Data from: mRNA sequencing-based DEGs: Licochalcone B suppresses oxidative stress and apoptosis accompanied by upregulating Nrf2/HO-1 pathway to ameliorate diabetic nephropathy in mice
Data files
Jan 30, 2026 version files 3.65 MB
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HFD_STZ_40LCB_vs_HFD_STZ_Differentially_Expressed_Genes.csv
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README.md
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Abstract
Introduction: Diabetic nephropathy (DN), as a complication of diabetes, is one of the major causes of end-stage renal disease. Licochalcone B (LCB), a flavonoid active component derived from licorice, is well known for its anti-inflammatory and antioxidant properties. However, the influence of LCB on DN remains unclear. This research investigated the effect of LCB on DN and elucidated the regulatory mechanism.
Methods: We employed male C57BL/6 mice to construct a DN mouse model induced by a high-fat diet (HFD)/streptozotocin (STZ). In vitro, a high glucose (HG)-induced injury model in HK-2 (human renal tubular epithelial) cells was used to further confirm the protective effects of LCB.
Results: LCB treatment (20 mg/kg and 40 mg/kg) decreased blood glucose levels, kidney injury, glycogen deposition, and collagen accumulation in the DN mice. Moreover, LCB at a dosage of 40 mg/kg reduced albumin, creatinine, and blood urea nitrogen levels by about 70.7%, 33.4%, and 45.6%, respectively, indicating an improvement in kidney function. In renal tissues, LCB suppressed oxidative stress and apoptosis in HFD/STZ-induced mice. Consistent with in vivo findings, LCB alleviated HG-induced oxidative stress and apoptosis in HK-2 cells. Transcriptome analysis revealed that LCB affects oxidative stress and renal function-related pathways to alleviate DN. Further mechanistic studies demonstrated that LCB treatment upregulates the expressions of heme oxygenase-1 (HO-1) and nuclear factor (erythroid-derived 2)-like 2 (Nrf2), suggesting activation of the Nrf2/HO-1 signaling pathway.
Conclusion: Taken together, this research demonstrates that LCB suppresses oxidative stress and apoptosis accompanied by modulating the Nrf2/HO-1 pathway to ameliorate DN, which provides a promising strategy for DN treatment.
Dataset DOI: 10.5061/dryad.zkh1893r3
Description of the data and file structure
The variables of the data file includes: Access number of the genes followed by the gene symbol, full information of the gene, gene expression expressed in log2(fold change). The data presented in this dataset provides information of the high-throughput mRNA sequencing-based DEGs in article “Licochalcone B suppresses oxidative stress and apoptosis accompanied by upregulating Nrf2/HO-1 pathway to ameliorate diabetic nephropathy in mice”.In brief, mice were reared with high-fat diet (HFD) for four weeks before being intraperitoneally injected with streptozotocin (STZ) for five days. Following STZ administration, mice in the treatment groups received LCB via gavage once every two days over an eight-week period. Afterward, kidney tissues were harvested for analysis. Extraction of total RNA was conducted from renal tissues in HFD/STZ-induced mice and HFD/STZ-induced mice administered with LCB. mRNA was captured from total RNA utilizing poly-T oligo-attached magnetic beads. Then, complementary DNA libraries were generated, and mRNA sequencing (mRNA-seq) was subjected to through the Illumina platform. The criteria for identifying up-regulated differentially expressed genes (DEGs) are: fold change (FC) > 1.5 and p < 0.05. The criteria for identifying down-regulated DEGs are: FC < 0.67 and p < 0.05. The column heading “symbol” indicates the name of DEGs. Missing data mentioned as n/a.
- ACCESS NUMBER: ESEMBL id (https://asia.ensembl.org/index.html) of the genes
- GENE: Gene name
- FULL INFORMATION: Description of the genes
- HFD STZ+40LCB vs HFD STZ FOLD CHANGE: Fold change in gene expression levels between HFD/STZ-induced mice treated with 40 mg/kg LCB and HFD/STZ-induced mice.
- HFD STZ+40LCB vs HFD STZ LOG2 (FOLD CHANGE): Log2(Fold change) in gene expression levels between HFD/STZ-induced mice treated with 40 mg/kg LCB and HFD/STZ-induced mice.
- P VALUE: P value of the genes
- ADJUST P VALUE: Adjusted p value of the genes
- HFD STZ REPLICATE 1:FPKM : FPKM value of the genes in biological replicate sample 1 from HFD/STZ-induced mice. FPKM is the abbreviation for "Fragments Per Kilobase of transcript per Million mapped fragments", which is the normalized expression value after standardizing the original count.
- HFD STZ REPLICATE 2:FPKM : FPKM value of the genes in biological replicate sample 2 from HFD/STZ-induced mice.
- HFD STZ REPLICATE 3:FPKM : FPKM value of the genes in biological replicate sample 3 from HFD/STZ-induced mice.
- HFD STZ REPLICATE 4:FPKM : FPKM value of the genes in biological replicate sample 4 from HFD/STZ-induced mice.
- HFD STZ REPLICATE 5:FPKM : FPKM value of the genes in biological replicate sample 5 from HFD/STZ-induced mice.
- HFD STZ+40LCB REPLICATE 1:FPKM : FPKM value of the genes in biological replicate sample 1 from HFD/STZ-induced mice treated with 40 mg/kg LCB.
- HFD STZ+40LCB REPLICATE 2:FPKM : FPKM value of the genes in biological replicate sample 2 from HFD/STZ-induced mice treated with 40 mg/kg LCB.
- HFD STZ+40LCB REPLICATE 3:FPKM : FPKM value of the genes in biological replicate sample 3 from HFD/STZ-induced mice treated with 40 mg/kg LCB.
- HFD STZ+40LCB REPLICATE 4:FPKM : FPKM value of the genes in biological replicate sample 4 from HFD/STZ-induced mice treated with 40 mg/kg LCB.
- HFD STZ+40LCB REPLICATE 5:FPKM : FPKM value of the genes in biological replicate sample 5 from HFD/STZ-induced mice treated with 40 mg/kg LCB.
Access information
Other publicly accessible locations of the data:
- Not applicable
Data was derived from the following sources:
- HFD_STZ_40LCB_vs_HFD_STZ_Differentially_Expressed_Genes.csv