Expression data from Botryococcus terribilis ethanol extract (BTEE)-treated RAW264 cells
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ABSTRACT:
PROVIDER: PRJNA915347 | ENA |
REPOSITORIES: ENA
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Project description:Gene expression profiling reveals anti-inflammatory effects of BTEE on lipopolysaccharide (LPS)-induced murine RAW264 cells We evaluated the pretreatment effect of BTEE on LPS-induced inflammation in RAW264 cells. Pretreatment with BTEE could significantly attenuate nitric oxide (NO) production and LPS-induced release of inflammatory mediators in RAW264 cells.
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Project description:In an attempt to elucidate the role of MiT/TFE families in the iron-mediated phenotypic changes of macrophages, we performed DNA microarray analysis using ferric chloride-stimulated RAW264 cells transfected with Tfe3/Tfeb or GFP. A number of genes upregulated by ferric chloride treatment in siGFP-transfected RAW264 cells were decreased in siTfe3/Tfeb-transfected cells, suggesting MiT/TFE families are involved in phenotypic changes of macrophages induced by iron.
2021-01-27 | GSE157472 | GEO
Project description:Comparative study of transcriptome expression in water extract and ethanol extract of Schisandra chinensis
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Project description:Objective: Hepatotoxicity has been reported for Emilia sonchifolia (L.) DC (Emilia sonchifolia). The plant material is typically prepared using two extraction methods for practical application: water extraction and ethanol extraction. However, our previous research only investigated its water extract. Therefore, this study aims to systematically evaluate the hepatotoxicity and underlying mechanisms of the ethanol extract of Emilia sonchifolia, thereby providing a more comprehensive scientific basis for its rational application and safety assessment. Methods: An acute toxicity preliminary screening study was conducted by orally administering Emilia sonchifolia ethanol extract to mice at doses ranging from 0 to 33.6 g/kg/day. Based on the results of the acute toxicity test preliminary screening study, mice were divided into a control group and an Emilia sonchifolia ethanol extract group (8.6 g/kg/day) for a 14-day delayed hepatotoxicity experiment based on clinical treatment duration. At the end of the intervention, hepatic pathological changes were examined using hematoxylin-eosin staining. Enzyme-linked immunosorbent assay (ELISA) was employed to quantify the levels of alanine aminotransferase , aspartate aminotransferase, total bilirubin, direct bilirubin, total bile acids, alkaline phosphatase, and γ-glutamyl transferase in serum, as well as malondialdehyde, superoxide dismutase, and catalase in liver tissue. Proteomics and metabolomics analyses were performed to investigate the mechanisms of hepatotoxicity induced by the ethanol extract. Additionally, the mRNA expression levels of Cyp3a41a, Cyp2c29, Ugt2b1, and Hsd3b3 in mice liver tissue were determined using quantitative reverse transcription polymerase chain reaction (qRT-PCR). Results: The acute toxicity preliminary screening study results showed that a dose of 12.0 g/kg or higher of the Emilia sonchifolia ethanol extract caused acute liver failure and death in mice. A dose of 8.6 g/kg or lower of the Emilia sonchifolia ethanol extract produced dose-dependent acute hepatotoxicity. Meanwhile, a dose of 8.6 g/kg of the Emilia sonchifolia ethanol extract induced delayed toxicities in mice. Proteomics and metabolomics results revealed that the hepatotoxicity induced by the ethanol extract of Emilia sonchifolia was associated with cholestasis and oxidative stress caused by disruptions in drug metabolism, steroid hormone biosynthesis, and primary bile acid biosynthesis. Validation experiments showed that the levels of Cyp2c29 were decreased, while the mRNA levels of Cyp3a41a, Ugt2b1, and Hsd3b3 were increased in the liver tissues of mice treated with the ethanol extract of Emilia sonchifolia. Additionally, serum levels of total bilirubin, direct bilirubin, total bile acids, alkaline phosphatase, and γ-glutamyl transferase were significantly elevated. Furthermore, in the livers of mice treated with the ethanol extract, malondialdehyde levels were increased, whereas superoxide dismutase and catalase levels were decreased. Conclusion: In summary, the ethanol extract of Emilia sonchifolia can induce hepatotoxicity in mice, and its mechanism is associated with cholestasis and oxidative stress mediated by disruptions in drug metabolism, steroid hormone biosynthesis, and primary bile acid biosynthesis.
2025-10-30 | PXD070070 |
Project description:We explored whether an ethanol extract of coptidis rhizoma (ECR) exhibited anti-teratoma activity and identified the main active components involved in the selective elimination of undifferentiated iPSCs.
2023-05-20 | GSE225709 | GEO
Project description:<p>Objective: Hepatotoxicity has been reported for Emilia sonchifolia (L.) DC (Emilia sonchifolia). The plant material is typically prepared using two extraction methods for practical application: water extraction and ethanol extraction. However, our previous research only investigated its water extract. Therefore, this study aims to systematically evaluate the hepatotoxicity and underlying mechanisms of the ethanol extract of Emilia sonchifolia, thereby providing a more comprehensive scientific basis for its rational application and safety assessment.</p><p>Methods: An acute toxicity preliminary screening study was conducted by orally administering Emilia sonchifolia ethanol extract to mice at doses ranging from 0 to 33.6 g/kg/day. Based on the results of the acute toxicity test preliminary screening study, mice were divided into a control group and an Emilia sonchifolia ethanol extract group (8.6 g/kg/day) for a 14-day delayed hepatotoxicity experiment based on clinical treatment duration. At the end of the intervention, hepatic pathological changes were examined using hematoxylin-eosin staining. Enzyme-linked immunosorbent assay (ELISA) was employed to quantify the levels of alanine aminotransferase , aspartate aminotransferase, total bilirubin, direct bilirubin, total bile acids, alkaline phosphatase, and γ-glutamyl transferase in serum, as well as malondialdehyde, superoxide dismutase, and catalase in liver tissue. Proteomics and metabolomics analyses were performed to investigate the mechanisms of hepatotoxicity induced by the ethanol extract. Additionally, the mRNA expression levels of Cyp3a41a, Cyp2c29, Ugt2b1, and Hsd3b3 in mice liver tissue were determined using quantitative reverse transcription polymerase chain reaction (qRT-PCR).</p><p>Results: The acute toxicity preliminary screening study results showed that a dose of 12.0 g/kg or higher of the Emilia sonchifolia ethanol extract caused acute liver failure and death in mice. A dose of 8.6 g/kg or lower of the Emilia sonchifolia ethanol extract produced dose-dependent acute hepatotoxicity. Meanwhile, a dose of 8.6 g/kg of the Emilia sonchifolia ethanol extract induced delayed toxicities in mice. Proteomics and metabolomics results revealed that the hepatotoxicity induced by the ethanol extract of Emilia sonchifolia was associated with cholestasis and oxidative stress caused by disruptions in drug metabolism, steroid hormone biosynthesis, and primary bile acid biosynthesis. Validation experiments showed that the levels of Cyp2c29 were decreased, while the mRNA levels of Cyp3a41a, Ugt2b1, and Hsd3b3 were increased in the liver tissues of mice treated with the ethanol extract of Emilia sonchifolia. Additionally, serum levels of total bilirubin, direct bilirubin, total bile acids, alkaline phosphatase, and γ-glutamyl transferase were significantly elevated. Furthermore, in the livers of mice treated with the ethanol extract, malondialdehyde levels were increased, whereas superoxide dismutase and catalase levels were decreased.</p><p>Conclusion: In summary, the ethanol extract of Emilia sonchifolia can induce hepatotoxicity in mice, and its mechanism is associated with cholestasis and oxidative stress mediated by disruptions in drug metabolism, steroid hormone biosynthesis, and primary bile acid biosynthesis.</p>
2025-10-30 | MTBLS13237 | MetaboLights
Project description:We report the transcriptomic response of a moderately growing subisolate from the culture of Botryococcus sp. CCALA-779 upon nitrogen deprivation (ND).
2015-08-03 | GSE71296 | GEO
Project description:Purpose: The aim is to analyze the translational kinetics of the basal and LPS-stimulated conditions of RAW264 macrophages focusing on ribosome density Method: RAW264 macrophages were cultured at 3.0 x 10^5 cells/ml in media (DMEM, 2mM Glutamine, 10% FBS, 100 units penicillin and 100µg streptomycin/mL) 24 hours prior to harvest. It was confirmed that the confluency of cells never surpassed 80 ~ 90%. Cell were harvested in their basal state or LPS stimulated condition (100 ng/ml for 30 min) and ribosome profiling (Ribo-Seq) and high-throughput mRNA sequencing (mRNA-Seq) were conducted. Ribosome protected fragments (RPF) were sequenced and the density was normalized by mRNA abundance. Result and conclusion: We discovered where in the ribosome translational arrest ocurs and how this happens. Translational stall was striking at A-site and P-site of ribosomal complex. The other arrest site was observed 3 to 5 residues away from the peptidyl transfer center of the exit tunnel, in which ribosomal density and hydrophobicity showed a significant negative correlation. mRNA and RPF of RAW264 macrophages were deep-sequenced with two independent biological replicates by Ion PGM sequencer
2015-11-01 | E-GEOD-60930 | biostudies-arrayexpress
Project description:The role of G-protein-coupled receptors (GPCRs) in the macrophage polarization remains not well understood. In this study, we illuminate the role of Gpr137b, a GPCR expressed strongly in macrophages, in macrophage polarization. We used RAW264 as a mouse macrophage-like cell line and generated Gpr137b-knockout (KO) cell clones using the CRISPR/Cas9 genome editing system. The Gpr137b-KO and wildtype cells were the treated with interleukin-4 (IL-4) to induce M2 polarization, and their gene expression was analyzed using microarrays.
2018-10-01 | GSE117578 | GEO