Cell biochemistry and biophysics
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Cell Biochem. Biophys. · Nov 2013
Adiponectin protects against hyperoxic lung injury and vascular leak.
Adiponectin (Ad), an adipokine exclusively secreted by the adipose tissue, has emerged as a paracrine metabolic regulator as well as a protectant against oxidative stress. Pharmacological approaches of protecting against clinical hyperoxic lung injury during oxygen therapy/treatment are limited. We have previously reported that Ad inhibits the NADPH oxidase-catalyzed formation of superoxide from molecular oxygen in human neutrophils. ⋯ Furthermore, the hyperoxia-induced lung injury, vascular leak, and lipid peroxidation were significantly attenuated in AdTg mice in vivo. Also, AdTg mice exhibited elevated levels of total thiols and GSH in the lungs as compared with WT mice. For the first time, our studies demonstrated that Ad protected against the hyperoxia-induced lung damage apparently through attenuation of oxidative stress and modulation of thiol-redox status.
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Cell Biochem. Biophys. · Nov 2013
DNA microarray and quantitative analysis reveal enhanced myocardial VEGF expression with stunted angiogenesis in human tetralogy of Fallot.
Tetralogy of Fallot (ToF) is a cyanotic congenital heart disease with prominent right ventricular hypertrophy (RVH) associated with impaired myocardial oxygen and nutrient supply. Consequently, the right ventricle may manifest in altered molecular phenotype with a number of adaptive and inherited gene profiles which are largely unknown. The aim of the present study was to investigate the myocardial differential gene expression profile and to assess myocardial vascularisation in patients with ToF. ⋯ VEGF staining in cardiomyocytes was increased in ToF-1 (1.5-fold, p < 0.05) as compared to ToF-2. Video image analysis revealed enhanced vascular density (p < 0.01) with enlarged myocyte cross sectional area (p < 0.01), but vascular wall thickness remained unchanged in ToF-1 patients as compared to age matched controls. Our data suggest that RVH is associated with profound changes in gene profile for a number of genes, where VEGF/VEGF-R system contributes to enhance, but stunted myocardial angiogenesis in patients with ToF.
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Cell Biochem. Biophys. · Nov 2013
Propofol administration modulates AQP-4 expression and brain edema after traumatic brain injury.
The increased intracranial pressure caused by brain edema following traumatic brain injury (TBI) always leads to poor patient prognosis. Aquaporin-4 (AQP-4) plays an important role in edema formation and resolution, which may provide a novel therapeutic target for edema treatment. In this present study, we found that propofol treatment, within a short time, after TBI significantly reduced brain edema in a controlled cortical injury rat model and suppressed in vivo expression of AQP-4. ⋯ We also found that both NFκB and p38/MAPK pathways were involved in IL-1β and TNF-α-induced AQP-4 expression and that propofol functions as a dual inhibitor of NFκB and p38/MAPK pathways. In conclusion, treatment with propofol, within a short time, after TBI attenuates cerebral edema and reduces the expression of AQP-4. Propofol modulates acute AQP-4 expression by attenuating IL-1β and TNF-α expression and inhibiting IL-1β and TNF-α induced AQP-4 expression.