In this study, we tested if the mechanism of protection of a calcium channel blocker, Verapamil (VER), was due to modulation of neutrophil infiltration after ischemia/reperfusion injury, in a rat renal ischemic model. Forty-four Sprague-Dawley rats were subjected to 75 min of warm ischemia and immediate contralateral nephrectomy. The animals were divided into two groups: the ischemic control (IC) group, which received normal saline, and the experimental group that received VER 1.25 mg/kg. The drug was administrated intravenously after ligation of the renal pedicle, before reperfusion. Survival was followed for 7 days. Laboratory tests included renal function tests, with serum creatinine (SCr) and blood urea nitrogen (BUN), light histology and neutrophil infiltration, measured by the myeloperoxidase test in renal tissue. Better survival rate was observed in the VER group (85% at 7 days vs control 50%) (P = 0.08). SCr and BUN at 48 and 72 hr showed a statistical significant difference between the two groups (VER lower than IC P < 0.05). Histological damage was significantly less in the VER group (P < 0.05). Neutrophil infiltration was significantly decreased in the VER group when compared to the IC group (P < 0.05). We concluded then, that VER had a downregulating effect on neutrophil infiltration and this might be an important mechanism of protection during the development of renal ischemic damage.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1006/jsre.1996.0148 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Framework Nucleic Acid-Based and Neutrophil-Based Nanoplatform Loading Baicalin with Targeted Drug Delivery for Anti-Inflammation Treatment.
ACS Nano
January 2025
State Key Laboratory of Oral Diseases, National Center for Stomatology, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan 610041, China.
Targeted drug delivery is a promising strategy for treating inflammatory diseases, with recent research focusing on the combination of neutrophils and nanomaterials. In this study, a targeted nanodrug delivery platform (Ac-PGP-tFNA, APT) was developed using tetrahedral framework nucleic acid (tFNA) along with a neutrophil hitchhiking mechanism to achieve precise delivery and anti-inflammatory effects. The tFNA structure, known for its excellent drug-loading capacity and cellular uptake efficiency, was used to carry a therapeutic agent─baicalin.
View Article and Find Full Text PDFPharmacological validation of a novel exopolysaccharide from sp. 139 to effectively inhibit cytokine storms.
Heliyon
July 2024
NHC Key Laboratory of Biotechnology of Antibiotics, CAMS Key Laboratory of Synthetic Biology for Drug Innovation, Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100050, China.
With the rapid development of immunotherapy in recent years, cytokine storm has been recognized as a common adverse effect of immunotherapy. The emergence of COVID-19 has renewed global attention to it. The cytokine storm's inflammatory response results in infiltration of large amounts of monocytes/macrophages in the lungs, heart, spleen, lymph nodes, and kidneys.
View Article and Find Full Text PDFLung endothelial cell senescence impairs barrier function and promotes neutrophil adhesion and migration.
Geroscience
January 2025
Department of Molecular Pharmacology and Physiology, University of South Florida, Morsani College of Medicine, 12901 Bruce B. Downs Blvd., Tampa, FL, USA.
Cellular senescence contributes to inflammation and organ dysfunction during aging. While this process is generally characterized by irreversible cell cycle arrest, its morphological features and functional impacts vary in different cells from various organs. In this study, we examined the expression of multiple senescent markers in the lungs of young and aged humans and mice, as well as in mouse lung endothelial cells cultured with a senescence inducer, suberoylanilide hydroxamic acid (SAHA), or doxorubicin (DOXO).
View Article and Find Full Text PDFMicroglial NLRP3-gasdermin D activation impairs blood-brain barrier integrity through interleukin-1β-independent neutrophil chemotaxis upon peripheral inflammation in mice.
Nat Commun
January 2025
Department of Microbiology and Immunology, Brain Korea 21 Project for Medical Science, Institute for Immunology and Immunological Diseases, Yonsei University College of Medicine, Seoul, Republic of Korea.
Blood-brain barrier (BBB) disintegration is a key contributor to neuroinflammation; however, the biological processes governing BBB permeability under physiological conditions remain unclear. Here, we investigate the role of NLRP3 inflammasome in BBB disruption following peripheral inflammatory challenges. Repeated intraperitoneal lipopolysaccharide administration causes NLRP3-dependent BBB permeabilization and myeloid cell infiltration into the brain.
View Article and Find Full Text PDFAblation of satellite cell-specific clock gene, Bmal1, alters force production, muscle damage, and repair following contractile-induced injury.
FASEB J
January 2025
Shirley Ryan AbilityLab, Chicago, Illinois, USA.
Following injury, skeletal muscle undergoes repair via satellite cell (SC)-mediated myogenic progression. In SCs, the circadian molecular clock gene, Bmal1, is necessary for appropriate myogenic progression and repair with evidence that muscle molecular clocks can also affect force production. Utilizing a mouse model allowing for inducible depletion of Bmal1 within SCs, we determined contractile function, SC myogenic progression and muscle damage and repair following eccentric contractile-induced injury.
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!