Transcriptome sequencing of palmitic acid-treated HepG2 cells upon intervention of curcumin or curcumin-copper complex
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE270357 | GEO | 2026/06/19
REPOSITORIES: GEO
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Project description:Purpose: The goals of this study are to compare NGS-derived gingiva transcriptome profiling (RNA-seq) of rats with or without experimental periodontitis and to explore the effect of curcumin/ZNPs hydrogel on the transcription of gingiva in rats with periodontitis. Methods: Six-week-old male Sprague-Dawley rats weighing 250–300 g (Dashuo company, China) were randomly divided into five groups (n = 5 per group): i) healthy control (Sham); ii) experimental periodontitis (EP); iii) experimental periodontitis treated by curcumin hydrogel (EP+Cur); iv) experimental periodontitis treated by ZNPs hydrogel (EP+ZNPs); v) experimental periodontitis treated by curcumin/ZNPs hydrogel (EP+Cur/ZNPs). Animals were anesthetized with isoflurane (5% induction, 2% maintenance, sealed until euthanized) and intramuscularly administered 0.1 mL penicillin (40,000 U/mL) for 7 days. EP was established by ligature with 4–0 silk thread around the bilateral maxillary first molars. Three days after ligature, P. gingivalis ATCC 33277 (107 CFU/mL) was smeared onto silk twice. Rats in the EP+Cur group were treated by curcumin hydrogel (Dalian Meilun Biotech Co., Ltd), EP+ZNPs group were treated by ZNPs hydrogel (Shanghai aladdin Biochemical Technology Co., Ltd), and EP+Cur/ZNPs group were treated by curcumin/ZNPs hydrogel. Total RNA was extracted with TRIzol® reagent (Thermo Fisher Scientific, Inc.). The TruSeq Stranded total RNA with RiboZero Plus kit (IIlumina, San Diego, CA) was used to obtain a sequencing library from 1μg of total RNA. Eukaryotic mRNA sequencing was performed on Illumina Novaseq 6000 by Shanghai Majorbio Bio-pharm Technology Co., Ltd. Raw gene counts with a minimum of two counts per million in at least one sample were used for downstream analyses. Differentially expressed genes were determined by the DESeq2 Bioconductor/R package. qRT–PCR validation was performed using TaqMan and SYBR Green assays. Results: Transcriptome analysis of 25 samples was completed in this project, and a total of 184.45 Gb Clean Data was obtained. The Clean Data of each sample reached 5.92 Gb and above, and the Q30 base percentage was above 92.75%. The Clean Reads of each sample were compared with the designated reference genome, and the comparison rate ranged from 93.38% to 95.1%. A total of 26188 expressed genes were detected in this analysis, including 22736 known genes and 3452 new genes; 57,961 expressed transcripts, including 29332 known transcripts and 28629 new transcripts. Conclusions: Our study represents the first detailed analysis of gingival transcriptomes of rats treated by Cur/ZnO gel, with biologic replicates, generated by RNA-seq technology.
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Project description:Background: Parkinson’s disease (PD), a severe threat in aging society, is a significant cause of disable. Curcumin, a polyphenol with hydrophobic properties, has been proved to against Parkinson. Our previous study provides an initial understanding of the neuroprotective mechanisms of curcumin in treating Parkinson’s disease. However, further exploration in this area is needed. The present study was designed to investigate the potential mechanism of curcumin for treating PD. Methods: The therapeutic efficacy of curcumin was evaluated using behavioral tests, immunofluorescence of tyrosine hydroxylase (TH). Network pharmacology and transcriptomics predicted the active pathway and bioprocess of curcumin in PD. Activation of the PI3K / AKT signaling pathway was confirmed by quantitative real-time PCR and immunofluorescence. Result: Curcumin restored the dyskinesia and dopaminergic neurons damage of MPTP-induced mice. The results of network pharmacology and transcriptomics showed that curcumin against Parkinson's disease by regulating inflammation, oxidative stress, and aging. The mechanisms of these were associated with activation of PI3K / AKT pathway. Conclusion: In conclusion, the mechanism of curcumin against PD was revealed by our study which lays a foundation for the application of curcumin in treating.
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Project description:Colorectal cancer (CRC) remains the leading cause of cancer-related death in the world. Aspirin (ASA) and curcumin (CUR) are widely investigated chemopreventive candidates for CRC. However, the precise mechanisms of their action and their combinatorial effects have not been evaluated. The purpose of the present study was to determine the effect of ASA, CUR, and their combination in azoxymethane/dextran sulfate sodium (AOM/DSS)-induced colitis-accelerated colorectal cancer (CAC). We also aimed to characterize the differential gene expression profiles in AOM/DSS-induced tumors as well as in tumors modulated by ASA and CUR using RNA-seq. Diets supplemented with 0.02% ASA, 2% CUR or 0.01% ASA + 1% CUR were given to mice from 1 week prior to the AOM injection until the experiment was terminated 22 weeks after AOM initiation. Our results showed that CUR had a superior inhibitory effect in colon tumorigenesis compared to that of ASA. The combination of ASA and CUR at a lower dose exhibited similar efficacy to that of a higher dose of CUR at 2%. RNA isolated from colonic tissue from the control group and from tumor samples from the experimental groups was subjected to RNA-seq. Transcriptomic analysis suggested that the low-dose combination of ASA and CUR modulated larger gene sets than the single treatment. These differentially expressed genes were situated in several canonical pathways important in the inflammatory network and liver metastasis in CAC. We identified a small subset of genes as potential molecular targets involved in the preventive action of the combination of ASA and CUR. Taken together, the current results provide the first evidence in support of the chemopreventive effect of a low-dose combination of ASA and CUR in CAC. Moreover, the transcriptional profile obtained in our study may provide a framework for identifying the mechanisms underlying the carcinogenesis process from normal colonic tissue to tumor development as well as the cancer inhibitory effects and potential molecular targets of ASA and CUR.
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