Date of Award

Summer 8-15-2021

Degree Type

Thesis

Degree Name

MS Biology

Department

Biology

Advisor

Heping Zhou, Ph.D.

Advisor

Heping Zhou, Ph.D.

Committee Member

Jane L. Ko, Ph.D.

Committee Member

Angela Klaus, Ph.D.

Committee Member

Daniel Nichols, Ph.D.

Keywords

Palmitate, Inflammation, BV2

Abstract

Obesity has become a pandemic health issue for the development of more serious illnesses such as insulin resistance, cardiovascular diseases, and hypertension. Among those pathological conditions, low grade chronic inflammation triggered by saturated fatty acids (SFA) such as palmitate (PA) has been suggested to be the culprit of crimes and various signaling modulators ranging from cellular surface receptors such as toll like receptors (TLRs) and G- protein – coupled receptor 40 (GPR40) to intracellular kinases like mitogen-activated protein kinase (MAPK) and protein kinase C (PKC) have been postulated. In this study, mouse BV2 cells were treated with different concentrations of PA and time and the mRNA expression levels of inflammatory cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β were examined. In order to determine how PA induced cytokine expression in BV2 cells, these cells were pre-treated with various pharmacological inhibitors followed by treatment with PA or BSA control, and the mRNA expressions of TNF-α, IL-6, and IL-1β were examined. Inhibition of PI3K and GPR40 by Wortmannin and DC260126 attenuated PA induced expression of these inflammatory cytokines, suggesting that PI3K and GPR40 might be involved in PA-induced production of inflammatory mediators in BV2 cells.

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