic><topic>Nitric-oxide synthase</topic><topic>Podocytes - physiology</topic><topic>Polarization</topic><topic>Proteins</topic><topic>Quinones - therapeutic use</topic><topic>RAW 264.7 Cells</topic><topic>RNA</topic><topic>Science & Technology</topic><topic>Stress, Physiological</topic><topic>Th1 Cells - immunology</topic><topic>Th2 Cells - immunology</topic><topic>Tumor necrosis factor</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumor necrosis factor-α</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhao, Xiaoyun</creatorcontrib><creatorcontrib>Zhang, Xilan</creatorcontrib><creatorcontrib>Shen, Dayue</creatorcontrib><creatorcontrib>Zheng, Dan</creatorcontrib><creatorcontrib>Li, Yuanping</creatorcontrib><creatorcontrib>Liao, Hui</creatorcontrib><collection>الدوريات العلمية والإحصائية - e-Marefa Academic and Statistical Periodicals</collection><collection>معرفة - المحتوى العربي الأكاديمي المتكامل - e-Marefa Academic Complete</collection><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access</collection><collection>Web of Science - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Journal of Immunology Research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhao, Xiaoyun</au><au>Zhang, Xilan</au><au>Shen, Dayue</au><au>Zheng, Dan</au><au>Li, Yuanping</au><au>Liao, Hui</au><au>Wang, Kai</au><au>Kai Wang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Protective Effects of Two Safflower Derived Compounds, Kaempferol and Hydroxysafflor Yellow A, on Hyperglycaemic Stress-Induced Podocyte Apoptosis via Modulating of Macrophage M1/M2 Polarization</atitle><jtitle>Journal of Immunology Research</jtitle><stitle>J IMMUNOL RES</stitle><addtitle>J Immunol Res</addtitle><date>2020-10-10</date><risdate>2020</risdate><volume>2020</volume><issue>2020</issue><spage>1</spage><epage>11</epage><pages>1-11</pages><artnum>2462039</artnum><issn>2314-8861</issn><eissn>2314-7156</eissn><abstract>Objective. The primary initiating mechanism in diabetes nephropathy (DN) is hyperglycemia-induced inflammation in which macrophage and podocyte play important roles. The present research is aimed at exploring the effects of kaempferol (Ka) and hydroxysafflor yellow A (HSYA) on classically activated (M1)/alternatively activated (M2) macrophage polarization and podocyte apoptosis under hyperglycaemic conditions in vitro. Methods. (1) RAW264.7 cells were treated with 11.1 mM glucose (NG), 33.3 mM glucose (HG), Ka 4–8 μM, and HSYA 100–200 μM separately. The expressions of inducible nitric oxide synthase (iNOS), tumor necrosis factor- (TNF-) α, mannose receptor (CD206), and arginase- (Arg-) 1 were quantified by Western blotting and real-time quantitative PCR. The collected supernatants from macrophage were named as (NG) MS, (HG) MS, (Ka) MS, and (HSYA) MS. (2) The podocyte survival rate was assessed by Bromodeoxyuridine assay, while TNF-α and interleukin- (IL-) 1β levels were evaluated by Elisa. Results. (1) Compared to the HG group, the Ka and HSYA 100 μM groups decreased iNOS and TNF-α levels and increased Arg-1 and CD206 expressions significantly (protein and mRNA: p<0.05, respectively). (2) The podocyte survival rate of Ka 8 μM was higher than that of HG, and the rates of (Ka) MS and (HSYA 100 μM) MS were higher than that of (HG) MS significantly (all: p<0.05). (3) TNF-α and IL-1β levels of Ka and HSYA 100 μM were significantly lower than those of the HG group, and both levels in the (Ka) MS and (HSYA) MS were lower than those in the (HG) MS group significantly (p<0.05, respectively). Conclusion. The protective effects of Ka and HSYA on podocyte apoptosis under hyperglycemic stress are related to their modulation on M1/M2 polarization and the lowering effects on TNF-α and IL-1β levels.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>33102606</pmid><doi>10.1155/2020/2462039</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0002-3631-4015</orcidid><orcidid>https://orcid.org/0000-0002-6940-0788</orcidid><orcidid>https://orcid.org/0000-0001-8095-811X</orcidid><orcidid>https://orcid.org/0000-0001-6325-062X</orcidid><orcidid>https://orcid.org/0000-0003-2667-1809</orcidid><orcidid>https://orcid.org/0000-0002-5692-5729</orcidid><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 2314-8861 |
ispartof | Journal of Immunology Research, 2020-10, Vol.2020 (2020), p.1-11, Article 2462039 |
issn | 2314-8861 2314-7156 |
language | eng |
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source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central Open Access; Web of Science - Science Citation Index Expanded - 2020<img src="https://exlibris-pub.s3.amazonaws.com/fromwos-v2.jpg" />; Wiley Online Library (Open Access Collection); PubMed Central; Alma/SFX Local Collection |
subjects | Animals Antibodies Apoptosis Arginase Bromodeoxyuridine Carthamus tinctorius - immunology Cell Differentiation Cells, Cultured Chalcone - analogs & derivatives Chalcone - therapeutic use Chinese medicine Cytokines - metabolism Dextrose Diabetes Diabetes mellitus Glucose Humans Hyperglycemia Hyperglycemia - drug therapy IL-1β Immunology Immunomodulation Inflammation Instrument industry Interleukins Kaempferol Kaempferols - therapeutic use Laboratories Life Sciences & Biomedicine Macrophages Macrophages - immunology Mannose Membranes Mice mRNA Nephropathy Nitric oxide Nitric-oxide synthase Podocytes - physiology Polarization Proteins Quinones - therapeutic use RAW 264.7 Cells RNA Science & Technology Stress, Physiological Th1 Cells - immunology Th2 Cells - immunology Tumor necrosis factor Tumor necrosis factor-TNF Tumor necrosis factor-α Western blotting |
title | Protective Effects of Two Safflower Derived Compounds, Kaempferol and Hydroxysafflor Yellow A, on Hyperglycaemic Stress-Induced Podocyte Apoptosis via Modulating of Macrophage M1/M2 Polarization |
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