Ontology highlight
ABSTRACT:
PROVIDER: PRJNA753953 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15430004.fastq.gz | Fastqsanger.gz | |||
| SRR15430005.fastq.gz | Fastqsanger.gz | |||
| SRR15430006.fastq.gz | Fastqsanger.gz | |||
| SRR15430007.fastq.gz | Fastqsanger.gz | |||
| SRR15430008.fastq.gz | Fastqsanger.gz |
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Project description:Objective: Benzbromarone (BBR) is an effective uric acid-lowering drug. However, it can induce severe liver damage in some patients. Studies have shown that BBR specifically exacerbates hepatic steatosis in obese individuals, leading to aggravated liver injury. The exact mechanism behind this phenomenon remains unclear. Methods: db/db mice were divided into four groups: Control, BBR administration (BBR), Pparg knockdown (Pparg-KD), and BBR administration with Pparg knockdown (BBR + Pparg-KD). One week after AAV8-shRNA-Pparg virus injection, mice were orally administered BBR for four weeks, and changes in blood glucose and body weight were measured. Subsequently, samples were collected, and plasma lipid levels, hepatic lipid content, and liver function parameters were determined. RNA-seq was performed to assess changes in the hepatic gene expression profile and analyze the protective effect of PPARγ knockdown on BBR-induced drug-induced liver injury. Results: Mice in the BBR group exhibited more severe levels of plasma lipids, hepatic lipids, and liver function parameters compared to the Control group. However, mice in the BBR + Pparg-KD group showed significant improvements in these indicators compared to the BBR group. Transcriptomic analysis revealed that BBR administration upregulated the expression of various lipid synthesis-related genes, primarily associated with the PPAR signaling pathway. Furthermore, PPARγ knockdown reversed the increased expression of these lipid synthesis genes. This suggests that PPARγ knockdown has a significant protective effect against BBR-induced drug-induced liver injury. Conclusion: Hepatocyte-specific knockdown of PPARγ can protect against BBR-induced exacerbation of hepatic steatosis and liver injury by inhibiting the promotion of lipid synthesis through PPARγ activation.
2025-01-29 | GSE274748 | GEO
Project description:Accumulating evidence suggests that berberine (BBR) exhibits anti-cancer effects in hepatocellular carcinoma (HCC). However, the mechanisms by which BBR regulates the immunological microenvironment in HCC has not been fully elucidated. In this study, we established a mouse model of orthotopic HCC and treated with varying doses of BBR. BBR showed effectiveness in reducing tumor burden in mice with HCC. Cytometry by time-of-flight depicted the alterations in the tumor immune landscape following BBR treatment, revealing the enhancement in the T lymphocytes effector function. In particular, BBR decreased the proportion of TCRbhiPD-1hiCD69+CD27+CD8a+ effector CD8+ T lymphocytes and increased the proportion of Ly6ChiTCRb+CD69+CD27+CD62L+ central memory CD8+ T lymphocytes. Single-cell RNA sequencing further elucidate the effects of BBR on transcriptional profiles of liver immune cell and confirmed the phenotypical heterogeneity of T lymphocytes in HCC immune microenvironment. Additionally, we found that BBR potentially regulated the antitumor immunity in HCC by modulating the receptor-ligand interaction among immune cells mediated by cytokines. In summary, our findings improve the understanding of BBR's impact on protecting against HCC, emphasizing BBR's role in regulating intrahepatic T cell heterogeneity. BBR has the potential to be a promising therapeutic strategy to hinder the advancement of HCC.
2025-05-21 | GSE271243 | GEO
Project description:Objective: Benzbromarone (BBR) is an effective uric acid-lowering drug, and studies have shown that BBR can exacerbate hepatic steatosis in obese individuals. However, the underlying mechanisms remain unclear. Methods: Primary hepatocytes isolated from C57/BL6 mice were cultured in vitro, and a high-fat culture model was simulated with 20mM oleic acid (OA) treatment. OA and bovine serum albumin (BSA) were mixed at a ratio of 1:4, pre-treated at 37°C for 1-2 hours, and then co-incubated with primary hepatocytes for 16 hours. The in vitro experiments were divided into four groups: control (BSA), control treatment group (BSA+BBR), high-fat group (OA), and high-fat treatment group (OA+BBR). After 16 hours of treatment, intracellular triglyceride (TAG) content was measured, and Bodipy staining was used to observe the number and morphological changes of lipid droplets. RNA-seq analysis was conducted to assess changes in the gene expression profile of hepatocytes with BBR treatment under BSA and OA conditions. Results: BBR significantly increased the intracellular TAG content in primary hepatocytes treated with OA, while no significant increase was observed in the BSA treatment group. Bodipy staining experiments also confirmed that BBR led to an increase in the number and size of lipid droplets under OA treatment. Transcriptomic data revealed that under both BSA and OA conditions, BBR upregulated the expression of a large number of genes related to lipid synthesis, which were associated with the activation of the PPARγ signaling pathway. Conclusion: BBR promotes the expression of genes involved in lipid synthesis in primary hepatocytes by activating PPARγ, leading to specific hepatic lipid accumulation under high-fat conditions.
2025-01-29 | GSE274374 | GEO
Project description:To investigate the mechanism of BBR improved intestinal mucosa induced by 5-fluorouracil-induced in mice
2024-08-15 | GSE215201 | GEO
Project description:Insulin resistance (IR) is likely to induce metabolic syndrome and type 2 diabetes mellitus (T2DM). Gluconeogenesis (GNG) is a complex metabolic process that may result in glucose generation from certain non-carbohydrate substrates. Chinese herbal medicine astragalus polysaccharides and berberine have been documented to ameliorate IR, and combined use of astragalus polysaccharide (AP) and berberine (BBR) are reported to synergistically produce an even better effect. However, what change may occur in the GNG signaling pathway of IR-HepG2 cells in this synergistic effect and whether AP-BBR attenuates IR by regulating the GNG signaling pathway remain unclear. For the first time, we discovered in this study that the optimal time of IR-HepG2 cell model formation was 48 hours after insulin intervention. AP-BBR attenuated IR in HepG2 cells and the optimal concentration was 10mg. AP-BBR reduced the intracellular H2O2 content with no significant effect on apoptosis of IR-HepG2 cells. In addition, a rapid change was observed in intracellular calcium current of the IR-HepG2 cell model, and AP-BBR intervention attenuated this change markedly. The gene sequencing results showed that the GNG signaling pathway was one of the signaling pathways of AP-BBR to attenuate IR in IR-Hepg2 cells. The expression of p-FoxO1Ser256 and PEPCK protein was increased and the expression of GLUT2 protein was decreased significantly in the IR-HepG2 cell model, and both of these effects could be reversed by AP-BBR intervention. AP-BBR attenuated IR in IR-HepG2 cells, probably by regulating the GNG signaling Pathway.
2019-11-14 | GSE139929 | GEO
Project description:RNA sequecing of isolated mouse islets from C57BL/6J mice fed high fat diet following control or AAV-mIP2-GCK injection.
2018-05-23 | GSE104581 | GEO