RESUMO
Because of the increasing demand for healthy and safe food, Monascus spp. have gained much attention as a sustainable source of natural food colorant. In this study, a novel integrated fermentation system consisting of surfactant and in situ extractant was established for efficiently producing yellow pigments by M. purpureus sjs-6. The maximum production of Monascus yellow pigment (669.2 U/mL) was obtained when 40% soybean oil (as extractant) was supplied at the beginning and 5 g/L Span-80 (as surfactant) was supplied at the 72nd h, which resulted in production 27.8-times of that of the control. Critical factors such as alleviating the product inhibition, increasing the membrane permeability, changing the hyphal morphology, and influencing the cell activity have been suggested as the underlying mechanisms. This system is of great significance for the bioprocess, which suffers product inhibition, and it can serve as a promising step for enhancing the yield of hydrophobic metabolites.
Assuntos
Fermentação , Monascus/metabolismo , Pigmentos Biológicos/biossíntese , Permeabilidade da Membrana Celular , Ácidos Graxos/metabolismo , Hexoses , Microscopia Acústica , Monascus/fisiologia , Monascus/ultraestrutura , Óleo de Soja , TensoativosRESUMO
Damage to the endothelial glycocalyx is a critical factor in increased pulmonary vascular permeability, which is the basic pathological feature of acute respiratory distress syndrome (ARDS). Neferine (Nef), a bisbenzylisoquinoline alkaloid isolated from green seed embryos of Nelumbo nucifera Gaertn, has extensive pharmacological activity. In this study, we showed that Nef reduced lung-capillary permeability, down-regulated the production of cytokines (IL-1ß, IL-6, TNF-α, and IL-10) and inhibited the activation of the NF-κB signaling pathway in mice with lipopolysaccharide (LPS)-induced ARDS. Further analysis indicated that Nef provided protection against endothelial glycocalyx degradation in LPS-induced ARDS mice (in vivo) and in LPS-stimulated human umbilical vein endothelial cells (in vitro). The glycocalyx-protective effect of Nef may be initiated by suppressing the production of mitochondrial ROS (mtROS) and decreasing oxidative damage. Nef was also found to promote glycocalyx restoration by accelerating the removal of mtROS in endothelial cells in LPS-induced ARDS. These results suggested the potential of Nef as a therapeutic agent for ARDS associated with Gram-negative bacterial infections and elucidated the mechanisms underlying the protection and restoration of the endothelial glycocalyx.