<HashMap><database>biostudies-arrayexpress</database><scores/><additional><submitter>Peisen Ruan</submitter><organism>Rattus norvegicus</organism><software>DESeq2 v1.30.0, StringTie v2.1.4</software><software>HISAT2 v2.1.0, StringTie v2.1.4</software><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/E-MTAB-17471</full_dataset_link><description>This study aimed to investigate the cardioprotective mechanism of baicalin (BAI) against myocardial ischemia-reperfusion injury (MIRI) in rats. We performed RNA-seq on left ventricular myocardial tissue from three groups: Sham (vehicle control), I/R (ischemia-reperfusion injury model), and I/R+BAI (baicalin treatment 100 mg/kg administered 10 min prior to reperfusion). The goal was to identify differentially expressed genes and key biological pathways affected by baicalin treatment. Transcriptomic analysis revealed that baicalin reversed I/R-induced activation of innate immune pathways, including complement activation, neutrophil degranulation, and TLR signaling.</description><repository>biostudies-arrayexpress</repository><sample_protocol>Growth Protocol - Male Sprague-Dawley rats (250-300 g, 8 weeks old) were housed in a specific pathogen-free facility under controlled conditions (22 ± 2°C, 50% ± 10% humidity, 12 h light/dark cycle) with free access to food and water.</sample_protocol><sample_protocol>Library Construction - RNA libraries were constructed using the NEBNext Ultra RNA Library Prep Kit (NEB) following the manufacturer's instructions. Briefly, mRNA was enriched from total RNA using oligo-dT magnetic beads, fragmented, and reverse-transcribed into cDNA. After end-repair, adapter ligation, and PCR amplification, the final cDNA libraries were quality-checked.</sample_protocol><sample_protocol>Sample Treatment - Rats were randomly assigned to three groups: Sham (Vehicle), I/R (ischemia-reperfusion injury model), and I/R+BAI (baicalin treatment). The I/R model was established by 45 min of left anterior descending coronary artery ligation followed by 24 h of reperfusion. Baicalin (100 mg/kg) was administered via intraperitoneal injection 10 minutes prior to reperfusion. The Vehicle group received an equivalent volume of saline containing 1% CMC-Na.</sample_protocol><sample_protocol>Nucleic Acid Extraction - Total RNA was extracted from myocardial tissue using TRIzol reagent (Invitrogen) according to the manufacturer's protocol. RNA quality and integrity were assessed using an Agilent 2100 Bioanalyzer. Only samples with RNA Integrity Number (RIN) greater than 7.0 were used for subsequent library preparation.</sample_protocol><sample_protocol>Sample Collection - Left ventricular myocardial tissue samples were collected from SD rats 24 hours after reperfusion. The heart was rapidly excised, rinsed with pre-cooled saline, and the left ventricle was dissected. Tissue samples were immediately flash-frozen in liquid nitrogen and stored at -80°C until RNA extraction.</sample_protocol><sample_protocol>Sequencing - Libraries were sequenced on a GenMind 9000 platform (or your actual platform) using a paired-end 150 bp sequencing strategy. Raw sequencing data were generated in FASTQ format.</sample_protocol><figure_sub>Organization</figure_sub><figure_sub>MINSEQE Score</figure_sub><figure_sub>Assays and Data</figure_sub><figure_sub>Processed Data</figure_sub><figure_sub>MAGE-TAB Files</figure_sub><data_protocol>Sequence Alignment - Raw sequencing reads were aligned to the Rattus norvegicus reference genome assembly rn6 using HISAT2 (v2.1.0) with default parameters. Aligned reads were then assembled and quantified at the gene level using StringTie (v2.1.4).</data_protocol><data_protocol>Data Transformation - Raw sequencing reads were quality-controlled using FastQC. Clean reads were aligned to the rat reference genome (rn6) using HISAT2. Gene expression was quantified using StringTie, and differential expression analysis was performed using the DESeq2 package with criteria |log2FC| > 1 and adjusted p-value &lt; 0.05. The processed data file contains the normalized gene count matrix.</data_protocol><omics_type>Unknown</omics_type><omics_type>Transcriptomics</omics_type><omics_type>Genomics</omics_type><omics_type>Proteomics</omics_type><instrument_platform>Illumina NovaSeq 6000</instrument_platform><study_type>RNA-seq of coding RNA</study_type><species>Rattus norvegicus</species><pubmed_title>Baicalin Attenuates Myocardial Ischemia-Reperfusion Injury by Interacting with the TLR4/MD-2 Complex and Suppressing the Complement-Neutrophil-NETs Amplification Axis</pubmed_title><pubmed_authors>Peisen Ruan</pubmed_authors><pubmed_authors>Jiapei Wang, Yao Zheng, Yan Wang, Zhuoya Dong, Hang Yu, Huan Chen, Yuxuan Zhu, Peisen Ruan, Hehe Chen</pubmed_authors></additional><is_claimable>false</is_claimable><name>RNA-seq of rat myocardial tissue to investigate the cardioprotective mechanism of baicalin in myocardial ischemia-reperfusion injury</name><description>This study aimed to investigate the cardioprotective mechanism of baicalin (BAI) against myocardial ischemia-reperfusion injury (MIRI) in rats. We performed RNA-seq on left ventricular myocardial tissue from three groups: Sham (vehicle control), I/R (ischemia-reperfusion injury model), and I/R+BAI (baicalin treatment 100 mg/kg administered 10 min prior to reperfusion). The goal was to identify differentially expressed genes and key biological pathways affected by baicalin treatment. Transcriptomic analysis revealed that baicalin reversed I/R-induced activation of innate immune pathways, including complement activation, neutrophil degranulation, and TLR signaling.</description><dates><release>2026-07-31T00:00:00Z</release><modification>2026-08-05T12:40:06.162Z</modification><creation>2026-08-05T12:39:49.213Z</creation></dates><accession>E-MTAB-17471</accession><cross_references><ENA>ERP203371</ENA><EFO>EFO_0002944</EFO><EFO>EFO_0004170</EFO><EFO>EFO_0003789</EFO><EFO>EFO_0004917</EFO><EFO>EFO_0005518</EFO><EFO>EFO_0003816</EFO><EFO>EFO_0003738</EFO><EFO>EFO_0004184</EFO><EFO>EFO_0003969</EFO></cross_references></HashMap>