Triptolide protects against podocyte injury in diabetic nephropathy by activating the Nrf2/HO-1 pathway and inhibiting the NLRP3 inflammasome pathway

Objectives: Diabetic nephropathy (DN) is the most common microvascular complication of diabetes mellitus. This study investigated the mechanism of triptolide (TP) in podocyte injury in DN. Methods: DN mouse models were established by feeding with a high-fat diet and injecting with streptozocin and M...

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Vydané v:	Renal failure Ročník 45; číslo 1; s. 2165103
Hlavní autori:	Lv, Chenlei, Cheng, Tianyang, Zhang, Bingbing, Sun, Ke, Lu, Keda
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	England Taylor & Francis 01.12.2023 Taylor & Francis Ltd Taylor & Francis Group
Predmet:	Animal models Animals Apoptosis Body weight Cell viability Clinical Study Creatinine Diabetes Diabetes Mellitus Diabetic Nephropathies - drug therapy Diabetic Nephropathies - metabolism Diabetic Nephropathies - prevention & control Diabetic nephropathy Heme oxygenase (decyclizing) Heme Oxygenase-1 - metabolism High fat diet Inflammasomes Inflammasomes - metabolism Inflammasomes - pharmacology Inflammation Mice Microvasculature MPC5 Nephropathy NF-E2-Related Factor 2 - metabolism NLR Family, Pyrin Domain-Containing 3 Protein - metabolism NLRP3 inflammasome Nrf2 Oxidative stress Podocytes - pathology Pyrin protein Pyroptosis Reactive oxygen species Reactive Oxygen Species - metabolism Renal function Streptozocin Triptolide Western blotting MPC5 Diabetic nephropathy triptolide NLRP3 inflammasome Nrf2 oxidative stress
ISSN:	0886-022X, 1525-6049, 1525-6049
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Abstract	Objectives: Diabetic nephropathy (DN) is the most common microvascular complication of diabetes mellitus. This study investigated the mechanism of triptolide (TP) in podocyte injury in DN. Methods: DN mouse models were established by feeding with a high-fat diet and injecting with streptozocin and MPC5 podocyte injury models were induced by high-glucose (HG), followed by TP treatment. Fasting blood glucose and renal function indicators, such as 24 h urine albumin (UAlb), serum creatinine (SCr), blood urea nitrogen (BUN), and kidney/body weight ratio of mice were examined. H&E and TUNEL staining were performed for evaluating pathological changes and apoptosis in renal tissue. The podocyte markers, reactive oxygen species (ROS), oxidative stress (OS), serum inflammatory cytokines, nuclear factor-erythroid 2-related factor 2 (Nrf2) pathway-related proteins, and pyroptosis were detected by Western blotting and corresponding kits. MPC5 cell viability and pyroptosis were evaluated by MTT and Hoechst 33342/PI double-fluorescence staining. Nrf2 inhibitor ML385 was used to verify the regulation of TP on Nrf2. Results: TP improved renal function and histopathological injury of DN mice, alleviated podocytes injury, reduced OS and ROS by activating the Nrf2/heme oxygenase-1 (HO-1) pathway, and weakened pyroptosis by inhibiting the nod-like receptor (NLR) family pyrin domain containing 3 (NLRP3) inflammasome pathway. In vitro experiments further verified the inhibition of TP on OS and pyroptosis by mediating the Nrf2/HO-1 and NLRP3 inflammasome pathways. Inhibition of Nrf2 reversed the protective effect of TP on MPC5 cells. Conclusions: Overall, TP alleviated podocyte injury in DN by inhibiting OS and pyroptosis via Nrf2/ROS/NLRP3 axis.
AbstractList	Objectives: Diabetic nephropathy (DN) is the most common microvascular complication of diabetes mellitus. This study investigated the mechanism of triptolide (TP) in podocyte injury in DN. Methods: DN mouse models were established by feeding with a high-fat diet and injecting with streptozocin and MPC5 podocyte injury models were induced by high-glucose (HG), followed by TP treatment. Fasting blood glucose and renal function indicators, such as 24 h urine albumin (UAlb), serum creatinine (SCr), blood urea nitrogen (BUN), and kidney/body weight ratio of mice were examined. H&E and TUNEL staining were performed for evaluating pathological changes and apoptosis in renal tissue. The podocyte markers, reactive oxygen species (ROS), oxidative stress (OS), serum inflammatory cytokines, nuclear factor-erythroid 2-related factor 2 (Nrf2) pathway-related proteins, and pyroptosis were detected by Western blotting and corresponding kits. MPC5 cell viability and pyroptosis were evaluated by MTT and Hoechst 33342/PI double-fluorescence staining. Nrf2 inhibitor ML385 was used to verify the regulation of TP on Nrf2. Results: TP improved renal function and histopathological injury of DN mice, alleviated podocytes injury, reduced OS and ROS by activating the Nrf2/heme oxygenase-1 (HO-1) pathway, and weakened pyroptosis by inhibiting the nod-like receptor (NLR) family pyrin domain containing 3 (NLRP3) inflammasome pathway. In vitro experiments further verified the inhibition of TP on OS and pyroptosis by mediating the Nrf2/HO-1 and NLRP3 inflammasome pathways. Inhibition of Nrf2 reversed the protective effect of TP on MPC5 cells. Conclusions: Overall, TP alleviated podocyte injury in DN by inhibiting OS and pyroptosis via Nrf2/ROS/NLRP3 axis. ObjectivesDiabetic nephropathy (DN) is the most common microvascular complication of diabetes mellitus. This study investigated the mechanism of triptolide (TP) in podocyte injury in DN.MethodsDN mouse models were established by feeding with a high-fat diet and injecting with streptozocin and MPC5 podocyte injury models were induced by high-glucose (HG), followed by TP treatment. Fasting blood glucose and renal function indicators, such as 24 h urine albumin (UAlb), serum creatinine (SCr), blood urea nitrogen (BUN), and kidney/body weight ratio of mice were examined. H&E and TUNEL staining were performed for evaluating pathological changes and apoptosis in renal tissue. The podocyte markers, reactive oxygen species (ROS), oxidative stress (OS), serum inflammatory cytokines, nuclear factor-erythroid 2-related factor 2 (Nrf2) pathway-related proteins, and pyroptosis were detected by Western blotting and corresponding kits. MPC5 cell viability and pyroptosis were evaluated by MTT and Hoechst 33342/PI double-fluorescence staining. Nrf2 inhibitor ML385 was used to verify the regulation of TP on Nrf2.ResultsTP improved renal function and histopathological injury of DN mice, alleviated podocytes injury, reduced OS and ROS by activating the Nrf2/heme oxygenase-1 (HO-1) pathway, and weakened pyroptosis by inhibiting the nod-like receptor (NLR) family pyrin domain containing 3 (NLRP3) inflammasome pathway. In vitro experiments further verified the inhibition of TP on OS and pyroptosis by mediating the Nrf2/HO-1 and NLRP3 inflammasome pathways. Inhibition of Nrf2 reversed the protective effect of TP on MPC5 cells.ConclusionsOverall, TP alleviated podocyte injury in DN by inhibiting OS and pyroptosis via Nrf2/ROS/NLRP3 axis. Objectives: Diabetic nephropathy (DN) is the most common microvascular complication of diabetes mellitus. This study investigated the mechanism of triptolide (TP) in podocyte injury in DN.Methods: DN mouse models were established by feeding with a high-fat diet and injecting with streptozocin and MPC5 podocyte injury models were induced by high-glucose (HG), followed by TP treatment. Fasting blood glucose and renal function indicators, such as 24 h urine albumin (UAlb), serum creatinine (SCr), blood urea nitrogen (BUN), and kidney/body weight ratio of mice were examined. H&E and TUNEL staining were performed for evaluating pathological changes and apoptosis in renal tissue. The podocyte markers, reactive oxygen species (ROS), oxidative stress (OS), serum inflammatory cytokines, nuclear factor-erythroid 2-related factor 2 (Nrf2) pathway-related proteins, and pyroptosis were detected by Western blotting and corresponding kits. MPC5 cell viability and pyroptosis were evaluated by MTT and Hoechst 33342/PI double-fluorescence staining. Nrf2 inhibitor ML385 was used to verify the regulation of TP on Nrf2.Results: TP improved renal function and histopathological injury of DN mice, alleviated podocytes injury, reduced OS and ROS by activating the Nrf2/heme oxygenase-1 (HO-1) pathway, and weakened pyroptosis by inhibiting the nod-like receptor (NLR) family pyrin domain containing 3 (NLRP3) inflammasome pathway. In vitro experiments further verified the inhibition of TP on OS and pyroptosis by mediating the Nrf2/HO-1 and NLRP3 inflammasome pathways. Inhibition of Nrf2 reversed the protective effect of TP on MPC5 cells.Conclusions: Overall, TP alleviated podocyte injury in DN by inhibiting OS and pyroptosis via Nrf2/ROS/NLRP3 axis.Objectives: Diabetic nephropathy (DN) is the most common microvascular complication of diabetes mellitus. This study investigated the mechanism of triptolide (TP) in podocyte injury in DN.Methods: DN mouse models were established by feeding with a high-fat diet and injecting with streptozocin and MPC5 podocyte injury models were induced by high-glucose (HG), followed by TP treatment. Fasting blood glucose and renal function indicators, such as 24 h urine albumin (UAlb), serum creatinine (SCr), blood urea nitrogen (BUN), and kidney/body weight ratio of mice were examined. H&E and TUNEL staining were performed for evaluating pathological changes and apoptosis in renal tissue. The podocyte markers, reactive oxygen species (ROS), oxidative stress (OS), serum inflammatory cytokines, nuclear factor-erythroid 2-related factor 2 (Nrf2) pathway-related proteins, and pyroptosis were detected by Western blotting and corresponding kits. MPC5 cell viability and pyroptosis were evaluated by MTT and Hoechst 33342/PI double-fluorescence staining. Nrf2 inhibitor ML385 was used to verify the regulation of TP on Nrf2.Results: TP improved renal function and histopathological injury of DN mice, alleviated podocytes injury, reduced OS and ROS by activating the Nrf2/heme oxygenase-1 (HO-1) pathway, and weakened pyroptosis by inhibiting the nod-like receptor (NLR) family pyrin domain containing 3 (NLRP3) inflammasome pathway. In vitro experiments further verified the inhibition of TP on OS and pyroptosis by mediating the Nrf2/HO-1 and NLRP3 inflammasome pathways. Inhibition of Nrf2 reversed the protective effect of TP on MPC5 cells.Conclusions: Overall, TP alleviated podocyte injury in DN by inhibiting OS and pyroptosis via Nrf2/ROS/NLRP3 axis. Diabetic nephropathy (DN) is the most common microvascular complication of diabetes mellitus. This study investigated the mechanism of triptolide (TP) in podocyte injury in DN. DN mouse models were established by feeding with a high-fat diet and injecting with streptozocin and MPC5 podocyte injury models were induced by high-glucose (HG), followed by TP treatment. Fasting blood glucose and renal function indicators, such as 24 h urine albumin (UAlb), serum creatinine (SCr), blood urea nitrogen (BUN), and kidney/body weight ratio of mice were examined. H&E and TUNEL staining were performed for evaluating pathological changes and apoptosis in renal tissue. The podocyte markers, reactive oxygen species (ROS), oxidative stress (OS), serum inflammatory cytokines, nuclear factor-erythroid 2-related factor 2 (Nrf2) pathway-related proteins, and pyroptosis were detected by Western blotting and corresponding kits. MPC5 cell viability and pyroptosis were evaluated by MTT and Hoechst 33342/PI double-fluorescence staining. Nrf2 inhibitor ML385 was used to verify the regulation of TP on Nrf2. TP improved renal function and histopathological injury of DN mice, alleviated podocytes injury, reduced OS and ROS by activating the Nrf2/heme oxygenase-1 (HO-1) pathway, and weakened pyroptosis by inhibiting the nod-like receptor (NLR) family pyrin domain containing 3 (NLRP3) inflammasome pathway. experiments further verified the inhibition of TP on OS and pyroptosis by mediating the Nrf2/HO-1 and NLRP3 inflammasome pathways. Inhibition of Nrf2 reversed the protective effect of TP on MPC5 cells. Overall, TP alleviated podocyte injury in DN by inhibiting OS and pyroptosis Nrf2/ROS/NLRP3 axis. Objectives: Diabetic nephropathy (DN) is the most common microvascular complication of diabetes mellitus. This study investigated the mechanism of triptolide (TP) in podocyte injury in DN. Methods: DN mouse models were established by feeding with a high-fat diet and injecting with streptozocin and MPC5 podocyte injury models were induced by high-glucose (HG), followed by TP treatment. Fasting blood glucose and renal function indicators, such as 24 h urine albumin (UAlb), serum creatinine (SCr), blood urea nitrogen (BUN), and kidney/body weight ratio of mice were examined. H&E and TUNEL staining were performed for evaluating pathological changes and apoptosis in renal tissue. The podocyte markers, reactive oxygen species (ROS), oxidative stress (OS), serum inflammatory cytokines, nuclear factor-erythroid 2-related factor 2 (Nrf2) pathway-related proteins, and pyroptosis were detected by Western blotting and corresponding kits. MPC5 cell viability and pyroptosis were evaluated by MTT and Hoechst 33342/PI double-fluorescence staining. Nrf2 inhibitor ML385 was used to verify the regulation of TP on Nrf2. Results: TP improved renal function and histopathological injury of DN mice, alleviated podocytes injury, reduced OS and ROS by activating the Nrf2/heme oxygenase-1 (HO-1) pathway, and weakened pyroptosis by inhibiting the nod-like receptor (NLR) family pyrin domain containing 3 (NLRP3) inflammasome pathway. In vitro experiments further verified the inhibition of TP on OS and pyroptosis by mediating the Nrf2/HO-1 and NLRP3 inflammasome pathways. Inhibition of Nrf2 reversed the protective effect of TP on MPC5 cells. Conclusions: Overall, TP alleviated podocyte injury in DN by inhibiting OS and pyroptosis via Nrf2/ROS/NLRP3 axis.
Author	Lv, Chenlei Lu, Keda Zhang, Bingbing Sun, Ke Cheng, Tianyang
Author_xml	– sequence: 1 givenname: Chenlei surname: Lv fullname: Lv, Chenlei organization: Department of Nephrology, The First Affiliated Hospital, Zhejiang Chinese Medical University – sequence: 2 givenname: Tianyang surname: Cheng fullname: Cheng, Tianyang organization: Department of Nephrology, The First Affiliated Hospital, Zhejiang Chinese Medical University – sequence: 3 givenname: Bingbing surname: Zhang fullname: Zhang, Bingbing organization: College of Pharmaceutical Sciences, Zhejiang Chinese Medical University – sequence: 4 givenname: Ke surname: Sun fullname: Sun, Ke organization: Department of Nephrology, The First Affiliated Hospital, Zhejiang Chinese Medical University – sequence: 5 givenname: Keda surname: Lu fullname: Lu, Keda organization: Department of Nephrology, The Third Affiliated Hospital, Zhejiang Chinese Medical University
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/36938748$$D View this record in MEDLINE/PubMed
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Cites_doi	10.1016/j.drudis.2015.06.003 10.1007/s12012-015-9342-y 10.2174/187221413804660971 10.3390/antiox10060823 10.3390/ijms23031252 10.3389/fphar.2022.783706 10.1042/CS20171459 10.1097/MD.0000000000005879 10.18632/aging.202460 10.3109/08923973.2015.1080265 10.1080/13813455.2021.1890129 10.3389/fphar.2022.857015 10.3892/etm.2013.1226 10.7150/ijbs.24032 10.1055/s-0042-106083 10.1016/j.ejmech.2022.114194 10.1016/0005-2760(86)90222-5 10.1007/s12010-021-03661-2 10.3389/fphar.2022.897046 10.3389/fphar.2022.897167 10.1371/journal.pone.0250666 10.1038/s41419-020-2544-7 10.1016/j.mce.2019.110490 10.1016/j.intimp.2021.108236 10.1007/s10565-022-09696-3 10.4196/kjpp.2021.25.6.533 10.3389/fphar.2022.894981 10.3390/molecules24071214 10.1089/gtmb.2021.0086 10.1016/j.mce.2018.08.002 10.1159/000518132 10.1016/j.metabol.2022.155155 10.3724/abbs.2021016 10.1016/j.cca.2021.09.003 10.1016/j.yexcr.2020.111849 10.2174/1872211309666150608095106 10.1615/JEnvironPatholToxicolOncol.2017019457 10.2215/CJN.11111016 10.3389/fmed.2021.747922 10.1155/2020/6126490 10.3390/nu13114050 10.1007/s11596-017-1689-9 10.1016/j.cellsig.2011.05.016 10.1016/j.cell.2016.03.046 10.1002/jcp.26092 10.1016/S2213-8587(20)30369-7 10.2174/1871530320666201208110209 10.3390/molecules27072109 10.1016/j.intimp.2022.108711 10.1039/D0NP00054J 10.1159/000452591 10.3389/fimmu.2020.592084 10.7150/ijbs.20485 10.1016/j.kint.2016.01.012 10.1016/j.canlet.2022.01.021 10.1111/jcmm.17304 10.1016/j.intimp.2022.108680 10.1016/j.omtn.2017.08.011 10.1016/j.biopha.2021.111308 10.1053/j.ackd.2021.09.010 10.1530/JOE-18-0578 10.1172/JCI121987 10.1038/s41401-020-00525-z 10.3390/ijms21072632 10.7150/ijbs.53769 10.1056/NEJMoa2024816 10.2147/JIR.S334996 10.1089/ars.2020.8038 10.1016/j.apsb.2020.12.020 10.1111/cpr.13052 10.3389/fcell.2022.832887 10.1007/s10565-019-09501-8 10.1007/s00018-016-2223-0 10.1080/21655979.2021.2012919 10.7150/ijbs.68977 10.1016/j.mam.2020.100889 10.1007/s40620-020-00749-6
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Keywords	MPC5 Diabetic nephropathy triptolide NLRP3 inflammasome Nrf2 oxidative stress
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PublicationTitle	Renal failure
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References	e_1_3_5_27_1 e_1_3_5_25_1 e_1_3_5_23_1 Liang X (e_1_3_5_29_1) 2020; 12 e_1_3_5_44_1 e_1_3_5_67_1 e_1_3_5_46_1 e_1_3_5_69_1 e_1_3_5_48_1 e_1_3_5_3_1 e_1_3_5_61_1 e_1_3_5_40_1 e_1_3_5_63_1 e_1_3_5_42_1 e_1_3_5_65_1 e_1_3_5_9_1 e_1_3_5_21_1 e_1_3_5_5_1 e_1_3_5_7_1 e_1_3_5_18_1 e_1_3_5_39_1 e_1_3_5_16_1 e_1_3_5_37_1 Sarafidis P (e_1_3_5_80_1) 2022 e_1_3_5_14_1 e_1_3_5_35_1 e_1_3_5_12_1 e_1_3_5_33_1 e_1_3_5_56_1 e_1_3_5_77_1 e_1_3_5_58_1 e_1_3_5_50_1 e_1_3_5_71_1 e_1_3_5_52_1 e_1_3_5_73_1 e_1_3_5_54_1 e_1_3_5_75_1 e_1_3_5_10_1 e_1_3_5_31_1 e_1_3_5_28_1 e_1_3_5_26_1 e_1_3_5_24_1 e_1_3_5_22_1 e_1_3_5_45_1 e_1_3_5_66_1 e_1_3_5_47_1 e_1_3_5_68_1 e_1_3_5_49_1 e_1_3_5_2_1 e_1_3_5_60_1 e_1_3_5_81_1 e_1_3_5_41_1 e_1_3_5_62_1 e_1_3_5_43_1 e_1_3_5_64_1 e_1_3_5_8_1 e_1_3_5_20_1 e_1_3_5_4_1 Chen Y (e_1_3_5_79_1) 2022; 2022 e_1_3_5_6_1 e_1_3_5_17_1 e_1_3_5_38_1 e_1_3_5_15_1 e_1_3_5_13_1 e_1_3_5_36_1 e_1_3_5_11_1 e_1_3_5_34_1 e_1_3_5_55_1 e_1_3_5_78_1 e_1_3_5_57_1 e_1_3_5_59_1 e_1_3_5_19_1 e_1_3_5_70_1 e_1_3_5_72_1 e_1_3_5_51_1 e_1_3_5_74_1 e_1_3_5_53_1 e_1_3_5_76_1 e_1_3_5_32_1 e_1_3_5_30_1
References_xml	– ident: e_1_3_5_61_1 doi: 10.1016/j.drudis.2015.06.003 – ident: e_1_3_5_70_1 doi: 10.1007/s12012-015-9342-y – ident: e_1_3_5_8_1 doi: 10.2174/187221413804660971 – ident: e_1_3_5_45_1 doi: 10.3390/antiox10060823 – ident: e_1_3_5_66_1 doi: 10.3390/ijms23031252 – volume: 2022 start-page: 6932188 year: 2022 ident: e_1_3_5_79_1 article-title: Ferulic acid protects human lens epithelial cells against ionizing radiation-induced oxidative damage by activating Nrf2/HO-1 signal pathway publication-title: Oxid Med Cell Longev – ident: e_1_3_5_23_1 doi: 10.3389/fphar.2022.783706 – ident: e_1_3_5_14_1 doi: 10.1042/CS20171459 – ident: e_1_3_5_57_1 doi: 10.1097/MD.0000000000005879 – ident: e_1_3_5_67_1 doi: 10.18632/aging.202460 – volume: 12 start-page: 800 issue: 3 year: 2020 ident: e_1_3_5_29_1 article-title: Triptolide potentiates the cytoskeleton-stabilizing activity of cyclosporine a in glomerular podocytes via a GSK3beta dependent mechanism publication-title: Am J Transl Res – ident: e_1_3_5_76_1 doi: 10.3109/08923973.2015.1080265 – ident: e_1_3_5_17_1 doi: 10.1080/13813455.2021.1890129 – ident: e_1_3_5_78_1 doi: 10.3389/fphar.2022.857015 – ident: e_1_3_5_53_1 doi: 10.3892/etm.2013.1226 – ident: e_1_3_5_55_1 doi: 10.7150/ijbs.24032 – ident: e_1_3_5_72_1 doi: 10.1055/s-0042-106083 – ident: e_1_3_5_21_1 doi: 10.1016/j.ejmech.2022.114194 – ident: e_1_3_5_60_1 doi: 10.1016/0005-2760(86)90222-5 – ident: e_1_3_5_27_1 doi: 10.1007/s12010-021-03661-2 – ident: e_1_3_5_34_1 doi: 10.3389/fphar.2022.897046 – ident: e_1_3_5_81_1 doi: 10.3389/fphar.2022.897167 – ident: e_1_3_5_52_1 doi: 10.1371/journal.pone.0250666 – ident: e_1_3_5_32_1 doi: 10.1038/s41419-020-2544-7 – ident: e_1_3_5_42_1 doi: 10.1016/j.mce.2019.110490 – ident: e_1_3_5_43_1 doi: 10.1016/j.intimp.2021.108236 – ident: e_1_3_5_74_1 doi: 10.1007/s10565-022-09696-3 – ident: e_1_3_5_77_1 doi: 10.4196/kjpp.2021.25.6.533 – ident: e_1_3_5_24_1 doi: 10.3389/fphar.2022.894981 – ident: e_1_3_5_63_1 doi: 10.3390/molecules24071214 – ident: e_1_3_5_4_1 doi: 10.1089/gtmb.2021.0086 – ident: e_1_3_5_73_1 doi: 10.1016/j.mce.2018.08.002 – ident: e_1_3_5_50_1 doi: 10.1159/000518132 – ident: e_1_3_5_6_1 doi: 10.1016/j.metabol.2022.155155 – ident: e_1_3_5_3_1 doi: 10.3724/abbs.2021016 – ident: e_1_3_5_47_1 doi: 10.1016/j.cca.2021.09.003 – ident: e_1_3_5_35_1 doi: 10.1016/j.yexcr.2020.111849 – ident: e_1_3_5_64_1 doi: 10.2174/1872211309666150608095106 – ident: e_1_3_5_65_1 doi: 10.1615/JEnvironPatholToxicolOncol.2017019457 – ident: e_1_3_5_7_1 doi: 10.2215/CJN.11111016 – ident: e_1_3_5_26_1 doi: 10.3389/fmed.2021.747922 – ident: e_1_3_5_37_1 doi: 10.1155/2020/6126490 – ident: e_1_3_5_2_1 doi: 10.3390/nu13114050 – ident: e_1_3_5_68_1 doi: 10.1007/s11596-017-1689-9 – ident: e_1_3_5_16_1 doi: 10.1016/j.cellsig.2011.05.016 – ident: e_1_3_5_19_1 doi: 10.1016/j.cell.2016.03.046 – ident: e_1_3_5_58_1 doi: 10.1002/jcp.26092 – ident: e_1_3_5_9_1 doi: 10.1016/S2213-8587(20)30369-7 – ident: e_1_3_5_56_1 doi: 10.2174/1871530320666201208110209 – ident: e_1_3_5_49_1 doi: 10.3390/molecules27072109 – ident: e_1_3_5_22_1 doi: 10.1016/j.intimp.2022.108711 – ident: e_1_3_5_25_1 doi: 10.1039/D0NP00054J – ident: e_1_3_5_59_1 doi: 10.1159/000452591 – ident: e_1_3_5_69_1 doi: 10.3389/fimmu.2020.592084 – ident: e_1_3_5_31_1 doi: 10.7150/ijbs.20485 – ident: e_1_3_5_62_1 doi: 10.1016/j.kint.2016.01.012 – ident: e_1_3_5_75_1 doi: 10.1016/j.canlet.2022.01.021 – ident: e_1_3_5_41_1 doi: 10.1111/jcmm.17304 – ident: e_1_3_5_48_1 doi: 10.1016/j.intimp.2022.108680 – ident: e_1_3_5_38_1 doi: 10.1016/j.omtn.2017.08.011 – ident: e_1_3_5_40_1 doi: 10.1016/j.biopha.2021.111308 – ident: e_1_3_5_12_1 doi: 10.1053/j.ackd.2021.09.010 – ident: e_1_3_5_39_1 doi: 10.1530/JOE-18-0578 – ident: e_1_3_5_54_1 doi: 10.1172/JCI121987 – ident: e_1_3_5_71_1 doi: 10.1038/s41401-020-00525-z – ident: e_1_3_5_51_1 doi: 10.3390/ijms21072632 – ident: e_1_3_5_28_1 doi: 10.7150/ijbs.53769 – year: 2022 ident: e_1_3_5_80_1 article-title: SGLT-2 inhibitors and nephroprotection in patients with diabetic and non-diabetic chronic kidney disease publication-title: Curr Med Chem – ident: e_1_3_5_10_1 doi: 10.1056/NEJMoa2024816 – ident: e_1_3_5_13_1 doi: 10.2147/JIR.S334996 – ident: e_1_3_5_36_1 doi: 10.1089/ars.2020.8038 – ident: e_1_3_5_11_1 doi: 10.1016/j.apsb.2020.12.020 – ident: e_1_3_5_30_1 doi: 10.1111/cpr.13052 – ident: e_1_3_5_5_1 doi: 10.3389/fcell.2022.832887 – ident: e_1_3_5_18_1 doi: 10.1007/s10565-019-09501-8 – ident: e_1_3_5_46_1 doi: 10.1007/s00018-016-2223-0 – ident: e_1_3_5_33_1 doi: 10.1080/21655979.2021.2012919 – ident: e_1_3_5_44_1 doi: 10.7150/ijbs.68977 – ident: e_1_3_5_20_1 doi: 10.1016/j.mam.2020.100889 – ident: e_1_3_5_15_1 doi: 10.1007/s40620-020-00749-6
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Snippet	Objectives: Diabetic nephropathy (DN) is the most common microvascular complication of diabetes mellitus. This study investigated the mechanism of triptolide... Diabetic nephropathy (DN) is the most common microvascular complication of diabetes mellitus. This study investigated the mechanism of triptolide (TP) in... ObjectivesDiabetic nephropathy (DN) is the most common microvascular complication of diabetes mellitus. This study investigated the mechanism of triptolide... Objectives Diabetic nephropathy (DN) is the most common microvascular complication of diabetes mellitus. This study investigated the mechanism of triptolide...
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SubjectTerms	Animal models Animals Apoptosis Body weight Cell viability Clinical Study Creatinine Diabetes Diabetes Mellitus Diabetic Nephropathies - drug therapy Diabetic Nephropathies - metabolism Diabetic Nephropathies - prevention & control Diabetic nephropathy Heme oxygenase (decyclizing) Heme Oxygenase-1 - metabolism High fat diet Inflammasomes Inflammasomes - metabolism Inflammasomes - pharmacology Inflammation Mice Microvasculature MPC5 Nephropathy NF-E2-Related Factor 2 - metabolism NLR Family, Pyrin Domain-Containing 3 Protein - metabolism NLRP3 inflammasome Nrf2 Oxidative stress Podocytes - pathology Pyrin protein Pyroptosis Reactive oxygen species Reactive Oxygen Species - metabolism Renal function Streptozocin Triptolide Western blotting
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Title	Triptolide protects against podocyte injury in diabetic nephropathy by activating the Nrf2/HO-1 pathway and inhibiting the NLRP3 inflammasome pathway
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