We examined the effect of dexamethasone (DXM) pretreatment on microvascular transport of macromolecules in ischemia-reperfusion injury. The rat cremaster muscle was splayed, placed in a Lucite intravital chamber, and suffused with bicarbonate buffer. The clearance of fluorescein isothiocyanate-dextran 150 (FITC-Dx 150) was measured as an index of microvascular transport. After determination of baseline data, the muscle was made ischemic for 2 hr by clamping its vascular pedicle, and subsequently reperfused for 2 hr. Ischemia-reperfusion produced a marked increase in clearance of FITC-Dx 150. After an initial peak of 13 times baseline value clearance fell to approximately 4 times baseline level 30 min into the reperfusion period. Clearance increased slowly throughout the remainder of the experiment, reaching 6 times baseline after 2 hr of reperfusion. The treated animals received DXM 3 hr prior to and immediately preceding the pedicle clamping. DXM reduced macromolecular clearance significantly after the first 30 min of reperfusion, and prevented the increase in clearance over time. After an initial peak, clearance values fell to near twice baseline in DXM-treated animals, and remained at this level for the 2 hr of reperfusion. Our data demonstrate that DXM attenuates the alternations in microvascular macromolecular transport produced by ischemia-reperfusion injury.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/0026-2862(89)90024-1 | DOI Listing |
PeerJ
January 2025
Department of Nephrology, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, Zhejiang, China.
Dysregulated specificity proteins (SPs), members of the C2H2 zinc-finger family, are crucial transcription factors (TFs) with implications for renal physiology and diseases. This comprehensive review focuses on the role of SP family members, particularly SP1 and SP3, in renal physiology and pathology. A detailed analysis of their expression and cellular localization in the healthy human kidney is presented, highlighting their involvement in fatty acid metabolism, electrolyte regulation, and the synthesis of important molecules.
View Article and Find Full Text PDFIran J Basic Med Sci
January 2025
Department of Urology, Renmin Hospital of Wuhan University, Wuhan, Hubei, 430060, China.
Objectives: To explore the effects of puerarin on renal ischemia/reperfusion injury and the possible mechanism.
Materials And Methods: The experimental mice were injected with puerarin (50 or 100 mg/kg) per day or equal sterile saline by intraperitoneal injection for one week, and a renal I/R injury model was constructed. HK-2 cells were incubated with puerarin (1 uM and 10 uM) before the H/R model.
Int J Biol Macromol
January 2025
Department of Thoracic Surgery, the First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, China. Electronic address:
Mitochondrial dysfunction and ferroptosis play crucial roles in myocardial ischemia/reperfusion (I/R) following heart transplantation. Microsomal glutathione s transferase 1 (MGST1) is widely distributed in mitochondria and has a protective effect against ferroptosis, and its involvement in myocardial I/R injury has not yet been elucidated. In this study, donor hearts from C57BL/6 male mice were subjected to 12 h of ex-vivo cold ischemia treatment and transplanted into the abdomen of recipient mice for 24 h of reperfusion.
View Article and Find Full Text PDFAm J Transplant
January 2025
Department of Urology, Osaka University Graduate School of Medicine, Suita, Japan; Department of Urology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan. Electronic address:
Antibody-mediated rejection (ABMR) remains a leading cause of graft loss during kidney transplantation. Ischemia reperfusion injury (IRI) has been reported to promote T-cell proliferation, leading to B-cell activation and subsequent production of donor-specific antibodies (DSA), which target antigens on the vascular endothelium. We hypothesize that a novel therapeutic strategy targeting highly toxic reactive oxygen species could mitigate oxidative stress and immune responses associated with IRI.
View Article and Find Full Text PDFBiomed Pharmacother
January 2025
Department of Cardiology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai 200120, China. Electronic address:
Purpose: Targeting mitochondrial ferroptosis presents a promising strategy for mitigating myocardial ischemia-reperfusion (I/R) injury. This study aims to evaluate the efficacy of the mitochondrial-targeted ferroptosis inhibitor SS-31@Fer-1 (elamipretide@ferrostatin1) in reducing myocardial I/R injury.
Methods: SS-31@Fer-1 was synthesized and applied to H9C2 cells subjected to hypoxia/reoxygenation (H/R) to assess its protective effects.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!