Effects of carbon nanodots on TNF-a-induced inflammatory gene expression in mouse spleen tissue

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

Abstract: The main cause of cardiovascular disease is known to be atherosclerosis, which is regulated by pro-inflammatory molecules such as IL-6, IL-1ß, Ho-1, MCP-1, TNF-a, VCAM1 IDT. The spleen is a vital part of the immune system and has been investigated for potential pathways that relate pro-inflammatory cytokines with macrophages. A new class of nanoparticles, Carbon Nanodots (CNDs), have been expressed as potential candidates for bioimaging, biosensing, and drug delivery. Some studies have also found that in vitro, CND have some anti-inflammatory effects. Recently, the spleen has been investigated as a potential pathway that may connect the pro-inflammatory cytokines with the inflammation-mediated atherosclerosis pathway. However, the effect of CNDs in the spleen have not been investigated. This study uses mice spleen tissue to investigate the effect of CNDs on TNF-a-mediated expressions of pro-inflammatory genes. C57BL/6 mice were treated with TNF-a (25 ug/kg bw), CNDs (2.5 mg/kg CNDs), both TNF-a and CNDs, or neither to serve as the control. The spleen tissue was harvested and homologized, and the isolated RNA was used to make cDNA. The cDNA was used to evaluate the expression of various genes related to the inflammatory response (IL-6, IL-1ß, Ho-1, MCP-1, Nrf2, TNF-a, VCAM1 IDT) was tested using RT-PCR. Our current results have shown there was a statistically significant decrease in TNF-a in the Ho-1 anti-inflammatory gene. Other experimental data are still in progress, which will allow for a better understanding of the actions of CNDs on spleen inflammation in vivo.

Additional Information

Publication
Honors Project
Language: English
Date: 2022
Keywords
cardiovascular disease, Carbon nanodots, anti-inflammatory gene expression, biomedical engineering

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