Gambogenic acid protects against high glucose-induced damage of renal tubular epithelial cells by inhibiting pyroptosis through regulating the AMPK–TXNIP pathway
Diabetic nephropathy, a chronic inflammatory disease, is characterized by hyperglycemia-stimulated pyroptosis of renal tubular epithelial cells. Gambogic acid, a primary component of gamboge resin, exerts detoxification, antioxidant, anticancer, anti-angiogenesis and anti-inflammatory capacities. Ho...
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| Veröffentlicht in: | Quality assurance and safety of crops & food 2022-04, Vol.14 (2), p.40-46 |
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| creator | Li, Ningxu Wen, Xiuying Tang, Mingjuan Peng, Xiangmei Sheng, Qizhi Liu, Ping |
| description | Diabetic nephropathy, a chronic inflammatory disease, is characterized by hyperglycemia-stimulated pyroptosis of renal tubular epithelial cells. Gambogic acid, a primary component of gamboge resin, exerts detoxification, antioxidant, anticancer, anti-angiogenesis and anti-inflammatory capacities. However, the nephroprotective effect of gambogic acid on diabetic nephropathy remains unknown. Human kidney (renal) epithelial cell line HK-2 was treated with dextrorotatory-glucose (D-glucose) to establish an in vitro cell model of diabetic nephropathy, followed by incubation with gambogic acid. CCK-8 was designed to detect cell viability. Enzyme-linked-immunosorbent serologic assay (ELISA) was used to detect the levels of inflammation-related factors. Pyroptosis and underlying mechanism were investigated by Western blot assay. High glucose treatment decreased the viability of HK-2 cell line, while gambogic acid incubation restored the reduced cell viability. High glucose-induced increase in the levels of tumor necrosis factor-α (TNF-α), Interleukin (IL)-6, Monocyte chemoattractant protein-1 (MCP-1) and IL-1β were reduced by gambogic acid. The protein expressions of NLR family pyrin domain containing 3 (NLRP3), N-terminal domain of gasdermin D (GSDMD-N), caspase-1, IL-1β and IL-18 were up-regulated in HK-2 cells after high glucose condition, while down-regulated by incubation of gambogic acid. Gambogic acid attenuated high glucose-induced increase of thioredoxin-interacting protein (TXNIP) and phosphorylated 5' adenosine monophosphate-activated protein kinase (p-AMPK) in HK-2 cell line. Gambogenic acid protected renal tubular epithelial cells against high glucose-induced inflammation and pyroptosis through suppression of AMPK–TXNIP pathway, providing a potential strategy for the prevention of diabetic nephropathy. |
| doi_str_mv | 10.15586/qas.v14i2.990 |
| format | Article |
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Gambogic acid, a primary component of gamboge resin, exerts detoxification, antioxidant, anticancer, anti-angiogenesis and anti-inflammatory capacities. However, the nephroprotective effect of gambogic acid on diabetic nephropathy remains unknown. Human kidney (renal) epithelial cell line HK-2 was treated with dextrorotatory-glucose (D-glucose) to establish an in vitro cell model of diabetic nephropathy, followed by incubation with gambogic acid. CCK-8 was designed to detect cell viability. Enzyme-linked-immunosorbent serologic assay (ELISA) was used to detect the levels of inflammation-related factors. Pyroptosis and underlying mechanism were investigated by Western blot assay. High glucose treatment decreased the viability of HK-2 cell line, while gambogic acid incubation restored the reduced cell viability. High glucose-induced increase in the levels of tumor necrosis factor-α (TNF-α), Interleukin (IL)-6, Monocyte chemoattractant protein-1 (MCP-1) and IL-1β were reduced by gambogic acid. The protein expressions of NLR family pyrin domain containing 3 (NLRP3), N-terminal domain of gasdermin D (GSDMD-N), caspase-1, IL-1β and IL-18 were up-regulated in HK-2 cells after high glucose condition, while down-regulated by incubation of gambogic acid. Gambogic acid attenuated high glucose-induced increase of thioredoxin-interacting protein (TXNIP) and phosphorylated 5' adenosine monophosphate-activated protein kinase (p-AMPK) in HK-2 cell line. Gambogenic acid protected renal tubular epithelial cells against high glucose-induced inflammation and pyroptosis through suppression of AMPK–TXNIP pathway, providing a potential strategy for the prevention of diabetic nephropathy.</description><identifier>ISSN: 1757-8361</identifier><identifier>EISSN: 1757-837X</identifier><identifier>DOI: 10.15586/qas.v14i2.990</identifier><language>eng</language><publisher>Brisbane: Codon Publications</publisher><subject>Acids ; Adenosine kinase ; Adenosine monophosphate ; AMP ; Angiogenesis ; Apoptosis ; Caspase-1 ; Cell viability ; Cells ; Cholecystokinin ; Detoxification ; Diabetes ; Diabetes mellitus ; Diabetic nephropathy ; Diabetic retinopathy ; Enzyme-linked immunosorbent assay ; Epithelial cells ; Epithelium ; Glucose ; Herbal medicine ; Hyperglycemia ; IL-1β ; Incubation ; Inflammation ; Inflammatory diseases ; Interleukin 18 ; Interleukins ; Kidneys ; Kinases ; Monocyte chemoattractant protein ; Monocyte chemoattractant protein 1 ; Monocytes ; Nephropathy ; Oxidative stress ; Protein expression ; Protein kinase ; Proteins ; Pyrin protein ; Pyroptosis ; Thioredoxin ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α ; Variance analysis</subject><ispartof>Quality assurance and safety of crops & food, 2022-04, Vol.14 (2), p.40-46</ispartof><rights>2022. This work is published under https://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c267t-5c7004093a944dd9af3f628aca6f6a2d92ab140dca9e0a1d485e2dde4a5e6a053</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27925,27926</link.rule.ids></links><search><creatorcontrib>Li, Ningxu</creatorcontrib><creatorcontrib>Wen, Xiuying</creatorcontrib><creatorcontrib>Tang, Mingjuan</creatorcontrib><creatorcontrib>Peng, Xiangmei</creatorcontrib><creatorcontrib>Sheng, Qizhi</creatorcontrib><creatorcontrib>Liu, Ping</creatorcontrib><title>Gambogenic acid protects against high glucose-induced damage of renal tubular epithelial cells by inhibiting pyroptosis through regulating the AMPK–TXNIP pathway</title><title>Quality assurance and safety of crops & food</title><description>Diabetic nephropathy, a chronic inflammatory disease, is characterized by hyperglycemia-stimulated pyroptosis of renal tubular epithelial cells. Gambogic acid, a primary component of gamboge resin, exerts detoxification, antioxidant, anticancer, anti-angiogenesis and anti-inflammatory capacities. However, the nephroprotective effect of gambogic acid on diabetic nephropathy remains unknown. Human kidney (renal) epithelial cell line HK-2 was treated with dextrorotatory-glucose (D-glucose) to establish an in vitro cell model of diabetic nephropathy, followed by incubation with gambogic acid. CCK-8 was designed to detect cell viability. Enzyme-linked-immunosorbent serologic assay (ELISA) was used to detect the levels of inflammation-related factors. Pyroptosis and underlying mechanism were investigated by Western blot assay. High glucose treatment decreased the viability of HK-2 cell line, while gambogic acid incubation restored the reduced cell viability. High glucose-induced increase in the levels of tumor necrosis factor-α (TNF-α), Interleukin (IL)-6, Monocyte chemoattractant protein-1 (MCP-1) and IL-1β were reduced by gambogic acid. The protein expressions of NLR family pyrin domain containing 3 (NLRP3), N-terminal domain of gasdermin D (GSDMD-N), caspase-1, IL-1β and IL-18 were up-regulated in HK-2 cells after high glucose condition, while down-regulated by incubation of gambogic acid. Gambogic acid attenuated high glucose-induced increase of thioredoxin-interacting protein (TXNIP) and phosphorylated 5' adenosine monophosphate-activated protein kinase (p-AMPK) in HK-2 cell line. Gambogenic acid protected renal tubular epithelial cells against high glucose-induced inflammation and pyroptosis through suppression of AMPK–TXNIP pathway, providing a potential strategy for the prevention of diabetic nephropathy.</description><subject>Acids</subject><subject>Adenosine kinase</subject><subject>Adenosine monophosphate</subject><subject>AMP</subject><subject>Angiogenesis</subject><subject>Apoptosis</subject><subject>Caspase-1</subject><subject>Cell viability</subject><subject>Cells</subject><subject>Cholecystokinin</subject><subject>Detoxification</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetic nephropathy</subject><subject>Diabetic retinopathy</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Epithelial cells</subject><subject>Epithelium</subject><subject>Glucose</subject><subject>Herbal medicine</subject><subject>Hyperglycemia</subject><subject>IL-1β</subject><subject>Incubation</subject><subject>Inflammation</subject><subject>Inflammatory diseases</subject><subject>Interleukin 18</subject><subject>Interleukins</subject><subject>Kidneys</subject><subject>Kinases</subject><subject>Monocyte chemoattractant protein</subject><subject>Monocyte chemoattractant protein 1</subject><subject>Monocytes</subject><subject>Nephropathy</subject><subject>Oxidative stress</subject><subject>Protein expression</subject><subject>Protein kinase</subject><subject>Proteins</subject><subject>Pyrin protein</subject><subject>Pyroptosis</subject><subject>Thioredoxin</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><subject>Variance 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acid protects against high glucose-induced damage of renal tubular epithelial cells by inhibiting pyroptosis through regulating the AMPK–TXNIP pathway</title><author>Li, Ningxu ; Wen, Xiuying ; Tang, Mingjuan ; Peng, Xiangmei ; Sheng, Qizhi ; Liu, Ping</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c267t-5c7004093a944dd9af3f628aca6f6a2d92ab140dca9e0a1d485e2dde4a5e6a053</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Acids</topic><topic>Adenosine kinase</topic><topic>Adenosine monophosphate</topic><topic>AMP</topic><topic>Angiogenesis</topic><topic>Apoptosis</topic><topic>Caspase-1</topic><topic>Cell viability</topic><topic>Cells</topic><topic>Cholecystokinin</topic><topic>Detoxification</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetic nephropathy</topic><topic>Diabetic retinopathy</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Epithelial cells</topic><topic>Epithelium</topic><topic>Glucose</topic><topic>Herbal medicine</topic><topic>Hyperglycemia</topic><topic>IL-1β</topic><topic>Incubation</topic><topic>Inflammation</topic><topic>Inflammatory diseases</topic><topic>Interleukin 18</topic><topic>Interleukins</topic><topic>Kidneys</topic><topic>Kinases</topic><topic>Monocyte chemoattractant protein</topic><topic>Monocyte chemoattractant protein 1</topic><topic>Monocytes</topic><topic>Nephropathy</topic><topic>Oxidative stress</topic><topic>Protein expression</topic><topic>Protein kinase</topic><topic>Proteins</topic><topic>Pyrin protein</topic><topic>Pyroptosis</topic><topic>Thioredoxin</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumor necrosis factor-α</topic><topic>Variance analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Ningxu</creatorcontrib><creatorcontrib>Wen, Xiuying</creatorcontrib><creatorcontrib>Tang, 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assurance and safety of crops & food</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Ningxu</au><au>Wen, Xiuying</au><au>Tang, Mingjuan</au><au>Peng, Xiangmei</au><au>Sheng, Qizhi</au><au>Liu, Ping</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Gambogenic acid protects against high glucose-induced damage of renal tubular epithelial cells by inhibiting pyroptosis through regulating the AMPK–TXNIP pathway</atitle><jtitle>Quality assurance and safety of crops & food</jtitle><date>2022-04-01</date><risdate>2022</risdate><volume>14</volume><issue>2</issue><spage>40</spage><epage>46</epage><pages>40-46</pages><issn>1757-8361</issn><eissn>1757-837X</eissn><abstract>Diabetic nephropathy, a chronic inflammatory disease, is characterized by hyperglycemia-stimulated pyroptosis of renal tubular epithelial cells. Gambogic acid, a primary component of gamboge resin, exerts detoxification, antioxidant, anticancer, anti-angiogenesis and anti-inflammatory capacities. However, the nephroprotective effect of gambogic acid on diabetic nephropathy remains unknown. Human kidney (renal) epithelial cell line HK-2 was treated with dextrorotatory-glucose (D-glucose) to establish an in vitro cell model of diabetic nephropathy, followed by incubation with gambogic acid. CCK-8 was designed to detect cell viability. Enzyme-linked-immunosorbent serologic assay (ELISA) was used to detect the levels of inflammation-related factors. Pyroptosis and underlying mechanism were investigated by Western blot assay. High glucose treatment decreased the viability of HK-2 cell line, while gambogic acid incubation restored the reduced cell viability. High glucose-induced increase in the levels of tumor necrosis factor-α (TNF-α), Interleukin (IL)-6, Monocyte chemoattractant protein-1 (MCP-1) and IL-1β were reduced by gambogic acid. The protein expressions of NLR family pyrin domain containing 3 (NLRP3), N-terminal domain of gasdermin D (GSDMD-N), caspase-1, IL-1β and IL-18 were up-regulated in HK-2 cells after high glucose condition, while down-regulated by incubation of gambogic acid. Gambogic acid attenuated high glucose-induced increase of thioredoxin-interacting protein (TXNIP) and phosphorylated 5' adenosine monophosphate-activated protein kinase (p-AMPK) in HK-2 cell line. Gambogenic acid protected renal tubular epithelial cells against high glucose-induced inflammation and pyroptosis through suppression of AMPK–TXNIP pathway, providing a potential strategy for the prevention of diabetic nephropathy.</abstract><cop>Brisbane</cop><pub>Codon Publications</pub><doi>10.15586/qas.v14i2.990</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acids Adenosine kinase Adenosine monophosphate AMP Angiogenesis Apoptosis Caspase-1 Cell viability Cells Cholecystokinin Detoxification Diabetes Diabetes mellitus Diabetic nephropathy Diabetic retinopathy Enzyme-linked immunosorbent assay Epithelial cells Epithelium Glucose Herbal medicine Hyperglycemia IL-1β Incubation Inflammation Inflammatory diseases Interleukin 18 Interleukins Kidneys Kinases Monocyte chemoattractant protein Monocyte chemoattractant protein 1 Monocytes Nephropathy Oxidative stress Protein expression Protein kinase Proteins Pyrin protein Pyroptosis Thioredoxin Tumor necrosis factor-TNF Tumor necrosis factor-α Variance analysis |
| title | Gambogenic acid protects against high glucose-induced damage of renal tubular epithelial cells by inhibiting pyroptosis through regulating the AMPK–TXNIP pathway |
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