Summary of Study ST002390

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR001537. The data can be accessed directly via it's Project DOI: 10.21228/M81B0N This work is supported by NIH grant, U2C- DK119886.

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This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.

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Study IDST002390
Study TitleThe metabolomic resetting effect of DMXAA in cisplatin-induced injured mouse kidney
Study SummaryA single injection of cisplatin was used to induce AKI in mice. To assess the effect of DMXAA, the mice were injected intraperitoneally with DMXAA or vehicle one hour before cisplatin injection, repeated every 24 hours. The mice were euthanized 72 hours after cisplatin injection, and renal tissues were collected for MS analysis.
Institute
Children's Hospital of Nanjing Medical University
Last NameLu
First NameLingling
AddressGuangzhou Road 72, Nanjing, Jiangsu, 210000, China
Emaillulingling89tara@163.com
Phone0086-25-8311-7435
Submit Date2022-12-05
Raw Data AvailableYes
Raw Data File Type(s)mzML
Analysis Type DetailLC-MS
Release Date2023-03-03
Release Version1
Lingling Lu Lingling Lu
https://dx.doi.org/10.21228/M81B0N
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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Project:

Project ID:PR001537
Project DOI:doi: 10.21228/M81B0N
Project Title:The metabolomic resetting effect of DMXAA in cisplatin-induced AKI
Project Type:MS quantitative analysis
Project Summary:Cisplatin-induced nephrotoxicity is the main adverse effect of cisplatin-based chemotherapy, which highly limits the clinical use of cisplatin. DMXAA, a flavonoid derivative as a known agonist of STING, has been served as a promising antivascular agent. Although cGAS-STING activation has been demonstrated to mediate cisplatin-induced AKI, the role of DMXAA in this condition is unclear. Here, we defined an unexpected and critical role of DMXAA in improving renal function, ameliorating renal tubular injury and cell apoptosis, suppressing inflammation in cisplatin-induced AKI. Moreover, we confirmed that DMXAA combated AKI in a STING-independent manner evidenced by its protection against AKI in STING knockout mice. Due to the established role of metabolic disorders in AKI, which could contribute to the injury and kidney recovery, we performed metabolomics using renal tissues from cisplatin-induced AKI mice with or without DMXAA treatment. Strikingly, the date revealed that DMXAA improved the metabolic disorders in kidneys of AKI mice, especially restored the tryptophan metabolism.
Institute:Children's Hospital of Nanjing Medical University
Department:Department of Nephrology, State Key Laboratory of Reproductive Medicine,
Laboratory:Nanjing Key Lab of Pediatrics, Jiangsu Key Laboratory of Pediatrics
Last Name:Lu
First Name:Lingling
Address:Guangzhou Road 72, Nanjing, Jiangsu, 210000, China
Email:lulingling89tara@163.com
Phone:0086-25-8311-7435
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