Does Folic Acid inhibit interleukin-1β induced iNOS expression, nitric oxide release, or p47phox,or expression in insulin secreting β-cells?
Govan, Jeane M.
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Type I diabetesis associated with β-cellapoptosis, also known as programmed cell death, in the pancreatic islets of Langerhans. Folic acid has been shown to have a positive impact in a variety of ways inthe human body. In this study, the role of folic acid in interleukin-lβ (IL-1β)-induced nitricoxide (•NO) release in pancreatic β-cells from the rat insulinoma cell line INS-1 was investigated.Pretreatment of INS-1 β-cells with folic acid decreased the •NO release from β-cells after 24 hours of exposure. The pretreatment of INS-1 β-cells with folic acid provided inconsistent results. For half of these experiments,there was a significant inhibition (-54%) of IL-1β-induced •NO release from these cells. In this set of experiments folic acid was also observed to inhibit IL-1β-induced inducible nitric oxide synthase (iNOS) and p47phox expressions. Thus,the data suggested that folic acid is an inhibitor of interleukin-1β-induced iNOS expression and •NO release that caused oxidative stress. A component of NADPH oxidase, p47phox, was phosphorylated, which was activated by IL-lβ. This activation caused an increase in oxidative stress that damaged the mitochondriain cells, releasing cytochrome c, thereby inducing apoptosis. The other set of experiments in this study suggested that folic acid had no significant effect on IL-1β induced •NO release (-10% inhibition) in INS-1 cells. There was no difference in nitrite release, iNOS or p47phox expressions. These data showed inconsistencies; further studies are needed to demonstrate the effect of folic acid on IL-1β on INS-1 cells.
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