Repeated positive acceleration exposure exacerbates endothelial dysfunction in high-fat-diet-induced hyperlipidemic rats

Abstract

IntroductionIt remains unclear whether exposure to repeated positive acceleration (+Gz) can exacerbate endothelial dysfunction on the basis of hyperlipidemia. The aim of this study was to investigate the effect of repeated +Gz exposure on endothelial function in high-fat-diet-induced hyperlipidemic rats.Material and methodsMale Sprague-Dawley rats were randomly divided into control, repeat +Gz exposure, high-fat diet (HFD), and +Gz + HFD groups. The rats in the +Gz group were exposed to +Gz and the rats in the HFD group were fed a diet with 2% cholesterol. The rats in the +Gz + HFD group received both the +Gz exposure and HFD. Eight weeks later, the endothelium-dependent relaxation of the aorta was tested and the ultrastructure of the endothelial cells was observed using transmission electron microscopy. Quantitative real-time polymerase chain reaction and Western blot were used to detect the mRNA and protein expression of endothelial function-associated proteins.ResultsRepeated +Gz exposure elevated the serum level of LDL-C in HFD rats. In the +Gz + HFD rats, the ACh-induced relaxation in the aorta rings was significantly attenuated and the endothelial cells of the aorta were dramatically damaged compared with HFD rats. Nitric oxide content and eNOS expression in the aortic tissue were markedly decreased and the oxidative stress was more serious in the +Gz + HFD rats compared with HFD rats. In addition, repeated +Gz exposure significantly increased serum ox-LDL level and LOX-1 expression in the aorta of HFD rats, thereby activating NF-κB p65 and upregulating the expression of interleukin 6, ICAM-1 and VAP-1.ConclusionsRepeated +Gz exposure promotes endothelial dysfunction in HFD-induced hyperlipidemic rats.

Formic Acid Induces Hypertension-Related Hemorrhage in hSSAOTG in Mice and Stroke Patients

“…To address whether SSAO overexpression is mediated by miR134/NF-kB p65 pathway (Fig. 3a) 22,23 , we transfected mimics of miR134 into cultured HASMC. The changes in mRNA levels of NF-kB p65 and SSAO were examined by Q-PCR; their protein contents were quanti ed by immuno uorescence (I.F.)…”

“…High-fat diets have been found to change the pro le of microRNAs including miR134 9 , and to enhance SSAO expression in blood vessels. MiR134 activates NF-kB 22 , and the phosphorylation of NF-kB p65 upregulates SSAO. In the present study, we provided evidence that miR134 upregulated SSAO in the cultured HASMC, wild-type mice and hSSAO TG mice fed with high-fat diet, especially, in hemorrhagic stroke patients.…”

Title High fat-induced upregulation of LOX-1 expression in RF/6A cells with high glucose

“…ICAM-1 is expressed at a low level on resting VEC and exerts its biological activity through binding with speci c receptors on the surface of VEC [29]. As a transmembrane protein of endothelial cells, ICAM-1 is vital for stabilization of intercellular interactions and promotion of leukocyte and endothelial cell migration [30,31].…”