Optimization and degradation studies of cellulose transesterification to palmitate esters in superbase ionic liquid.

Cellulose palmitates (CPs) were synthesized with varying degrees of substitution (DS) via a catalyst-free, homogeneous transesterification of cellulose in a novel superbase ionic liquid (SB-IL) system, specifically 5-methyl-1,5,7-triaza-bicyclo[4.3.0]non-6-enium acetate [mTBNH][OAc], combined with dimethyl sulfoxide (DMSO) as a co-solvent, using vinyl palmitate as the acylating agent. We examined the influence of reaction temperature, reaction time, and the molar ratio of vinyl palmitate to anhydroglucose unit (AGU) on the DS, which ranged from 0.5 to 2.3 under the given conditions. Notably, the reaction order of the three hydroxy groups was C6-OH > C2-OH > C3-OH. To elucidate the chemical structure of CPs and confirm the transesterification process, various spectroscopic techniques including 1H nuclear magnetic resonance (NMR), 13C NMR, heteronuclear single quantum correlation (HSQC), and solid-state NMR were employed. Higher reaction temperatures and extended reaction times led to a decrease in the DS of CPs, potentially due to the degradation of some of the involved chemicals during the transesterification process. We also investigated the stability of the pure ionic liquid (IL) and the IL + DMSO solvent system at elevated temperatures by heating them at 100 °C for 5 h, confirming their chemical integrity through 1H NMR analysis. Additionally, we assessed the compatibility between the solvent system and cellulose by subjecting a mixture of cellulose and the solvent system to 100 °C for 5 h. To compare the structures of untreated cellulose and regenerated cellulose, Fourier transform infrared (FT-IR) spectroscopy was employed. Furthermore, we determined the molar mass of both untreated cellulose and regenerated cellulose, as well as CPs synthesized at higher reaction temperatures and longer durations, using intrinsic viscosity measurements. Lastly, we examined the solubility properties of CPs.

AM1638, a GPR40-Full Agonist, Inhibited Palmitate- Induced ROS Production and Endoplasmic Reticulum Stress, Enhancing HUVEC Viability in an NRF2-Dependent Manner.

BACKGRUOUND: G protein-coupled receptor 40 (GPR40) is a key molecule in diabetes and fatty liver, but its role in endothelial dysfunction remains unclear. Our objective in this study was to determine whether GPR40 agonists protect endothelial cells against palmitatemediated oxidative stress. METHODS: Human umbilical vein endothelial cells (HUVECs) were used to investigate effects of various GPR40 agonists on vascular endothelium. RESULTS: In HUVECs, AM1638, a GPR40-full agonist, enhanced nuclear factor erythroid 2-related factor 2 (NRF2) translocation to the nucleus and heme oxygenase-1 (HO-1) expression, which blocked palmitate-induced superoxide production. Those antioxidant effects were not detected after treatment with LY2922470 or TAK875, GPR40-partial agonists, suggesting that GPR40 regulates reactive oxygen species (ROS) removal in a ligand-dependent manner. We also found that palmitate-induced CCAAT/enhancer-binding protein homologous protein expression; X-box binding protein-1 splicing, nuclear condensation, and fragmentation; and caspase-3 cleavage were all blocked in an NRF2-dependent manner after AM1638 treatment. Both LY2922470 and TAK875 also improved cell viability independent of the NRF2/ROS pathway by reducing palmitate-mediated endoplasmic reticulum stress and nuclear damage. GPR40 agonists thus have beneficial effects against palmitate in HUVECs. In particular, AM1638 reduced palmitate-induced superoxide production and cytotoxicity in an NRF2/HO-1 dependent manner. CONCLUSION: GPR40 could be developed as a good therapeutic target to prevent or treat cardiovascular diseases such as atherosclerosis.