Treatment with Apocynin Limits the Development of Acute Graft-versus-Host Disease in Mice.

In this study, we have evaluated the role of ROS in GVHD pathogenesis by treatment of recipient mice with apocynin (apo), an inhibitor of intracellular translocation of cytosolic components of NADPH oxidase complex. The pharmacological blockade of NADPH oxidase resulted in prolonged survival and reduced GVHD clinical score. This reduction in GVHD was associated with reduced levels of ROS and TBARS in target organs of GVHD in apocynin-treated mice at the onset of the mortality phase. These results correlated with reduced intestinal and liver injuries and decreased levels of proinflammatory cytokines and chemokines. Mechanistically, pharmacological blockade of the NADPH oxidase was associated with inhibition of recruitment and accumulation of leukocytes in the target organs. Additionally, the chimerism remained unaffected after treatment with apocynin. Our study demonstrates that ROS plays an important role in mediating GVHD, suggesting that strategies aimed at blocking ROS production may be useful as an adjuvant therapy in patients subjected to bone marrow transplantation. PMID: 31781685 [PubMed - in process]
Source: Journal of Immunology Research - Category: Allergy & Immunology Tags: J Immunol Res Source Type: research

Related Links:

CONCLUSIONS BAI suppressed bilirubin-induced neuron apoptosis and inflammation by deactivating p38 MAPK signaling. PMID: 32633271 [PubMed - in process]
Source: Medical Science Monitor - Category: Research Tags: Med Sci Monit Source Type: research
Condition:   Sjogren's Syndrome Intervention:   Other: Biomarker detection Sponsor:   Centre Hospitalier Universitaire de Nīmes Not yet recruiting
Source: ClinicalTrials.gov - Category: Research Source Type: clinical trials
Abstract An essential property associated with leptospiral virulence is the pathogen's ability to translocate across host cells, enabling Leptospira to evade the host immune response, disseminate, and establish infection. Cell monolayer translocation assay allows for the quantification of Leptospira strain's competence to cross cell barriers while measuring the integrity of the polarized eukaryotic cell monolayer during this process. PMID: 32632868 [PubMed - in process]
Source: Mol Biol Cell - Category: Molecular Biology Authors: Tags: Methods Mol Biol Source Type: research
Journal of the American Chemical SocietyDOI: 10.1021/jacs.0c05502
Source: Journal of the American Chemical Society - Category: Chemistry Authors: Source Type: research
AbstractA 68-year-old man was followed up with chronic kidney disease. Follow-up CT incidentally detected a tumor at the left kidney and multiple small nodular shadows in the lungs bilaterally. The patient underwent needle biopsy and was diagnosed with Xp11.2 translocation renal cell carcinoma (RCC) pathologically. Hence, laparoscopic nephrectomy was performed. Fluorescence in situ hybridization analysis revealed a break-apart of the transcription factor E3 (TFE3) genes in the left tumor. After 2  months postoperatively, nivolumab and ipilimumab were administered thrice intravenously, considering the intermediate risk...
Source: International Cancer Conference Journal - Category: Cancer & Oncology Source Type: research
Epigenetic factors have been proven to contribute to pituitary adenoma formation. 5-hydroxymethylcytosine (5hmC), which is catalyzed by ten-eleven translocation 2 (TET2), is related to DNA demethylation. In order to explore the pathogenesis of non-functioning pituitary adenomas (NFPAs), we detected genomic 5hmC levels in 57 NFPAs and 5 normal pituitary glands, and TET2 expression, distribution and TET2 alteration. Genomic 5hmC levels in NFPAs were significantly lower than those in normal pituitary glands (0.38‰ (0.24‰, 0.61‰) vs. 2.47‰ (1.56‰, 2.83‰), P
Source: Frontiers in Endocrinology - Category: Endocrinology Source Type: research
In conclusion, curcumin regulates autophagy by controlling TFEB through the inhibition of GSK-3β, and increases antioxidant gene expression in human neuroblastoma cells. These results contribute to the development of novel cellular therapies for neurodegenerative diseases. PMID: 32623920 [PubMed - as supplied by publisher]
Source: Free Radical Research - Category: Research Tags: Free Radic Res Source Type: research
TNF‑α promotes the malignant transformation of intestinal stem cells through the NF‑κB and Wnt/β‑catenin signaling pathways. Oncol Rep. 2020 Aug;44(2):577-588 Authors: Zhao X, Ma L, Dai L, Zuo D, Li X, Zhu H, Xu F Abstract Cancer stem cells are responsible for tumorigenesis, progression, recurrence and metastasis. Intestinal stem cells (ISCs) are regarded as the origin of intestinal neoplasia. Inflammation also serves an important role in intestinal neoplasia. To explore the molecular mechanisms underlying the inflammation‑mediated induction of intestinal tumorigenesis, the pre...
Source: Oncology Reports - Category: Cancer & Oncology Tags: Oncol Rep Source Type: research
An elongated tract of polyQ in the carboxyl‑terminus of human α1A calcium channel induces cell apoptosis by nuclear translocation. Oncol Rep. 2020 Jul;44(1):156-164 Authors: Sun J, Sun X, Li Z, Ma D, Lv Y Abstract An aberrant elongated tract of glutamine residues (polyQ) in proteins induces multiple diseases treated in the clinic. In our previous study of progressive myoclonic epilepsy (PME), using whole‑exome sequencing, a mutant Cav2.1 protein with an aberrant elongated polyQ tract was identified in PME patients. To investigate the molecular mechanism and cell biology of this aberrant elong...
Source: Oncology Reports - Category: Cancer & Oncology Tags: Oncol Rep Source Type: research
Type 2 diabetes (T2D) is a metabolic disease characterized by increased inflammation, NOD-like receptors (NLRs) activation and gut dysbiosis. Our research group has recently reported that intestinal Th17 response limits gut dysbiosis and LPS translocation to visceral adipose tissue (VAT), protecting against metabolic syndrome. However, whether NOD2 receptor contributes intestinal Th17 immunity, modulates dysbiosis-driven metabolic tissue inflammation, and obesity-induced T2D remain poorly understood. In this context, we observed that mice lacking NOD2 fed a high-fat diet (HFD) display severe obesity, exhibit greater adipos...
Source: Frontiers in Immunology - Category: Allergy & Immunology Source Type: research
More News: Allergy & Immunology | Bone Marrow Transplant | Liver | Liver Transplant | Stem Cell Therapy | Stem Cells | Study | Translocation | Transplants | Urology & Nephrology