RNA sequence analysis of rat acute experimental pancreatitis with and without fatty liver: a gene expression profiling comparative study

Wang, Qian; Yan, Hongkai; Wang, Gang; Qiu, Zhaoyan; Bai, Bin; Wang, Shiqi; Yu, Pengfei; Feng, Quanxin; Zhao, Qingchuan; He, Xianli; Liu, Chaoxu

doi:10.1038/s41598-017-00821-5

Cited by 15 publications

(10 citation statements)

References 53 publications

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“…RNA sequencing is a useful technology with an advantage in discovering novel tissue-and disease-specific ncRNAs, whereas microarray and qRT-PCR can only measure the expression levels of known ncRNAs 10 , 16 . To date, RNA sequencing has been widely used in transcriptome profiles analyses 17 .…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA expression patterns in lung tissues of chronic cigarette smoke induced COPD mouse model

Zhang

Sun

et al. 2018

Sci Rep

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Long non-coding RNAs (lncRNAs) have critical regulatory roles in protein-coding gene expression. Aberrant expression profiles of lncRNAs have been observed in various human diseases. In this study, we investigated transcriptome profiles in lung tissues of chronic cigarette smoke (CS)-induced COPD mouse model. We found that 109 lncRNAs and 260 mRNAs were significantly differential expressed in lungs of chronic CS-induced COPD mouse model compared with control animals. GO and KEGG analyses indicated that differentially expressed lncRNAs associated protein-coding genes were mainly involved in protein processing of endoplasmic reticulum pathway, and taurine and hypotaurine metabolism pathway. The combination of high throughput data analysis and the results of qRT-PCR validation in lungs of chronic CS-induced COPD mouse model, 16HBE cells with CSE treatment and PBMC from patients with COPD revealed that NR_102714 and its associated protein-coding gene UCHL1 might be involved in the development of COPD both in mouse and human. In conclusion, our study demonstrated that aberrant expression profiles of lncRNAs and mRNAs existed in lungs of chronic CS-induced COPD mouse model. From animal models perspective, these results might provide further clues to investigate biological functions of lncRNAs and their potential target protein-coding genes in the pathogenesis of COPD.

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Section: Introductionmentioning

confidence: 99%

Long non-coding RNA expression patterns in lung tissues of chronic cigarette smoke induced COPD mouse model

Zhang

Sun

et al. 2018

Sci Rep

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“…Among them, PPAR signaling was an extremely important pathway. The PPAR signaling pathway has been considered to be related to the pathological processes of fatty liver development in rats with acute pancreatitis [ 17 ]. PPARA was a nuclear hormone receptor and important regulator of lipid metabolism in the liver.…”

Section: Discussionmentioning

confidence: 99%

Use of Network Pharmacology to Investigate the Mechanism by Which Allicin Ameliorates Lipid Metabolism Disorder in HepG2 Cells

Cheng

2021

Evidence-Based Complementary and Alternative Medicine

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Allicin has been well documented to exhibit a wide spectrum of biological activities, especially lipid-lowering activity, as a promising candidate for the management of nonalcoholic fatty liver disease (NALFD). However, the mechanisms underlying the therapeutic effects of allicin require further investigation. It is tempting to think of combining network pharmacology and experimental validation to investigate the mechanism by which allicin ameliorates lipid metabolism disorder in HepG2 cells. We established a cell model of hepatic steatosis induced by PA to investigate the antisteatotic effects of allicin. The studies showed that allicin reduced PA-induced lipid accumulation using Nile red staining and TC and TG assays. Then, 219 potential targets of allicin were successfully predicted by PharmMapper. According to Reactome Pathway Analysis, 44 potential targets related to lipid metabolism were screened out. Molecular signaling cascades mediated by allicin included PPARA, PPARG, FABP4, and FABP6 by cytoHubba and qPCR analysis. Results revealed that allicin activated the gene expression of PPARA and FABP6 and suppressed the gene expression of FABP4 and PPARG. Thus, the present study united the methods of network pharmacology and experimental validation to investigate the protein targets of allicin on PA-induced lipid metabolism disorders to supply a reference for related application for the first time.

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“…High triglyceride level is also a risk factor, serum triglyceride level higher than 5.6 mmol/L significantly increases the mortality rate (OR = 2.75, 95% CI = 1.28–5.92, p < 0.01) [ 16 ]. An experimental study in rat AP model demonstrated that the presence of FLD increased pro-inflammatory cytokine production, which may worsen the course of the disease [ 17 ]. Cross-sectional studies confirmed that AP is often accompanied by FLD, with a prevalence between 18–43% [ 18 , 19 ].…”

Section: Introductionmentioning

confidence: 99%

Fatty Liver Disease and Non-Alcoholic Fatty Liver Disease Worsen the Outcome in Acute Pancreatitis: A Systematic Review and Meta-Analysis

Váncsa

Németh

Hegyi

et al. 2020

JCM

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The prevalence of fatty liver disease (FLD) and that of non-alcoholic fatty liver disease (NAFLD) share some risk factors known to exacerbate the course of acute pancreatitis (AP). This meta-analysis aimed to investigate whether FLD or NAFLD carry a higher risk of untoward outcomes in AP. In accordance with PRISMA guidelines, we performed a systematic search in seven medical databases for cohort studies that compared the outcomes of AP for the presence of FLD or NAFLD, and we calculated pooled odds ratio (OR) or weighted mean difference (WMD) with 95% confidence interval (CI). We included 13 articles in our meta-analysis. AP patients with FLD were more likely to die (5.09% vs 1.89%, OR = 3.56, CI = 1.75–7.22), develop severe AP (16.33% vs 7.87%, OR = 2.67, CI = 2.01–3.56), necrotizing pancreatitis (34.83% vs 15.75%, OR = 3.08, CI = 2.44–3.90) and had longer in-hospital stay (10.8 vs 9.2 days, WMD = 1.46, OR = 0.54–2.39). Patients with NAFLD were more likely to have severe AP and longer hospital stay. Both FLD and NAFLD proved to be independent risk factors of a more severe disease course (OR = 3.68, CI = 2.16–6.29 and OR = 3.39, CI = 1.52–7.56 for moderate/ severe vs. mild AP, respectively). FLD and NAFLD worsen the outcomes of AP, which suggests that incorporating FLD or NAFLD into prognostic scoring systems of AP outcomes might improve the prediction of severity and contribute to a more individualized patient care.

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RNA sequence analysis of rat acute experimental pancreatitis with and without fatty liver: a gene expression profiling comparative study

Cited by 15 publications

References 53 publications

Long non-coding RNA expression patterns in lung tissues of chronic cigarette smoke induced COPD mouse model

Long non-coding RNA expression patterns in lung tissues of chronic cigarette smoke induced COPD mouse model

Use of Network Pharmacology to Investigate the Mechanism by Which Allicin Ameliorates Lipid Metabolism Disorder in HepG2 Cells

Fatty Liver Disease and Non-Alcoholic Fatty Liver Disease Worsen the Outcome in Acute Pancreatitis: A Systematic Review and Meta-Analysis

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