Microencapsulation of fish oil by spray drying, spray freeze-drying, freeze-drying, and microwave freeze-drying: Microcapsule characterization and storage stability.

The objective of this paper was to evaluate the effect of spray drying (SD), spray freeze-drying (SFD), freeze-drying (FD), and microwave freeze-drying (MFD) on the characteristics of fish oil (FO) microcapsules. The physicochemical properties, morphology, fatty acid composition, and stability of the microcapsules were analyzed. The encapsulation efficiencies of microcapsules dried by SD, SFD, FD, and MFD were 86.98%, 77.79%, 63.29%, and 57.89%, respectively. SD microcapsules exhibited superior properties in terms of effective loading capacity, color, and flowability. Conversely, SFD microcapsules demonstrated improved solubility. Microencapsulation positively affected the thermal stability of FO, but the content of unsaturated fatty acids decreased. The findings from the storage experiment indicated that the oxidative stability of SD fish oil microcapsules was marginally lower compared to microcapsules produced through three alternative drying techniques, all of which were based on the FD concept. The comparison of various drying methods and their effects on the quality of FO microcapsules offers valuable insights that can serve as a foundation for the industrial production of high-quality microcapsules.

Effect of gum arabic and thermal modification of whey protein isolate on the characteristics of Cornus officinalis flavonoid microcapsules.

Whey protein isolates (WPIs) were treated at 50, 60, 70, and 80°C to obtain thermally modified WPI. Gum arabic (GA) and thermal modification of WPI were used as novel wall materials to improve the quality of Cornus officinalis flavonoid (COF) microcapsules using microwave freeze-drying technique in this study. Results showed that all the thermal modification treatment decreased emulsifying activity index of WPI, whereas the solubility and emulsifying stability index (ESI) of WPI gradually increased with the increase of heating temperature. Compared to the untreated protein, the thermal modification treatment at 70°C increased the solubility and ESI of WPI by 14.91% ± 0.71% and 26.70% ± 0.94%, respectively. The microcapsules prepared with the modified protein at 60°C had the highest encapsulation efficiency (95.13% ± 2.36%), the lowest moisture content (1.42% ± 0.34%), and the highest solubility (84.41% ± 0.91). Scanning electron microscopy images showed that COF microcapsules were uniformly spherical, and the sizes of the microcapsules were in the following order: 12.42 ± 0.37 µm (80°C) > 11.7 ± 0.23 µm (untreated group) > 9.44 ± 0.33 µm (60°C) > 9.24 ± 0.14 µm (50°C) > 7.69 ± 0.29 µm (70°C). In the simulated in vitro digestion experiments, the release rate of COF microcapsules in the gastric digestion phase was less than that in the intestinal digestion phase, and it reached 66.46% at intestinal digestion phase. These results suggested that heated WPI and GA could be an effective nanocarrier to enhance the stability of COF.

Anti-high mobility group box-1 antibody attenuated vascular smooth muscle cell phenotypic switching and vascular remodelling after subarachnoid haemorrhage in rats.

Although cerebral vascular smooth muscle cell (VSMC) phenotypic switching is involved in the vascular dysfunction after subarachnoid haemorrhage (SAH), the precise mechanisms are still unclear. High mobility group box-1 (HMGB1) has been identified as a modulator in VSMC proliferation. The purpose of this study was to investigate the potential role of HMGB1 in the VSMC phenotypic switching following SAH. An endovascular perforation SAH model was used in our experiments. The expression levels of HMGB1, α-smooth muscle actin (α-SMA), osteopontin (OPN), smooth muscle myosin heavy chain (SM-MHC), embryonic smooth muscle myosin heavy chain (Smemb), TXA2, PAR-1 and AT1 receptor were evaluated by Western blot analyses. Iba1-positive cells and apoptotic cells were determined by immunofluorescence staining and TUNEL staining, respectively. Vasoconstriction of the isolated basilar artery was stimulated by thrombin and KCl. We found that HMGB1 expression was markedly increased following SAH, and anti-HMGB1 mAb significantly reversed VSMC phenotypic switching and vascular remodelling in rats. However, the effects of HMGB1 on VSMC phenotypic switching were partly blocked in the presence of SC79, a potent activator of phosphatidylinositol-3-kinase-AKT (PI3K/AKT). Furthermore, the enhanced vasoconstriction and decreased cerebral cortical blood flow induced by SAH were reversed by anti-HMGB1 mAb. Finally, we found that anti-HMGB1 mAb attenuated microglial activation and brain oedema, ameliorating neurological dysfunction. These results indicated that HMGB1 is a useful regulator of VSMC phenotypic switching and vascular remodelling following SAH and might be exploited as a novel therapeutic target for delayed cerebral ischaemia.