Carbon nanodots in endothelial cells and C57BL/6 mice: a study of toxicity and anti-inflammatory effect

UNCG Author/Contributor (non-UNCG co-authors, if there are any, appear on document)
Safeera Khan (Creator)
Institution
The University of North Carolina at Greensboro (UNCG )
Web Site: http://library.uncg.edu/
Advisor
Zhenquan Jia

Abstract: The advancement of therapy for cardiovascular disease (CVD) is paramount to public health, as it is the leading global cause of mortality [1]. Nanomedicine provides new opportunities in the ongoing efforts to reduce the economic and healthcare consequences of CVD. Carbon nanodots (CNDs) green-synthesized from microwave pyrolysis of ethylenediamine and citric acid are spherical, ~3 nm in diameter, and possess exceptional hydrophilic, biocompatible, fluorescent, and anti-oxidant properties. However, there is no current report on how these CNDs affect the cardiovascular system, particularly their potential in mediating endothelial dysfunction and cardiovascular disease (CVD). As a known biomarker of inflammation, Oxidized-LDL (Ox-LDL) induces inflammatory gene expression and monocyte extravasation that leads to atherosclerotic development. This study examines the role of CNDs in mediating Ox-LDL induced inflammation in human microvascular endothelial cells (HMEC-1). Our results demonstrate that CNDs can reduce Ox-LDL induced monocyte adhesion in HMEC-1s, which demonstrates their anti-inflammatory effects. The relative gene expression of the cytokine interleukin-8 (IL-8) was reduced by the addition of CNDs, which implies their action in mediating monocyte recruitment to the site of inflammation. While reactive oxygen species (ROS) perform many essential functions, their overproduction disrupts cellular oxidative balance, induces EC dysfunction, and leads to an inflammatory state. Studying the action of CNDs through Electron paramagnetic resonance (EPR) spectroscopy showed direct superoxide and hydroxyl radical-scavenging by CNDs. This result implies that the anti-inflammatory effects of CNDs seen in vitro are attributed to their direct scavenging of ROS. Furthermore, CNDs were found to ameliorate the cytotoxicity caused by Ox-LDL in HMEC-1s. Viability assays showed CNDs were not cytotoxic at measured concentrations to HMEC-1s in vitro. Animal studies involving mice did not show any morphological or physical changes between the CND and control groups. These collective results demonstrate the potential of CNDs to reduce inflammation and cytotoxicity caused by Ox-LDL in HMEC-1s, which implies their use in the development of novel therapy for cardiovascular disease.

Additional Information

Publication
Thesis
Language: English
Date: 2018
Keywords
Carbon Nanodots, Cardiovascular Disease
Subjects
Nanomedicine
Nanostructured materials
Vascular endothelial cells
Low density lipoproteins
Cardiovascular system $x Diseases

Email this document to