Analysis of microRNA expression profiles induced by Yiqifumai Powder Injection in rats with chronic heart failure
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PROVIDER: PRJNA417231 | ENA |
REPOSITORIES: ENA
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Project description:To investigate the mechanism of Yiqifumai Powder Injectionthe on treating chronic heart diseases. We have employed a microRNAs microarray to identify the pivotal miRNAs altered by Yiqifumai compared to chronic heart injury and control group samples. 7 miRNAs accord with a 4-fold change (or more) or 1/4 (or less) and reverse rate between 1 and 2 were picked out as the reversible miRNAs for their expression after Yiqifumai treatment reversed significantly compared to model group. Among them, miR-21-3p and miR-542-3p were reported to associate with cardiac hypertrophy and tumer poliferation,respectively and they were validated by RT-PCR, which showed the consistent results as the microarray ones.
2017-11-07 | GSE106547 | GEO
Project description:Background: Yiqifumai Injection (YQFM) is clinically used to treat various cardiovascular diseases including chronic heart failure (CHF). The efficacy of YQFM for treating heart failure has been suggested, but the mechanism of action for pharmacological effects of YQFM is unclear. Methods: Echocardiography detection, left ventricular intubation evaluation, histopathology and immunohistochemical examination were performed in CHF rats to evaluate the cardioprotective effect of YQFM. Rat miRNA microarray and bioinformatics analysis were employed to investigate the differentially expressed microRNAs. In vitro models of AngII-induced hypertrophy and t-BHP induced oxidative stress in H9c2 myocardial cells were used to validate the anti-hypertrophy and anti-apoptosis effects of YQFM. Measurement of cell surface area, ATP content and cell viability, Real-time PCR and Western blot were performed. Results: YQFM significantly improved the cardiac function of CHF rats by increasing left ventricular ejection fraction and fractional shortening, decreasing left ventricular internal diameter and enhancing cardiac output. Seven microRNAs which have a reversible regulation by YQFM treatment were found. Among them, miR-21-3p and miR-542-3p are related to myocardial hypertrophy and cell proliferation, respectively and were further verified by RT-PCR. Target gene network was established and potential related signaling pathways were predicted. YQFM could significantly alleviate AngII induced hypertrophy in cellular model. It also significantly increased cell viabilities and ATP content in t-BHP induced apoptotic cell model. Western blot analysis showed that YQFM could increase the phosphorylation of Akt. Conclusion: Our findings provided scientific evidence to uncover the mechanism of action of YQFM on miRNAs regulation against CHF by miRNA expression profile technology. The results indicated that YQFM has a potential effect on alleviate cardiac hypertrophy and apoptosis in chronic heart failure.
| S-EPMC5808162 | biostudies-literature
Project description:Background: Vitamin D deficiency is associated with cardiac hypertrophy and heart failure, and vitamin D therapy prevents the progression of cardiac hypertrophy in animal models. Here, we examine whether vitamin D therapy regresses pre-existing cardiac hypertrophy, and prevents the progression to heart failure. Methods and Results: When male Dahl salt-sensitive (DSS) rats are fed a high salt (HS) diet, all rats develop cardiac hypertrophy after 5 weeks (H). Thereafter, rats were treated with vehicle (V), paricalcitol (PC, an active vitamin D analog at 200ng, IP 3x/wk), enalapril (EP, 90ug/day), and PC+EP. All groups were continued on the HS diet and evaluated after 4 weeks of therapy. The PC and PC+EP, but not the V and EP-only groups, showed significant regression of pre-existing cardiac hypertrophy. The signs of decompensated heart failure were evident in the vehicle-treated group; these heart failure parameters significantly improved with PC, EP or PC+EP therapy. The expression of PKCe, which is regulated by Ca2+ and known to stimulate cardiac hypertrophy, was significantly increased in the vehicle group, and PC, EP or PC+EP effectively decreased PKCe activation. We also observed normalization of genetic alterations during progression to heart failure with PC treatment. Conclusions: PC treatment resulted in both the regression of pre-existing cardiac hypertrophy, and the attenuation of the progression to heart failure, compared to improvement in progression to heart failure by EP alone. These beneficial findings in the heart were associated with inhibition of PKCe activation, and reversal of gene alterations. Male Dahl salt-sensitive rats (Harlan Sprague–Dawley, Somerville, NJ) were bred and fed a normal diet until 6 weeks of age. To generate pressure overload cardiac hypertrophy, they were then fed a high salt (6%NaCl) diet for the next 5 weeks. Data for baseline hypertrophic group (H) was obtained at the end of 11 weeks. Among H group animals, they were divided as follows and treated for an additional 4 weeks: 1) continuation of the HS diet with vehicle injection (H+V); 2) continuation of the HS diet with paricalcitol (19-nor-1,25-(OH)2 D2) (PC) (200ng IP 3x/wk) injection (H+PC); 3) continuation of the HS diet with low dose enalapril (EP), an angiotensin-converting enzyme inhibitor, infusion via osmotic pump and vehicle injection (H+EP+V); and 4) continuation of the HS diet with low dose EP infusion via osmotic pump and PC (200ng IP 3x/wk) injection (H+EP+PC). PC was prepared with 95% propylene glycol and 5% ethyl alcohol solution and administered three times a week on Monday, Wednesday, and Friday for 4 consecutive weeks. Vehicle groups received vehicle injections on the same schedule. Two groups of rats were implanted with pumps to deliver EP for 4 weeks. Since the reduction in blood pressure (BP) from high doses of EP would have effects on cardiac hypertrophy and progression to heart failure, we used low dose EP at 90ug/day, a maximum dose that did not significantly decrease BP in these rats, to study the effects of EP and PC that are independent of BP.
2010-09-14 | E-GEOD-24110 | biostudies-arrayexpress
Project description:We aimed to identify gene variants associated with heart failure by using a rat model of the human disease. We performed invasive cardiac hemodynamic measurements in F2 crosses between spontaneously hypertensive heart failure rats (SHHF) and reference strains. We combined linkage analyses with genome-wide expression profiling .
2008-09-01 | E-TABM-418 | biostudies-arrayexpress
Project description:The effect of krill powder, a mixed source of protein and n-3 PUFAs from Antarctic Krill (Euphausia superba), on hepatic gene expression was analyzed in CBA/J mice. Mice were fed a low-fat control diet or a 3% (w/w) krill powder low-fat diet for three months. Gene expression profiling on liver samples revealed that the krill powder supplemented diet modulated a large number of pathways compared to the control diet, and we focused on the genes involved in metabolic processes. Pathways involved β-oxidation, glucose metabolism, and amino acid catabolism were downregulated. In contrast, genes involved in the mitochondrial electron transport chain were upregulated. Thus, a krill powder supplemented diet had potent and specific effects on energy metabolism and oxidative phosphorylation at the gene level. This indicates that krill powder supplementation could be an approach to prevent age-related decline in mitochondrial respiratory chain function and weight loss.
2021-11-25 | GSE46049 | GEO
Project description:ASS lime injection - injection site
| PRJEB6137 | ENA
Project description:We describe a unique phenotype, blastulation failure, in three primary infertile males with oligoasthenoteratozoospermia (OAT) who underwent intracytoplasmic sperm injection (ICSI), resulting in multiple good-quality cleavage embryos that repeatedly failed to achieve blastulation or implantation. Single-cell analysis revealed that the arrested embryos had complex spermatozoa-derived chromosomal abnormalities, major embryonic genome activation failure, and overactivation of stress and apoptosis pathways at the transcriptional level. We further identified mutations in the meiosis-specific kinetochore factor MEIKIN gene in these males, causing OAT and chromosomal chaos in the spermatozoa. This study is the first to establish a connection between the genetic etiology of OAT and a novel embryo development arrest phenotype, indicating potenial risks of ICSI for OAT patients and providing a new explanation for recurrent implantation failure.
2024-06-30 | GSE234683 | GEO
Project description:ContextInjection of YiQiFuMai (YQFM) powder, a modern Chinese plant-derived medical preparation, has a therapeutic effect in heart failure (HF). However, its therapeutic mechanism remains largely unknown.ObjectiveTo investigate the molecular mechanisms of YQFM in HF.Materials and methodsKinase inhibition profiling assays with 2 mg/mL YQFM were performed against a series of 408 kinases. In addition, the effects of kinase inhibition were validated in cardiomyocyte cell line H9c2. In vivo, HF with reduced ejection fraction (HFrEF) was induced by permanent left anterior descending (LAD) coronary artery ligation for 6 weeks in male Sprague-Dawley rats. Then, HFrEF mice were treated with 0.46 g/kg YQFM or placebo once a day for 2 weeks. Echocardiography, immunohistochemistry, histological staining and Western blotting analysis were performed to assess the myocardial damage and molecular mechanisms.ResultsKinase inhibition profiling analysis demonstrated that mitogen-activated protein kinases (MAPKs) mediated the signalling cascades of YQFM during HF therapy. Meanwhile, p38 and extracellular signal-regulated kinases (ERK1/2) were inhibited after YQFM treatment in H9c2 cells. In rats, the control group had lower left ventricular ejection fraction (LVEF) at 37 ± 1.7% compared with the YQFM group at 54 ± 1.1% (p < 0.0001). Cardiac fibrosis levels in control group rats were significantly higher than YQFM group (30.5 ± 3.0 vs. 14.1 ± 1.0, p < 0.0001).ConclusionsOur collective in vitro and in vivo experiments demonstrated that YQFM improves left ventricular (LV) function and inhibits fibrosis in HFrEF rats by inhibiting MAPK signalling pathways.
| S-EPMC8903779 | biostudies-literature
Project description:Proteomic analysis of the changes in kidney upon chronic heart failure in a rat model. Heart failure develops due to surgically created aorto-venoufistula.
2018-09-24 | PXD009296 | Pride