Background: Ischemic reperfusion (I/R) injury of the kidney is closely associated with delayed graft function, increased acute rejection, and late allograft dysfunction. Splenectomy reduced hepatic I/R injury by inhibiting leukocyte infiltration in the liver, release of TNF-α, cell apoptosis, and expression of caspase-3. Thus, we investigated the effects of splenectomy on renal I/R injury in the rat.
Methods: Male Wistar rats were assigned to four groups: sham operation (sham group), sham operation+splenectomy (sham+SPLN group), right nephrectomy followed by clamping the left renal pedicle for 30min (I/R 30 group), and I/R 30+splenectomy (I/R 30+SPLN group). Renal function was determined by measuring the concentration of blood urea nitrogen (BUN) and serum creatinine (S-Cr). The serum level of tumor necrosis factor-α (TNF-α) was measured as the marker for inflammation. Left kidneys were obtained 24h after reperfusion. TUNEL assay was assessed for cell apoptosis. Spleens were obtained immediately (0-h group) and 3h after reperfusion (3-h group). The removed spleens were histologically evaluated.
Results: The BUN and S-Cr levels were significantly lower in the I/R 30+SPLN group than in the I/R 30 group (p<0.05 for both). Apoptotic cells were significantly lower in the I/R 30+SPLN group than in the I/R 30 group. The serum level of TNF-α, which was increased after I/R, was significantly lower in the I/R 30+SPLN group than in the I/R 30 group (p<0.05). Spleen weights were significantly lower in the 3-h group than in the 0-h group (p<0.05).
Conclusion: These results suggest that splenectomy reduces renal I/R injury, and this effect may occur by an anti-inflammatory pathway and inhibition of cell apoptosis.
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http://dx.doi.org/10.1016/j.trim.2012.03.005 | DOI Listing |
Drug Des Devel Ther
January 2025
Department of Anesthesiology, Beijing Friendship Hospital, Capital Medical University, Beijing, People's Republic of China.
Purpose: This study aimed to assess the protective effect of a clinical dose esketamine on cerebral ischemia/reperfusion (I/R) injury and to reveal the potential mechanisms associated with microglial polarization and autophagy.
Methods: Experimental cerebral ischemia was induced by middle cerebral artery occlusion (MCAO) in adult rats and simulated by oxygen-glucose deprivation (OGD) in BV-2 microglial cells. Neurological and sensorimotor function, cerebral infarct volume, histopathological changes, mitochondrial morphological changes, and apoptosis of ischemic brain tissues were assessed in the presence or absence of esketamine and the autophagy inducer rapamycin.
World J Cardiol
January 2025
Cardiac Care Unit, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, Zhejiang Province, China.
Background: Myocardial ischemia/reperfusion (I/R) injury, which is associated with high morbidity and mortality, is a main cause of unexpected myocardial injury after acute myocardial infarction. However, the underlying mechanism remains unclear. Circular RNAs (circRNAs), which are formed from protein-coding genes, can sequester microRNAs or proteins, modulate transcription and interfere with splicing.
View Article and Find Full Text PDFFood Funct
January 2025
The Affiliated Changsha Hospital of Xiangya School of Medicine, Central South University, Changsha 410000, China.
A balanced diet is essential for maintaining human health. Increasing evidence suggests that dietary and nutritional interventions contribute to disease management and are associated with reduced healthcare costs and economic burden. Ferroptosis, a novel type of regulated cell death (RCD) driven by lipid peroxidation, has been shown to be involved in various pathological conditions, including diabetes, ischemia/reperfusion (I/R) injury, inflammation-related diseases, and cancer.
View Article and Find Full Text PDFJ Biochem Mol Toxicol
February 2025
Department of Cardiology, Affiliated Hospital of Hebei University, Baoding, China.
Ischemia-reperfusion (I/R) injury is a significant clinical problem impacting the heart and other organs, such as the kidneys and liver. This study explores the protective effects of oxycodone on myocardial I/R injury and its underlying mechanisms. Using a myocardial I/R model in Sprague-Dawley (SD) rats and an oxygen-glucose deprivation/reoxygenation (OGD/R) model in H9c2 cells, we administered oxycodone and inhibited AMP-activated protein kinase (AMPK) with Compound C (C.
View Article and Find Full Text PDFCell Death Dis
January 2025
Key Laboratory of Cellular Physiology at Shanxi Medical University, Ministry of Education, and the Department of Physiology, School of Basic Medicine, Shanxi Medical University, Taiyuan, China.
Programmed necrosis/necroptosis greatly contributes to the pathogenesis of cardiac disorders including myocardial infarction, ischemia/reperfusion (I/R) injury and heart failure. However, the fundamental mechanism underlying myocardial necroptosis, especially the mitochondria-dependent death pathway, is poorly understood. Synaptotagmin-1 (Syt1), a Ca sensor, is originally identified in nervous system and mediates synchronous neurotransmitter release.
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