Metformin improves renal injury of MRL/lpr lupus-prone mice via the AMPK/STAT3 pathway
ObjectiveLupus nephritis (LN) is a major complication and cause of death among patients with SLE. This research used in vivo and in vitro experiments to explore the therapeutic potential of metformin in kidney injury from LN-induced inflammation.MethodsIn vivo study, 8-week-old MRL/MpJ-Faslpr/J (MRL...
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| Published in | Lupus science & medicine Vol. 9; no. 1; p. e000611 |
|---|---|
| Main Authors | , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
Lupus Foundation of America
01.04.2022
BMJ Publishing Group LTD BMJ Publishing Group |
| Series | Original research |
| Subjects | |
| Online Access | Get full text |
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| Abstract | ObjectiveLupus nephritis (LN) is a major complication and cause of death among patients with SLE. This research used in vivo and in vitro experiments to explore the therapeutic potential of metformin in kidney injury from LN-induced inflammation.MethodsIn vivo study, 8-week-old MRL/MpJ-Faslpr/J (MRL/lpr) mice were randomly divided into two groups (n=12 each): daily administration of 0.3 mg/mL metformin in drinking water and control (water only). Body weight and urinary samples were measured biweekly. Mice were sacrificed after 8-week treatment to harvest serum, lymph nodes, spleen and kidneys. In vitro study, human kidney-2 (HK-2) cells were pretreated with 1 mM metformin for 1 hour and then stimulated with 20 µg/mL lipopolysaccharides (LPS) or 10 ng/mL tumour necrosis factor-α (TNF-α) for another 48 hours. Protein was collected for subsequent analysis.ResultsWe found that metformin administration improved renal function in MRL/lpr lupus-prone mice, measured by decreased urea nitrogen and urinary proteins. Metformin reduced immunoglobulin G and complement C3 deposition in glomeruli. The treatment also downregulated systemic and renal inflammation, as seen in decreased renal infiltration of F4/80-positive macrophages and reduced splenic and renal MCP-1 (monocyte chemoattractant protein-1) and TNF-α, and renal IL-1β (interleukin 1β) expression. Metformin administration decreased renal expression of necroptosis markers p-RIPK1 (phosphorylated receptor-interacting protein kinase 1) and p-MLKL, along with tubular injury marker KIM-1 (kidney injury molecule-1) in lupus mice. In addition, metformin alleviated the necroptosis of HK-2 cells stimulated by LPS and TNF-α, evidencing by a decrease in the expression of necroptosis markers p-RIPK1, p-RIPK3 and p-MLKL, and the inflammasome-related markers NLRP3 (NLR family pyrin domain containing 3), ASC (apoptosis-associated speck-like protein containing a CARD), caspase-1. Mechanistically, metformin treatment upregulated p-AMPK (phosphorylated AMP-activated protein kinase) and downregulated p-STAT3 (phosphorylated signal transducer and activator of transcription 3) expression in the kidneys. Moreover, AMPKα2 knockdown abolished the protective effects of metformin in vitro.ConclusionsMetformin alleviated kidney injury in LN though suppressing renal necroptosis and inflammation via the AMPK/STAT3 pathway. |
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| AbstractList | Lupus nephritis (LN) is a major complication and cause of death among patients with SLE. This research used in vivo and in vitro experiments to explore the therapeutic potential of metformin in kidney injury from LN-induced inflammation.OBJECTIVELupus nephritis (LN) is a major complication and cause of death among patients with SLE. This research used in vivo and in vitro experiments to explore the therapeutic potential of metformin in kidney injury from LN-induced inflammation.In vivo study, 8-week-old MRL/MpJ-Faslpr/J (MRL/lpr) mice were randomly divided into two groups (n=12 each): daily administration of 0.3 mg/mL metformin in drinking water and control (water only). Body weight and urinary samples were measured biweekly. Mice were sacrificed after 8-week treatment to harvest serum, lymph nodes, spleen and kidneys. In vitro study, human kidney-2 (HK-2) cells were pretreated with 1 mM metformin for 1 hour and then stimulated with 20 µg/mL lipopolysaccharides (LPS) or 10 ng/mL tumour necrosis factor-α (TNF-α) for another 48 hours. Protein was collected for subsequent analysis.METHODSIn vivo study, 8-week-old MRL/MpJ-Faslpr/J (MRL/lpr) mice were randomly divided into two groups (n=12 each): daily administration of 0.3 mg/mL metformin in drinking water and control (water only). Body weight and urinary samples were measured biweekly. Mice were sacrificed after 8-week treatment to harvest serum, lymph nodes, spleen and kidneys. In vitro study, human kidney-2 (HK-2) cells were pretreated with 1 mM metformin for 1 hour and then stimulated with 20 µg/mL lipopolysaccharides (LPS) or 10 ng/mL tumour necrosis factor-α (TNF-α) for another 48 hours. Protein was collected for subsequent analysis.We found that metformin administration improved renal function in MRL/lpr lupus-prone mice, measured by decreased urea nitrogen and urinary proteins. Metformin reduced immunoglobulin G and complement C3 deposition in glomeruli. The treatment also downregulated systemic and renal inflammation, as seen in decreased renal infiltration of F4/80-positive macrophages and reduced splenic and renal MCP-1 (monocyte chemoattractant protein-1) and TNF-α, and renal IL-1β (interleukin 1β) expression. Metformin administration decreased renal expression of necroptosis markers p-RIPK1 (phosphorylated receptor-interacting protein kinase 1) and p-MLKL, along with tubular injury marker KIM-1 (kidney injury molecule-1) in lupus mice. In addition, metformin alleviated the necroptosis of HK-2 cells stimulated by LPS and TNF-α, evidencing by a decrease in the expression of necroptosis markers p-RIPK1, p-RIPK3 and p-MLKL, and the inflammasome-related markers NLRP3 (NLR family pyrin domain containing 3), ASC (apoptosis-associated speck-like protein containing a CARD), caspase-1. Mechanistically, metformin treatment upregulated p-AMPK (phosphorylated AMP-activated protein kinase) and downregulated p-STAT3 (phosphorylated signal transducer and activator of transcription 3) expression in the kidneys. Moreover, AMPKα2 knockdown abolished the protective effects of metformin in vitro.RESULTSWe found that metformin administration improved renal function in MRL/lpr lupus-prone mice, measured by decreased urea nitrogen and urinary proteins. Metformin reduced immunoglobulin G and complement C3 deposition in glomeruli. The treatment also downregulated systemic and renal inflammation, as seen in decreased renal infiltration of F4/80-positive macrophages and reduced splenic and renal MCP-1 (monocyte chemoattractant protein-1) and TNF-α, and renal IL-1β (interleukin 1β) expression. Metformin administration decreased renal expression of necroptosis markers p-RIPK1 (phosphorylated receptor-interacting protein kinase 1) and p-MLKL, along with tubular injury marker KIM-1 (kidney injury molecule-1) in lupus mice. In addition, metformin alleviated the necroptosis of HK-2 cells stimulated by LPS and TNF-α, evidencing by a decrease in the expression of necroptosis markers p-RIPK1, p-RIPK3 and p-MLKL, and the inflammasome-related markers NLRP3 (NLR family pyrin domain containing 3), ASC (apoptosis-associated speck-like protein containing a CARD), caspase-1. Mechanistically, metformin treatment upregulated p-AMPK (phosphorylated AMP-activated protein kinase) and downregulated p-STAT3 (phosphorylated signal transducer and activator of transcription 3) expression in the kidneys. Moreover, AMPKα2 knockdown abolished the protective effects of metformin in vitro.Metformin alleviated kidney injury in LN though suppressing renal necroptosis and inflammation via the AMPK/STAT3 pathway.CONCLUSIONSMetformin alleviated kidney injury in LN though suppressing renal necroptosis and inflammation via the AMPK/STAT3 pathway. Objective Lupus nephritis (LN) is a major complication and cause of death among patients with SLE. This research used in vivo and in vitro experiments to explore the therapeutic potential of metformin in kidney injury from LN-induced inflammation.Methods In vivo study, 8-week-old MRL/MpJ-Faslpr/J (MRL/lpr) mice were randomly divided into two groups (n=12 each): daily administration of 0.3 mg/mL metformin in drinking water and control (water only). Body weight and urinary samples were measured biweekly. Mice were sacrificed after 8-week treatment to harvest serum, lymph nodes, spleen and kidneys. In vitro study, human kidney-2 (HK-2) cells were pretreated with 1 mM metformin for 1 hour and then stimulated with 20 µg/mL lipopolysaccharides (LPS) or 10 ng/mL tumour necrosis factor-α (TNF-α) for another 48 hours. Protein was collected for subsequent analysis.Results We found that metformin administration improved renal function in MRL/lpr lupus-prone mice, measured by decreased urea nitrogen and urinary proteins. Metformin reduced immunoglobulin G and complement C3 deposition in glomeruli. The treatment also downregulated systemic and renal inflammation, as seen in decreased renal infiltration of F4/80-positive macrophages and reduced splenic and renal MCP-1 (monocyte chemoattractant protein-1) and TNF-α, and renal IL-1β (interleukin 1β) expression. Metformin administration decreased renal expression of necroptosis markers p-RIPK1 (phosphorylated receptor-interacting protein kinase 1) and p-MLKL, along with tubular injury marker KIM-1 (kidney injury molecule-1) in lupus mice. In addition, metformin alleviated the necroptosis of HK-2 cells stimulated by LPS and TNF-α, evidencing by a decrease in the expression of necroptosis markers p-RIPK1, p-RIPK3 and p-MLKL, and the inflammasome-related markers NLRP3 (NLR family pyrin domain containing 3), ASC (apoptosis-associated speck-like protein containing a CARD), caspase-1. Mechanistically, metformin treatment upregulated p-AMPK (phosphorylated AMP-activated protein kinase) and downregulated p-STAT3 (phosphorylated signal transducer and activator of transcription 3) expression in the kidneys. Moreover, AMPKα2 knockdown abolished the protective effects of metformin in vitro.Conclusions Metformin alleviated kidney injury in LN though suppressing renal necroptosis and inflammation via the AMPK/STAT3 pathway. Lupus nephritis (LN) is a major complication and cause of death among patients with SLE. This research used in vivo and in vitro experiments to explore the therapeutic potential of metformin in kidney injury from LN-induced inflammation. In vivo study, 8-week-old MRL/MpJ-Faslpr/J (MRL/lpr) mice were randomly divided into two groups (n=12 each): daily administration of 0.3 mg/mL metformin in drinking water and control (water only). Body weight and urinary samples were measured biweekly. Mice were sacrificed after 8-week treatment to harvest serum, lymph nodes, spleen and kidneys. In vitro study, human kidney-2 (HK-2) cells were pretreated with 1 mM metformin for 1 hour and then stimulated with 20 µg/mL lipopolysaccharides (LPS) or 10 ng/mL tumour necrosis factor-α (TNF-α) for another 48 hours. Protein was collected for subsequent analysis. We found that metformin administration improved renal function in MRL/lpr lupus-prone mice, measured by decreased urea nitrogen and urinary proteins. Metformin reduced immunoglobulin G and complement C3 deposition in glomeruli. The treatment also downregulated systemic and renal inflammation, as seen in decreased renal infiltration of F4/80-positive macrophages and reduced splenic and renal MCP-1 (monocyte chemoattractant protein-1) and TNF-α, and renal IL-1β (interleukin 1β) expression. Metformin administration decreased renal expression of necroptosis markers p-RIPK1 (phosphorylated receptor-interacting protein kinase 1) and p-MLKL, along with tubular injury marker KIM-1 (kidney injury molecule-1) in lupus mice. In addition, metformin alleviated the necroptosis of HK-2 cells stimulated by LPS and TNF-α, evidencing by a decrease in the expression of necroptosis markers p-RIPK1, p-RIPK3 and p-MLKL, and the inflammasome-related markers NLRP3 (NLR family pyrin domain containing 3), ASC (apoptosis-associated speck-like protein containing a CARD), caspase-1. Mechanistically, metformin treatment upregulated p-AMPK (phosphorylated AMP-activated protein kinase) and downregulated p-STAT3 (phosphorylated signal transducer and activator of transcription 3) expression in the kidneys. Moreover, AMPKα2 knockdown abolished the protective effects of metformin in vitro. Metformin alleviated kidney injury in LN though suppressing renal necroptosis and inflammation via the AMPK/STAT3 pathway. ObjectiveLupus nephritis (LN) is a major complication and cause of death among patients with SLE. This research used in vivo and in vitro experiments to explore the therapeutic potential of metformin in kidney injury from LN-induced inflammation.MethodsIn vivo study, 8-week-old MRL/MpJ-Faslpr/J (MRL/lpr) mice were randomly divided into two groups (n=12 each): daily administration of 0.3 mg/mL metformin in drinking water and control (water only). Body weight and urinary samples were measured biweekly. Mice were sacrificed after 8-week treatment to harvest serum, lymph nodes, spleen and kidneys. In vitro study, human kidney-2 (HK-2) cells were pretreated with 1 mM metformin for 1 hour and then stimulated with 20 µg/mL lipopolysaccharides (LPS) or 10 ng/mL tumour necrosis factor-α (TNF-α) for another 48 hours. Protein was collected for subsequent analysis.ResultsWe found that metformin administration improved renal function in MRL/lpr lupus-prone mice, measured by decreased urea nitrogen and urinary proteins. Metformin reduced immunoglobulin G and complement C3 deposition in glomeruli. The treatment also downregulated systemic and renal inflammation, as seen in decreased renal infiltration of F4/80-positive macrophages and reduced splenic and renal MCP-1 (monocyte chemoattractant protein-1) and TNF-α, and renal IL-1β (interleukin 1β) expression. Metformin administration decreased renal expression of necroptosis markers p-RIPK1 (phosphorylated receptor-interacting protein kinase 1) and p-MLKL, along with tubular injury marker KIM-1 (kidney injury molecule-1) in lupus mice. In addition, metformin alleviated the necroptosis of HK-2 cells stimulated by LPS and TNF-α, evidencing by a decrease in the expression of necroptosis markers p-RIPK1, p-RIPK3 and p-MLKL, and the inflammasome-related markers NLRP3 (NLR family pyrin domain containing 3), ASC (apoptosis-associated speck-like protein containing a CARD), caspase-1. Mechanistically, metformin treatment upregulated p-AMPK (phosphorylated AMP-activated protein kinase) and downregulated p-STAT3 (phosphorylated signal transducer and activator of transcription 3) expression in the kidneys. Moreover, AMPKα2 knockdown abolished the protective effects of metformin in vitro.ConclusionsMetformin alleviated kidney injury in LN though suppressing renal necroptosis and inflammation via the AMPK/STAT3 pathway. |
| Author | Zhu, Shao-ping Wu, Hong-luan An, Ning Su, Hong-yong Li, Hui-yuan Liu, Hua-feng Pan, Qing-jun Huang, Xiao-rong Yang, Chen Lu, Xing Chen, Xiao-cui Liu, Ze-jian Huang, Li-feng Wu, Dan |
| AuthorAffiliation | 1 Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang, Institute of Nephrology , Affiliated Hospital of Guangdong Medical University , Zhanjiang , Guangdong , China 2 Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases co-sponsored by province and city , Zhanjiang , Guangdong , China 3 Laboratory Animal Center , Guangdong Medical University , Zhanjiang , Guangdong , China |
| AuthorAffiliation_xml | – name: 1 Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang, Institute of Nephrology , Affiliated Hospital of Guangdong Medical University , Zhanjiang , Guangdong , China – name: 2 Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases co-sponsored by province and city , Zhanjiang , Guangdong , China – name: 3 Laboratory Animal Center , Guangdong Medical University , Zhanjiang , Guangdong , China |
| Author_xml | – sequence: 1 givenname: Xiao-cui surname: Chen fullname: Chen, Xiao-cui organization: Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases co-sponsored by province and city, Zhanjiang, Guangdong, China – sequence: 2 givenname: Dan surname: Wu fullname: Wu, Dan organization: Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases co-sponsored by province and city, Zhanjiang, Guangdong, China – sequence: 3 givenname: Hong-luan surname: Wu fullname: Wu, Hong-luan organization: Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases co-sponsored by province and city, Zhanjiang, Guangdong, China – sequence: 4 givenname: Hui-yuan surname: Li fullname: Li, Hui-yuan organization: Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases co-sponsored by province and city, Zhanjiang, Guangdong, China – sequence: 5 givenname: Chen orcidid: 0000-0001-8937-4508 surname: Yang fullname: Yang, Chen organization: Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases co-sponsored by province and city, Zhanjiang, Guangdong, China – sequence: 6 givenname: Hong-yong surname: Su fullname: Su, Hong-yong organization: Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases co-sponsored by province and city, Zhanjiang, Guangdong, China – sequence: 7 givenname: Ze-jian surname: Liu fullname: Liu, Ze-jian organization: Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases co-sponsored by province and city, Zhanjiang, Guangdong, China – sequence: 8 givenname: Xiao-rong surname: Huang fullname: Huang, Xiao-rong organization: Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases co-sponsored by province and city, Zhanjiang, Guangdong, China – sequence: 9 givenname: Xing surname: Lu fullname: Lu, Xing organization: Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases co-sponsored by province and city, Zhanjiang, Guangdong, China – sequence: 10 givenname: Li-feng surname: Huang fullname: Huang, Li-feng organization: Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases co-sponsored by province and city, Zhanjiang, Guangdong, China – sequence: 11 givenname: Shao-ping surname: Zhu fullname: Zhu, Shao-ping organization: Laboratory Animal Center, Guangdong Medical University, Zhanjiang, Guangdong, China – sequence: 12 givenname: Qing-jun surname: Pan fullname: Pan, Qing-jun organization: Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases co-sponsored by province and city, Zhanjiang, Guangdong, China – sequence: 13 givenname: Ning surname: An fullname: An, Ning email: an347@163.com organization: Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases co-sponsored by province and city, Zhanjiang, Guangdong, China – sequence: 14 givenname: Hua-feng surname: Liu fullname: Liu, Hua-feng email: liu@263.net organization: Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases co-sponsored by province and city, Zhanjiang, Guangdong, China |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/35414608$$D View this record in MEDLINE/PubMed |
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| DOI | 10.1136/lupus-2021-000611 |
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| Keywords | Lupus Nephritis Lupus Erythematosus, Systemic Therapeutics |
| Language | English |
| License | This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/. Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ. |
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| PublicationTitle | Lupus science & medicine |
| PublicationTitleAbbrev | Lupus Sci Med |
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| Snippet | ObjectiveLupus nephritis (LN) is a major complication and cause of death among patients with SLE. This research used in vivo and in vitro experiments to... Lupus nephritis (LN) is a major complication and cause of death among patients with SLE. This research used in vivo and in vitro experiments to explore the... Objective Lupus nephritis (LN) is a major complication and cause of death among patients with SLE. This research used in vivo and in vitro experiments to... |
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| SubjectTerms | AMP-Activated Protein Kinases - metabolism AMP-Activated Protein Kinases - pharmacology Animals Antidiabetics Apoptosis Creatinine Humans Inflammation Kidney - metabolism Kidneys Kinases Laboratory animals Lipopolysaccharides - metabolism Lipopolysaccharides - pharmacology Lipopolysaccharides - therapeutic use Lupus Lupus Erythematosus, Systemic Lupus Erythematosus, Systemic - complications Lupus Erythematosus, Systemic - drug therapy Lupus Nephritis Lupus Nephritis - complications Lupus Nephritis - drug therapy Metformin - pharmacology Metformin - therapeutic use Mice Mice, Inbred MRL lpr Monoclonal antibodies NLR Family, Pyrin Domain-Containing 3 Protein - metabolism Proteins Signal Transduction - physiology STAT3 Transcription Factor - metabolism STAT3 Transcription Factor - pharmacology STAT3 Transcription Factor - therapeutic use Therapeutics Tumor Necrosis Factor-alpha - metabolism Tumor Necrosis Factor-alpha - pharmacology Tumor Necrosis Factor-alpha - therapeutic use Tumor necrosis factor-TNF |
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| Title | Metformin improves renal injury of MRL/lpr lupus-prone mice via the AMPK/STAT3 pathway |
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