Ischemia/reperfusion (I/R) injury is a multifactorial process that affects liver function after transplantation and resectional surgery. Alterations in hepatic microcirculation and decreased hepatic flow can cause local hypoxia and consequently liver damage, which is worsened by reperfusion. The aim of this study was to evaluate if treatment with L-arginine improved hepatic function in rats with I/R injury. Animals were treated with L-arginine, ischemized for 30 min, and reperfused for 3 h. Plasmatic levels of GOT, GPT, lipid hydroperoxides (LOOH), and total thiol groups (RSH) were evaluated. In addition, we analyzed hepatic LOOH and RSH levels, DNA fragmentation, heme oxygenase 1 (HO-1) expression, and histological modifications. Our results demonstrate a significant improvement in hepatic function of I/R rats compared to the control group. Treatment with L-arginine increased the expression of HO-1. These data suggest that L-arginine could be useful in preventing oxidative damage during hepatic surgery.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1002/micr.20206 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
HMOX1-LDHB interaction promotes ferroptosis by inducing mitochondrial dysfunction in foamy macrophages during advanced atherosclerosis.
Dev Cell
December 2024
Department of Cardiology, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China; Heilongjiang Provincial Key Laboratory of Panvascular Disease, Harbin 150086, China; The Key Laboratory of Myocardial Ischemia, Chinese Ministry of Education, Harbin 150081, China; State Key Laboratory of Frigid Zone Cardiovascular Diseases, Harbin 150080, China. Electronic address:
Advanced atherosclerosis is the pathological basis for acute cardiovascular events, with significant residual risk of recurrent clinical events despite contemporary treatment. The death of foamy macrophages is a main contributor to plaque progression, but the underlying mechanisms remain unclear. Bulk and single-cell RNA sequencing demonstrated that massive iron accumulation in advanced atherosclerosis promoted foamy macrophage ferroptosis, particularly in low expression of triggering receptor expressed on myeloid cells 2 (TREM2) foamy macrophages.
View Article and Find Full Text PDFReduction in Renal Heme Oxygenase-1 Is Associated with an Aggravation of Kidney Injury in Shiga Toxin-Induced Murine Hemolytic-Uremic Syndrome.
Toxins (Basel)
December 2024
Department of Anesthesiology and Intensive Care Medicine, Jena University Hospital, Am Klinikum 1, 07747 Jena, Germany.
Hemolytic-uremic syndrome (HUS) is a systemic complication of an infection with Shiga toxin (Stx)-producing enterohemorrhagic , primarily leading to acute kidney injury (AKI) and microangiopathic hemolytic anemia. Although free heme has been found to aggravate renal damage in hemolytic diseases, the relevance of the heme-degrading enzyme heme oxygenase-1 (HO-1, encoded by ) in HUS has not yet been investigated. We hypothesized that HO-1 also important in acute phase responses in damage and inflammation, contributes to renal pathogenesis in HUS.
View Article and Find Full Text PDFAchilles tenocytes from diabetic and non diabetic donors exposed to hyperglycemia respond differentially to inflammatory stimuli and stretch.
J Anat
December 2024
Institute of Anatomy and Cell Biology, Paracelsus Medical University, Nuremberg, Germany.
Diabetes mellitus type 2 (DMT2) promotes Achilles tendon (AS) degeneration and exercise could modulate features of DMT2. Hence, this study investigated whether tenocytes of non DMT2 and DMT2 rats respond differently to normo- (NG) and hyperglycemic (HG) conditions in the presence of tumor necrosis factor (TNF)α or cyclic stretch. AS tenocytes, isolated from DMT2 (fa/fa) or non DMT2 (lean, fa/+) adult Zucker Diabetic Fatty (ZDF) rats, were treated with 10 ng/mL TNFα either under NG or HG conditions (1 g/L vs.
View Article and Find Full Text PDF[Luteolin inhibits proliferation of lung cancer A549 cells by increasing ROS production and inhibiting the AKT/mTOR signaling pathway and HO-1 expression].
Nan Fang Yi Ke Da Xue Xue Bao
December 2024
School of Public Health, Bengbu Medical University, Bengbu 233000, China.
Objectives: To investigate the mechanism of luteolin for inhibiting proliferation of lung cancer A549 cells.
Methods: A549 cells treated with different concentrations of luteolin for 48 h were evaluated for changes in cell viability, proliferation, reactive oxygen species (ROS) production and apoptosis using MTT assay, plate cloning assay, EdU staining, DCFH-DA assay and Hoechst33258 staining. The changes in cell autophagy were examined with MDC staining, and the expressions of apoptosis-related proteins (Bax, Bcl-2, and cleaved caspase-9), autophagy-related proteins (LC3B, Beclin 1, and P62), AKT/mTOR pathway proteins, and HO-1 protein were detected using Western blotting.
Elucidating Ligand Interactions and Small-Molecule Activation in the Pyrrolnitrin Biosynthetic Enzyme PrnB.
J Biol Chem
December 2024
Department of Chemistry, University of Georgia, Athens, GA 30602. Electronic address:
Pyrrolnitrin, a potent antifungal compound originally discovered in Pseudomonas strains, is biosynthesized through a secondary metabolic pathway involving four key enzymes. Central to this process is PrnB, a heme enzyme that catalyzes the complex transformation of 7-Cl-L-tryptophan. Despite its structural similarity to indoleamine 2,3-dioxygenase (IDO) and tryptophan 2,3-dioxygenase (TDO) and its classification within the histidine-ligated heme-dependent aromatic oxygenase (HDAO) superfamily, PrnB has remained relatively unexplored due to challenges in reconstituting its in vitro activity.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!