Dopamine-derived nanoparticles for the protection of irradiation-induced intestinal injury by maintaining intestinal homeostasis.

Radiotherapy of abdominal and pelvic tumors almost inevitably injures the intestine by oxidative stress and causes inflammation. Regrettably, traditional radioprotective agents for irradiation (IR) induced intestinal injury suffer from challenges such as poor solubility, unsatisfactory bioactivity and undesired adverse reactions, which significantly limit their usefulness. Polydopamine nanoparticles (PDA-NPs) have shown promising potential in scavenging reactive oxygen species (ROS) and suppressing inflammation. In this study, PDA-NPs were prepared by a simple method and their physical properties were characterized. Mice received two doses of PDA-NPs by oral gavage 22 h apart, and were irradiated with X-rays 2 h after the last gavage. The protective effect of PDA-NPs and possible mechanisms of protection against IR-induced intestinal injury were explored. The results showed that PDA-NPs were spherical and well dispersed, with good shape uniformity, compact structure, good colloid dispersion stability, concentration-dependent light absorption, and accurate quantification. Importantly, PDA-NPs reduced mortality and prolonged the average survival time of mice after IR. Furthermore, PDA-NPs protected mice from IR-induced injury to crypt-villus units and maintained intestinal barrier function in the intestine. In particular, PDA-NPs significantly inhibited the depletion of Lgr5+ intestinal stem cells (ISCs) and promoted cell regeneration after IR, which indicated that the regeneration ability of ISCs was maintained and the repair of intestinal structure and function was promoted. Finally, PDA-NPs significantly suppressed the apoptosis, inflammatory pyroptosis and DNA damage of intestinal cells induced by ionizing radiation. Altogether, our study suggested that PDA-NPs may have great potential in protecting the intestines from ionizing radiation damage.

Organic Hollow Mesoporous Silica as a Promising Sandalwood Essential Oil Carrier.

As film-forming agents, fillers and adsorbents, microplastics are often added to daily personal care products. Because of their chemical stability, they remain in the environment for thousands of years, endangering the safety of the environment and human health. Therefore, it is urgent to find an environmentally friendly substitute for microplastics. Using n-octyltrimethoxysilane (OTMS) and tetraethoxysilane (TEOS) as silicon sources, a novel, environmentally friendly, organic hollow mesoporous silica system is designed with a high loading capacity and excellent adsorption characteristics in this work. In our methodology, sandalwood essential oil (SEO) was successfully loaded into the nanoparticle cavities, and was involved in the formation of Pickering emulsion as well, with a content of up to 40% (w/w). The developed system was a stable carrier for the dispersion of SEO in water. This system can not only overcome the shortcomings of poor water solubility and volatility of sandalwood essential oil, but also act as a microplastic substitute with broad prospects in the cosmetics and personal care industry, laying a foundation for the preparation and applications of high loading capacity microcapsules in aqueous media.

Protection of agarwood essential oil aroma by nanocellulose-graft-polylactic acid.

Essential oil products are often volatile, and their aromas cannot be effectively preserved over long periods of time. In this study, nanocellulose crystals were modified, and an amphiphilic copolymer was prepared by ring-opening polymerisation to produce wall materials. A nanocellulose crystal-grafted polylactic acid copolymer was successfully synthesised and characterised using nuclear magnetic resonance spectrometry, Fourier transform infrared spectrometry, X-ray diffraction, and thermogravimetric analysis. Because of the amphiphilic properties of the synthesised copolymer, an agarwood essential oil nanoemulsion system was prepared. Using transmission electron microscopy and dynamic laser light scattering, the nanoemulsion was observed to have an apparent shell-core structure. The nanoemulsion was uniformly distributed, and the system had good stability. Finally, the electronic nose results showed that the nanocellulose crystal-grafted polylactic acid copolymer micelle effectively protected agarwood essential oil aromas.

Carbon Monoxide-Releasing Molecule-3 Suppresses Tumor Necrosis Factor-α- and Interleukin-1ß-Induced Expression of Junctional Molecules on Human Gingival Fibroblasts via the Heme Oxygenase-1 Pathway.

Human gingival fibroblast barrier dysfunction caused by inflammation contributes to gingivitis and can lead to inflammatory periodontal disease. The disease features include upregulated epithelial permeability, increased inflammatory mediators, and downregulated junctional complex molecules. Carbon monoxide- (CO-) releasing molecule-3 (CORM-3) is a water-soluble compound that has demonstrated anti-inflammatory effects in in vitro and in vivo studies. In this study, we aimed to investigate the effects of CORM-3 on the expression of tight and adherens junction molecules on human gingival fibroblasts (HGFs) stimulated with tumor necrosis factor-α (TNF-α) and interleukin-1ß (IL-1ß). HGFs were cultured from the explants of normal human gingival tissues, which were stimulated in the presence or absence of CORM-3. Epithelial barrier function was evaluated by paracellular permeability and junctional complex molecule expression analyses. The protein and mRNA expression levels of adherens junction molecules (VE-cadherin and ß-catenin) and tight junction molecules (zona occludens-1, ZO-1) were studied using western blot analysis and reverse transcription-quantitative polymerase chain reaction (RT-PCR). The mRNA and protein expression levels of these cytokines were also analyzed in HGFs transiently transfected with HO-1 small interfering RNA (siRNA) in response to TNF-α and IL-1ß stimulation. CORM-3 reduced permeability and enhanced the expression of junctional complex molecules (ZO-1, VE-cadherin, and ß-catenin) in TNF-α- and IL-1ß-induced HGFs. However, these effects of CORM-3 were attenuated when HO-1 siRNA was transiently transfected in HGFs. These findings indicate that CORM-3 exerts anti-inflammatory effects on TNF-α- and IL-1ß-stimulated HGFs via the HO-1 pathway, which suggests the promising potential of CORM-3 in the treatment of inflammatory periodontal disease.