Huangxueyishen formular attenuates Chronic renal failure by promoting activation of p38/MAPK signaling pathway
Ontology highlight
ABSTRACT:
ORGANISM(S): Rattus Rattus
SUBMITTER: 
Cheng Hu
PROVIDER: PXD043416 | iProX | Fri Jun 30 00:00:00 BST 2023
REPOSITORIES: iProX
Similar Datasets
Project description:Renal failure is characterized by important biological changes resulting in profound pleomorphic physiological effects termed “uremia”, whose molecular causation is not well understood. The data was used to study gene expression changes in uremia using whole genome microarray analysis of peripheral blood from subjects with end-stage renal failure (n=63) and healthy controls (n=20) to obtain insight into the molecular and biological causation of this syndrome. The study was conducted at the University of British Columbia and approved by the human ethics research board. A 3:1 case-control design was employed to compare gene expression in patients with chronic renal failure and healthy controls. Patients with stage 5 renal disease aged 18 to 75 years, who were clinically stable awaiting renal transplantation, were not receiving immunosuppressive medications, and who provided written informed consent were enrolled into the study. Patients were treated according to Canadian Guidelines for Chronic Kidney Disease (13). Normal controls of comparable age and gender to the patients who were screened to ensure freedom from known illness and medical therapy served as comparators.
2012-04-11 | E-GEOD-37171 | biostudies-arrayexpress
Project description:Kidney transplants that develop dysfunction or proteinuria after one year post transplant are at considerable risk for progression to renal failure. Identifying the molecules associated with graft failure could potentially lead to interventions that would slow the progression of organ failure. We analyzed the relationship between gene expression in late biopsies for cause in human kidney transplants and subsequent graft loss, and assessed the predictive value of gene expression. We evaluated the performance of these genes in an independent , and in a population of early biopsies that have a very low risk of subsequent graft failure. All consenting renal transplant patients undergoing biopsies for cause as standard of care between 09/2004 and 10/2007 at the university of Alberta or between 11/2006 and 02/2007 at the University of Illinois were included in the analysis. In addition, biopsies obtained from Minnesota between 09/2006 and 09/2007 were used as an independent . In addition to the cores required for standard histopathology, we collected one core for gene expression studies. the relationship between gene expression in the biopsy and subsequent graft loss was analyzed. This dataset is part of the TransQST collection.
2010-05-24 | E-GEOD-21374 | biostudies-arrayexpress
Project description:This experiment was designed to study the alteration in expression of mRNA is kidney following recovery from transient acute renal failure. The model used was a 52 min. bilateral renal artery clamping, followed by reperfusion, which resulted in a transient loss of renal function, followed by a functional recovery. All tissue in this study was harvested 35 days post-surgery, when renal function was restored, and renal structure largelyy normal. For controls, sham-operated animals were used. An N of 6 post-ischemia reperfusion animals were used with 6 sham-operated controls. For hybridization studies, RNA from one of six post-ischemic acute renal failure animals were compared with with RNA from kidney of six sham-operated control animals. Each ARF vs. sham-operated comparison was performed twice, alternating the cy3 and cy5 label between the two hybridizations for each pair. A second set of hybridizations was carried out using sham vs. sham hybridizations. This was done to get a quantitative analysis of the variation of the biological and microarry platform.
2010-06-10 | E-GEOD-1714 | biostudies-arrayexpress
Project description:Objective: To investigate the treatment and mechanism of lanthanum hydroxide on hyperphosphate-induced vascular calcification in chronic renal failure. Methods: Develop a rat model of CKD hyperphosphatemia. Rats were randomly allocated to the model, lanthanum hydroxide, lanthanum carbonate, Calcium carbonate groups. Determination of serum biochemical indicators and the determination of pathological analysis of kidney tissue, Von Kossa staining and CT scan on the aortic vessels. The proteomic analysis of aortic tissue in Vivo. A calcified VSMCs model was established. The calcium content and ALP activity were measured. RT-PCR measures the mRNA expression level of SM22α, Runx2, BMP-2 and TRAF6. Western Blot measures the protein expression level of SM22α, Runx2, BMP-2, TRAF6 and NF-κB. Results: Through the detection of serum biochemical indicators and pathological analysis of kidney tissue, it can be summaryed that lanthanum hydroxide has the effect of delaying the progression of renal failure and protecting renal function. We found that the administration of lanthanum hydroxide delayed the development of vascular calcification induced by hyperphosphatemia in CKD. It can be concluded that lanthanum hydroxide may affect vascular calcification through the NF-κB pathway. , To deal with Lanthanum chloride (LaCl3) inhibited phosphate induced calcification, osteo-/chondrogenic transdifferentiation, and NF-κB signaling in cultured VSMCs. Lanthanum hydroxide significantly reduces the expression of Runx2, BMP-2, TRAF6 and NF-κB. Conclusion: Lanthanum hydroxide has a protective effect on the kidneys, and can delay the development of vascular calcification by reducing serum phosphorus concentration.
2021-09-09 | PXD023081 | Pride
Project description:This experiment was designed to study the alteration in expression of mRNA is kidney following recovery from transient acute renal failure. The model used was a 52 min. bilateral renal artery clamping, followed by reperfusion, which resulted in a transient loss of renal function, followed by a functional recovery. All tissue in this study was harvested 35 days post-surgery, when renal function was restored, and renal structure largelyy normal. For controls, sham-operated animals were used. An N of 6 post-ischemia reperfusion animals were used with 6 sham-operated controls. For hybridization studies, RNA from one of six post-ischemic acute renal failure animals were compared with with RNA from kidney of six sham-operated control animals. Each ARF vs. sham-operated comparison was performed twice, alternating the cy3 and cy5 label between the two hybridizations for each pair. A second set of hybridizations was carried out using sham vs. sham hybridizations. This was done to get a quantitative analysis of the variation of the biological and microarry platform. Keywords: parallel sample
2005-01-26 | GSE1714 | GEO
Project description:<p><strong>OBJECTIVE:</strong> Patients with renal failure suffer from symptoms caused by uraemic toxins, possibly of gut microbial origin, as deduced from studies in animals. The aim of the study is to characterise relationships between the intestinal microbiome composition, uraemic toxins and renal failure symptoms in human end-stage renal disease (ESRD).</p><p><strong>DESIGN:</strong> Characterisation of gut microbiome, serum and faecal metabolome and human phenotypes in a cohort of 223 patients with ESRD and 69 healthy controls. Multidimensional data integration to reveal links between these datasets and the use of chronic kidney disease (CKD) rodent models to test the effects of intestinal microbiome on toxin accumulation and disease severity.</p><p><strong>RESULTS:</strong> A group of microbial species enriched in ESRD correlates tightly to patient clinical variables and encode functions involved in toxin and secondary bile acids synthesis; the relative abundance of the microbial functions correlates with the serum or faecal concentrations of these metabolites. Microbiota from patients transplanted to renal injured germ-free mice or antibiotic-treated rats induce higher production of serum uraemic toxins and aggravated renal fibrosis and oxidative stress more than microbiota from controls. Two of the species, Eggerthella lenta and Fusobacterium nucleatum, increase uraemic toxins production and promote renal disease development in a CKD rat model. A probiotic Bifidobacterium animalis decreases abundance of these species, reduces levels of toxins and the severity of the disease in rats.</p><p><strong>CONCLUSION:</strong> Aberrant gut microbiota in patients with ESRD sculpts a detrimental metabolome aggravating clinical outcomes, suggesting that the gut microbiota will be a promising target for diminishing uraemic toxicity in those patients.</p>
2020-10-20 | MTBLS700 | MetaboLights
Project description:A chronic heart failure model was prepared using thoracic aortic narrowing surgery, and cardiac function, serum markers and renal pathologic changes were evaluated in comparison model mice at weeks 4, 8, 12, and 16 after surgery. Proteomic analysis was performed on mouse kidneys 16 weeks after operation
2024-01-04 | PXD048237 | iProX
Project description:Persistently elevated glycolysis in kidney has been demonstrated to promote chronic kidney disease. However, the underlying mechanism remains largely unclear. Here, we observed that PFKFB3, a key glycolytic enzyme, was remarkably induced in kidney proximal tubular cells following ischemia-reperfusion injury in mice, as well as in multiple etiologies of chronic kidney disease patients. Proximal tubular epithelial-specific deletion of PFKFB3 significantly reduced renal lactate levels, mitigated inflammation and fibrosis, and preserved renal function in the IRI mouse model. To explore the mechanism of PFKFB3 in renal fibrosis, we performed RNA-sequencing (RNA-seq) on the kidney cortices from IRI mice. Of note, we found that PFKFB3-mediated kidney tubular glycolytic reprogramming markedly enhanced H4K12la lactylation. To further explore the potential functional significance of H4K12la in renal fibrosis, we performed genome-wide cleavage under targets and tagmentation (CUT&Tag) analysis to identify candidate genes regulated by H4K12la in sham and IRI kidney. Following CUT&Tag, H4K12la-associated DNAs were amplified using non-biased conditions, labeled, and sequenced with Illumina NovaSeq 6000.
2024-05-01 | GSE266243 | GEO
Project description:Persistently elevated glycolysis in kidney has been demonstrated to promote chronic kidney disease. However, the underlying mechanism remains largely unclear. Here, we observed that PFKFB3, a key glycolytic enzyme, was remarkably induced in kidney proximal tubular cells following ischemia-reperfusion injury in mice, as well as in multiple etiologies of chronic kidney disease patients. Proximal tubular epithelial-specific deletion of PFKFB3 significantly reduced renal lactate levels, mitigated inflammation and fibrosis, and preserved renal function in the IRI mouse model. To explore the mechanism of PFKFB3 in renal fibrosis, we performed RNA-sequencing (RNA-seq) on the kidney cortices from IRI mice. Of note, we found that PFKFB3-mediated kidney tubular glycolytic reprogramming markedly enhanced H4K12la lactylation. To further explore the potential functional significance of H4K12la in renal fibrosis, we performed genome-wide cleavage under targets and tagmentation (CUT&Tag) analysis to identify candidate genes regulated by H4K12la in sham and IRI kidney. Following CUT&Tag, H4K12la-associated DNAs were amplified using non-biased conditions, labeled, and sequenced with Illumina NovaSeq 6000.
2024-05-01 | GSE266242 | GEO
Project description:Biomarkers for early detection of chronic kidney disease are needed, as millions of patients suffer from chronic diseases predisposing them to kidney failure. Protein microarrays may hold utility in the discovery of auto-antibodies in other conditions not commonly considered auto-immune diseases. We hypothesized that proteins are released as a consequence of damage at a cellular level during end-organ damage from renal injury, not otherwise recognized as self-antigens, and an adaptive humoral immune response to these proteins might be detected in the blood, as a non-invasive tracker of this injury. The resultant antibodies (Ab) detected in the blood would serve as effective biomarkers for occult renal injury, enabling earlier clinical detection of chronic kidney disease than currently possible, due to the redundancy of the serum creatinine as a biomarker for early kidney injury. To screen for novel autoantibodies in chronic kidney disease, 24 protein microarrays were used to compare serum Ab from patients with chronic kidney disease against matched controls. From a panel of 38 antigens with increased Ab binding, 4 were validated in 71 individuals, with (n=50) and without (n=21) renal insufficiency. Significant elevations in the titer of novel auto-Ab were noted against Angiotensinogen (AGT) and PRKRIP1 in renal insufficiency. Current validation is underway to evaluate if these auto-Ab can provide means to follow the evolution of chronic kidney disease in patients with early stages of renal insufficiency, and if these rising titers of these auto-Ab correlate with the rate of progression of chronic kidney disease.
2010-08-13 | GSE23609 | GEO