Objective: To investigate the effects and mechanism of doxorubicin preconditioning in providing ischemic tolerance for rats abdomen island flaps.
Methods: Twenty-four healthy adult Sprague Dawley rats, 12 males and 12 females, were randomly divided into 3 groups (n = 8): control group (group A), ischemic preconditioning group (group B), and doxorubicin preconditioning group (group C). After the abdomen island flap (6 cm x 3 cm in size) based on the superficial inferior epigastric neurovascular bundle was prepared, group A had no further treatment; group B was given a 10-minute ischemia followed by a 10-minute reperfusion for 4 times; and group C was given pretreatment with doxorubicin (1 mg/kg) by injection of the inferior epigastric vein. After 24 hours, the inferior epigastric vessels were blocked by vascular clamp for 4 hours, followed by reperfusion 2 hours to prepare ischemia/reperfusion (I/R) injury model. The rat survival was observed after operation; at 0, 8, 12, 24, and 30 hours after I/R injury, the malonyldiadehyde (MDA) and superoxide dismutase (SOD) levels were measured. At 7 days after I/R injury, the survival rate of flap were calculated and the flaps were harvested for histological observation.
Results: During experiment, 5 rats died (1 rat in groups A and B respectively, 3 rats in group C) and were added. The survival rates of the flap in group A (10.10% +/- 0.43%) was lower than those in group B (91.63% +/- 1.76%) and in group C (92.75% +/- 1.48%) at 7 days after I/R injury, showing significant differences (P < 0.05), and there was no significant difference between groups B and C (t = 0.29, P = 0.77). Significant difference was found in MDA level and SOD level between group A and groups B, C after 8 hours (P < 0.05), and there was no significant difference between groups B and C (P > 0.05). Histological observation showed that inflammatory cells infiltration was more obvious and hyperplasia of fibers was weaker in group A than in groups B and C.
Conclusion: Doxorubicin preconditioning can provide ischemic tolerance for rats abdomen island flaps and protect flaps from the I/R injury. The possible mechanism may be related to that doxorubicin can induce endogenous protections.
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Apoptosis
January 2025
Department of Cardiac Surgery, First Affiliated Hospital of Sun Yat-sen University, 58 Zhongshan II Rd, Guangzhou, 510080, China.
Recent studies have suggested that sVEGFR3 is involved in cardiac diseases by regulating lymphangiogenesis; however, results are inconsistent. The aim of this study was to investigate the function and mechanism of sVEGFR3 in myocardial ischemia/reperfusion injury (MI/RI). sVEGFR3 effects were evaluated in vivo in mice subjected to MI/RI, and in vitro using HL-1 cells exposed to oxygen-glucose deprivation/reperfusion.
View Article and Find Full Text PDFAnn Chir Plast Esthet
January 2025
Department of Plastic, Reconstructive, and Aesthetic Surgery, Faculty of Medicine, Çukurova University, Adana, Turkey.
Background: Hydrogen sulfide (HS) is a widely studied gasotransmitter, and its protective effect against ischemia-reperfusion damage has been explored in several studies. Therefore, a requirement exists for a comprehensive study about HS effects on ischemia-reperfusion damage in flap surgery. The aim of this study is to examine the effect of hydrogen sulfide by creating ischemia-reperfusion injury in the vascular-stemmed island flap prepared from the rat groin area.
View Article and Find Full Text PDFArch Biochem Biophys
January 2025
Department of Critical Care Medicine, the First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province 150001, China; Heilongjiang Provincial Key Laboratory of Critical Care Medicine, Harbin 150001, China; Central Laboratory of The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China. Electronic address:
Background: Ischemia-reperfusion injury (IRI) often results in renal impairment. While the presence of neutrophil extracellular traps (NETs) is consistently observed, their specific impact on IRI is not yet defined. Sivelestat sodium, an inhibitor of neutrophil elastase which is crucial for NET formation, may offer a therapeutic approach to renal IRI, warranting further research.
View Article and Find Full Text PDFFront Biosci (Landmark Ed)
January 2025
Department of Cardiology, Affiliated Hospital of Jiangnan University, 214122 Wuxi, Jiangsu, China.
Background: Myocardial ischemia-reperfusion (I/R) injury refers to cell damage that occurs as a consequence of the restoration of blood circulation following reperfusion therapy for cardiovascular diseases, and it is a primary cause of myocardial infarction. The search for nove therapeutic targets in the context of I/R injury is currently a highly active area of research. p70 ribosomal S6 kinase (S6K1) plays an important role in I/R induced necrosis, although the specific mechanisms remain unclear.
View Article and Find Full Text PDFFront Biosci (Landmark Ed)
January 2025
Department of Cardiology, The Second Affiliated Hospital of Chongqing Medical University, 401336 Chongqing, China.
Background: Myocardial ischemia-reperfusion (I/R) injury and coronary microcirculation dysfunction (CMD) are observed in patients with myocardial infarction after vascular recanalization. The antianginal drug trimetazidine has been demonstrated to exert a protective effect in myocardial ischemia-reperfusion injury.
Objectives: This study aimed to investigate the role of trimetazidine in endothelial cell dysfunction caused by myocardial I/R injury and thus improve coronary microcirculation.
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