A study of the effect of carbon nanodots on TNF-a induced human aortic endothelial inflammation

Abstract

Atherosclerosis, a prevalent contributor to cardiovascular disease (CVD) on a global scale, is primarily triggered by inflammation, which plays a critical role in initiating the disease process. This inflammatory response leads to endothelial cell dysfunction or damage, ultimately resulting in the formation of plaque buildup within the inner walls of arteries. The emerging nanomaterials provide new prospects to lower the economic and healthcare costs associated with CVD. Carbon nanodots (CNDs), a type of nanoparticle, are particularly attractive due to their biocompatibility, fluorescent capabilities, and potential antioxidant properties. While much research has been conducted on the use of CNDs as bioimaging and drug-delivery tools, their potential anti-inflammatory effects, particularly in the cardiovascular system, have yet to receive much attention. The aorta is particularly vulnerable to atherosclerosis, being the largest affected area. In this study, HAEC (human aortic endothelial cells) were chosen as the cell line due to their capability to express endothelial cell surface biomarkers, and their common use in vascular research has provided a comprehensive understanding of cell lines. However, the impact of CNDs on HAEC has not been investigated yet. In this study, the impact of CNDs on TNF-a induced inflammation in HAEC was studied. Our results demonstrate CNDs inhibited the production of inflammatory genes, such as IL-8, E-Selectin, and CCL2, in vitro in response to TNF-a. With concentrations of up to 0.6 mg/mL used, CNDs did not show any cytotoxic capabilities in our results in HAEC. Fluorescence microscopy data indicated that HAEC were able to uptake CNDs at the concentrations used. The NF-?B Luciferase Reporter Cell assay results showed that CNDs have the ability to reduce TNF-a-mediated increase in NF-kB activity. The results of the Nrf2 pathways also indicated that CNDs can activate Nrf2 transcription, thus leading to an increase in Nrf2-mediated upregulation of various antioxidant genes, including HO-1, GCLC, NQO-1, and GR. Through these results, it can be suggested that the anti-inflammatory effects of CNDs can be related to the downregulation of the NF-?B pathway and the up-regulation of the Nrf2 pathway signaling. This is the first study to examine the effects of CNDs on human aorta endothelial inflammation. [This abstract may have been edited to remove characters that will not display in this system. Please see the PDF for the full abstract.]]]> 2023 English http://libres.uncg.edu/ir/uncg/f/Amin_uncg_0154M_13858.pdf oai:libres.uncg.edu/39109 2023-07-11T15:48:04Z UNCG Gait variability, cognitive control, and brain BOLD signal variability in healthy, young adults Angelino, Shena A. NC DOCKS at The University of North Carolina at Greensboro <![CDATA[Gait variability has been studied in various diseases and in aging, however variability is observed even in young, healthy adults. Variability in stride time can be characterized in terms of short-term, or step-by-step variability, and long-term variability. It is plausible that these temporal parameters in gait have similar neural origins to the dual modes of cognitive control since both require goal-oriented, higher-order processing. A handful of frontoparietal areas have been widely observed to be important for the dynamic nature of these abilities. The purpose of this study is to test the hypothesis that the adaptability of this frontoparietal network, as defined by the variability of the blood oxygen level-dependent (BOLD) signal, underlies a relationship between cognitive control strategies and stride time variability. We recruited twenty healthy young adults between 18 and 35 years old (10 females; average age = 23.6 ± 3.9 years old) to measure performance on a stepping-in-place task, cognitive control, and BOLD signal variability using resting-state functional MRI. A Pearson correlation wase used to determine the association between proactive and reactive cognitive control strategies and long and short-term gait variability, and a partial least squares correlation was used to determine if there is a pattern of BOLD signal variability in a set of frontoparietal regions that jointly explains these cognitive-gait relationships. There was no relationship between cognitive control strategy and long- or short-term variability, however there was a pattern of BOLD variability, primarily in control and salience/ventral attention network regions, that was associated with both short-term gait variability, and to a lesser extent, long-term gait variability (Permutation p = 0.0323). These findings provide evidence of gait variability as a marker of brain variability in healthy, young adults and may open the door to understanding its role as a biomarker of brain health