Vegetable-oils-based pressure-sensitive adhesives (PSAs) are being developed as a substitute for petrochemical-based PSAs for application in daily life. However, vegetable-oils-based PSAs face the problems of unsatisfactory binding strengths and easy aging. In this work, the grafting of antioxidants (tea polyphenol palmitates, caffeic acid, ferulic acid, gallic acid, butylated hydroxytoluene, tertiary butylhydroquinone, butylated hydroxyanisole, propyl gallate (PG), tea polyphenols) was introduced into an epoxidized soybean oils (ESO)/di-hydroxylated soybean oils (DSO)-based PSA system to improve the binding strengths and aging-resistant properties. PG was screened out as the most suitable antioxidant in the ESO/DSO-based PSA system. Under optimal conditions (ESO/DSO mass ratio of 9/3, 0.8% PG, 55% rosin ester (RE), 8% phosphoric acid (PA), 50 °C, and 5 min), the peel adhesion, tack, and shear adhesion of the PG-grafted ESO/DSO-based PSA increased to 1.718 N/cm, 4.62 N, and >99 h, respectively, in comparison with the control (0.879 N/cm, 3.59 N, and 13.88 h), while peel adhesion residue reduced to 12.16% in comparison with the control (484.07%). The thermal stability of the ESO/DSO-based PSA was enhanced after PG grafting. PG, RE, PA, and DSO were partially crosslinked in the PSA system, with the rest being free in the network structures. Thus, antioxidant grafting is a feasible method for improving the binding strengths and aging-resistant properties of vegetable-oils-based PSAs.

Obesity is an important risk factor for exacerbating chronic diseases such as cardiovascular disease and cancer. High serum level of saturated free fatty acids such as palmitate is an important contributor for obesity-induced diseases. Here, we examined the contribution of inflammasome activation in vascular cells to free fatty acid-induced endothelial dysfunction and vascular injury in obesity. Our findings demonstrated that high fat diet-induced impairment of vascular integrity and enhanced vascular permeability in the myocardium in mice were significantly attenuated by Nlrp3 gene deletion. In microvascular endothelial cells (MVECs), palmitate markedly induces Nlrp3 inflammasome complex formation leading to caspase-1 activation and IL1β production. By fluorescence microscopy and flow cytometry, we observed that such palmitate-induced Nlrp3 inflammasome activated was accompanied by a reduction in inter-endothelial tight junction proteins ZO-1/ZO-2. Such palmitate-induced decrease of ZO-1/ZO-2 was also correlated with an increase in the permeability of endothelial monolayers treated with palmitates. Moreover, palmitate-induced alterations in ZO-1/ZO-2 or permeability were significantly reversed by an inflammasome activity inhibitor, YVAD, or a high mobility group box 1 (HMGB1) activity inhibitor glycyrrhizin. Lastly, blockade of cathepsin B with Ca-074Me significantly abolished palmitate-induced activation of Nlrp3 inflammasomes, down-regulation of ZO-1/ZO-2, and enhanced permeability in MVECs or their monolayers. Together, these data strongly suggest that activation of endothelial inflammasomes due to increased free fatty acids produces HMGB1, which disrupts inter-endothelial junctions and increases paracellular permeability of endothelium contributing to early onset of endothelial injury during obesity.

Inflammation and the inflammasome complex formation are associated with numerous diseases, and palmitates or lipopolysaccharides (LPS) have been identified as potential links between these disorders. Recently, edible insects such as the Gryllus bimaculatus (GB) and the larva of Tenebrio molitor have emerged as alternative food sources. In the present study, the effect of GB on LPS‑ or palmitate‑induced production of inflammatory cytokines, the formation of the inflammasome complex, reactive oxygen species (ROS) generation, endoplasmic reticulum (ER) stress and cell death was investigated in RAW264.7 cells. The results revealed that GB extract downregulated the production of inflammatory cytokines (such as TNF‑α, IL‑1β and IL‑6). Since the role of the MAP kinase and NF‑κB signalling pathways in the production of inflammatory cytokines is well established, the translocation of p65 into the nucleus and the phosphorylation of IκB and MAP kinases were further examined. Both these processes were upregulated following LPS and palmitate treatment, but they were inhibited by the GB extract. Moreover, GB extract decreased LPS/palmitate‑induced inflammasome complex formation (assessed via analysing the levels of the apoptosis‑associated speck‑like protein containing a caspase‑recruitment domain, NOD‑like receptor family pyrin domain containing 3, cleaved caspase‑1 and IL‑1β), the generation of ROS, ER stress and cell death. Treatment with SB203580 (a p38 inhibitor), SP600125 (a JNK inhibitor) and pyrrolidinedithiocarbamate ammonium (an NF‑κB inhibitor) decreased the production of inflammatory cytokines, as well as helped in the recovery of LPS/palmitate‑induced cell death. Overall, GB extract served an inhibitory role in LPS/palmitate‑induced inflammation via inhibiting the MAP kinase and NF‑κB signalling pathways, inflammasome complex formation, ROS generation, ER stress and cell death.