DOI: 10.5061/dryad.zkh1893r3
title: 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

description: 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.
description: # 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 Dataset DOI:
 [10.5061/dryad.zkh1893r3](https://doi.org/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) &gt; 1.5 and p
 &lt; 0.05. The criteria for identifying down-regulated DEGs are: FC &lt;
 0.67 and p &lt; 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](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