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7-hydroxycoumarin-β-D-glucuronide protects against cisplatin-induced acute kidney injury via inhibiting p38 MAPK-mediated apoptosis in mice

GSE341145 Mus musculus (mouse) RNA-seq (gene expression) 20 samples Submitted 2026/07/28 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 20 samples

What it is
RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism
Mus musculus (mouse)
Samples
20 samples: 5 × Con vs 5 × M vs 5 × E2-15 vs 5 × E2-30Groups are read from the sample names, not from the paper. Check the list below.
Data you can get
A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Summary (written by the submitters)
Cisplatin is a common chemotherapeutic agent limited by severe nephrotoxicity, which easily induces acute kidney injury (AKI) in tumor patients. 7-hydroxycoumarin-β-D-glucuronide (7-HCG), a major kidney-enriched metabolite of coumarins from Hydrangea paniculata, was previously found to accumulate specifically in renal tissue with long elimination half-life.
Read the full summary ↓
In this study, male C57BL/6 mice were pretreated with 7-HCG at three doses, followed by intraperitoneal cisplatin injection to establish AKI model. Renal tissue mRNA sequencing was performed on control, cisplatin model, 15 mg/kg and 30 mg/kg 7-HCG groups to explore transcriptomic changes. Transcriptome analysis revealed that 7-HCG reversed dysregulated MAPK signaling and apoptosis pathways triggered by cisplatin. Further validation confirmed that 7-HCG reduced renal ROS production, suppressed phosphorylation of p38/ERK/JNK, and downregulated pro-apoptotic proteins Bax and cleaved-caspase3. This dataset provides transcriptomic evidence illustrating the protective mechanism of 7-HCG against cisplatin nephrotoxicity through p38 MAPK/apoptosis axis inhibition. All raw RNA-seq reads and processed gene expression matrices are deposited here for public reuse.
This dataset
Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE341145_RAW.tar (it can run to tens of gigabytes).

3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

What the files usually look like: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1499665 and SRA study SRP720670. Searching any of these in the dataset finder brings you back here.

Study design
5 × Con vs 5 × M vs 5 × E2-15 vs 5 × E2-30

Supports a between-group comparison across 20 samples.

How we read this: 4 replicated groups read from 20 sample titles; they account for 20 of them. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study
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Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.