Abstract
Despite the promise of its therapeutic benefits, curcumin as a free molecule has failed to demonstrate significant clinical success. Arguably, its inherently poor stability and rapid clearance is a significant reason for these negative outcomes. The incorporation of curcumin into the backbone of a crosslinked hydrogel that utilizes poly(beta-amino ester) (PBAE) chemistry can provide a tunable protective network with the ability to release at a controlled rate while improving its therapeutic potential. Kinetics of curcumin conjugated PBAE microparticles controlled release delivery system in the presence of oxidative environments was studied for the first time, where consumption rates of active curcumin and release products were obtained. The constituent amount of curcumin present in solution was improved by incorporating the active into the network in comparison to curcumin as a free drug. Modeling curcumin conjugated PBAE microparticles will provide a design platform to improve translation and overall success in delivering a therapeutic agent that matches levels of oxidative stress.
Highlights
The cytosolic balance between reactive oxygen species and antioxidants is essential to the physiological health of a cell [1]
We report on the consumption of curcumin as a free molecule and the degradation product release and consumption profile from three controlled release curcumin conjugated poly(beta-amino ester) (PBAE) MP systems
Curcumin and acryloyl chloride were reacted in a 1:3 molar ratio in anhydrous THF in the presence of triethylamine for 24 h in the dark to produce Curcumin multiacrylate (CMA) comprised of 45% curcumin diacrylate, 55% curcumin triacrylate and 0.9% curcumin monoacrylate characterized by reverse-phase high performance liquid chromatography (HPLC) (Water Phenomenex C18 column, 5 mm, 250 mm  4.6 mm (ID) on a Shimadzu Prominence LC-20 AB HPLC system) coupled with a UV-Visible (UV-Vis) detector set at 420 nm
Summary
The cytosolic balance between reactive oxygen species and antioxidants is essential to the physiological health of a cell [1]. This interferes with the intracellular regulation, leading to the formation of superoxide anions These free radicals are linked to a specific inflammasome, nucleotide-binding domain and leucine-rich repeat containing Proteins 1 (NRLP1) that activates pro-inflammatory cytokines, such as interleukin 1b (IL-1b) [9]. The activation and upregulation of these receptors activate matrix metalloproteinases, which can cause tissue damage and lead to apoptosis and cell death [11] These detrimental cell signaling cascades continue to inhibit proliferation of healthy epithelial cells, which lead to the formation of severe ulcers within the oral cavity [8]. Temporary treatments such as topical anesthetics and analgesics are implemented during prognosis [6]; a successful drug to scavenge free radicals and maintain homeostasis to reduce the onset of OM for all patients does not exist and is in high demand
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