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This study aimed to investigate the effects of MCC950 in a rat model of sepsis-associated encephalopathy (SAE). Adult male rats were randomly assigned to 12 groups according to the surgery or treatment received and evaluation times. The SAE model was established using the cecal ligation and puncture (CLP) method.

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Background: Myocardial ischemia-reperfusion injury (MIRI) is an important complication in the treatment of heart failure, and its treatment has not made satisfactory progress. Nitroxyl (HNO) showed protective effects on the heart failure, however, the effect and underlying mechanism of HNO on MIRI remain largely unclear.

Methods: MIRI model in this study was established to induce H9C2 cell injury through hypoxia/reoxygenation (H/R) in vitro.

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Hemolytic anemia (HA) is characterized by massive destruction of red blood cells (RBCs) and insufficient oxygen supply, which can lead to shock, organ failure, even death. Recent studies have preliminarily demonstrated the therapeutic effectiveness of whole blood exchange (WBE) in the management of acute hemolytic anemia and exhibited potential for reducing the duration of corticosteroid treatment, while the underlying mechanism of WBE therapy was not investigated in preclinical study. Hence, we investigate the therapeutic mechanisms of WBE in HA through established continued WBE therapy in rats creatively.

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Background/aims: MOTS-c belongs to a group of mitochondrial peptides involved in metabolic processes in the body. This peptide has garnered increasing attention since its discovery in 2015 because of its potential to ameliorate metabolic parameters in animals with diabetes or insulin resistance. MOTS-c is involved in muscle metabolism; however, little is known about its role in fiber differentiation.

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Leptin drives glucose metabolism to promote cardiac protection via OPA1-mediated HDAC5 translocation and Glut4 transcription.

Funct Integr Genomics

January 2025

Department of Cardiology, Guizhou Provincial People`s Hospital, 83 Zhongshan East Road, Guiyang City, 550002, Guizhou Province, China.

Metabolic reprogramming, the shifting from fatty acid oxidation to glucose utilization, improves cardiac function as heart failure (HF) progresses. Leptin plays an essential role in regulating glucose metabolism. However, the crosstalk between leptin and metabolic reprogramming is poorly understood.

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