RESUMO
Fungal infection possesses the characteristics of high invasion depth and easy formation of a biofilm under the skin, which greatly hinders the treatment process. Here, traditional Chinese medicine moxa is carbonized and modified with zinc oxide (ZnO) nanosheets to synthesize carbonized moxa@ZnO (CMZ) with the dual response properties of yellow light (YL) and ultrasound (US) for synergistic antifungal therapy. CMZ with narrow bandgap can respond to long-wavelength YL that is highly safe and helpful for skin repair. Simultaneously, CMZ with a piezoelectric effect can further enhance the photocatalytic efficiency under the stimulation of US with high tissue penetration. Gene mechanism investigation indicates that when exposed to US and YL irradiation, CMZ-based therapy can adjust the expression of genes associated with fungal virulence, metabolic activity, mycelial growth and biofilm development, thus efficaciously eradicating planktonic Candida albicans (C. albicans) and mature biofilm. Importantly, despite the 1.00 cm thick tissue barrier, CMZ can rapidly eliminate 99.9% of C. albicans within 4 min, showing a satisfactory deep fungicidal efficacy. The in vivo therapeutic effect of this strategy is demonstrated in both open wound and deep cutaneous infection tests, speaking of dramatically better efficacy than the traditional fungicide ketoconazole (KTZ).
Assuntos
Micoses , Óxido de Zinco , Antifúngicos/farmacologia , Óxido de Zinco/farmacologia , Cetoconazol , Candida albicans , Biofilmes , Testes de Sensibilidade MicrobianaRESUMO
Ferritin, a distinctive iron-storage protein, possesses a unique cage-like nanoscale structure that enables it to encapsulate and deliver a wide range of biomolecules. Recent advances prove that ferritin can serve as an efficient 8 nm diameter carrier for various bioinorganic nutrients, such as minerals, bioactive polyphenols, and enzymes. This review offers a comprehensive summary of ferritin's structural features from different sources and emphasizes its functions in iron supplementation, calcium delivery, single- and coencapsulation of polyphenols, and enzyme package. Additionally, the influence of innovative food processing technologies, including manothermosonication, pulsed electric field, and atmospheric cold plasma, on the structure and function of ferritin are examined. Furthermore, the limitations and prospects of ferritin in food and nutritional applications are discussed. The exploration of ferritin as a multifunctional protein with the capacity to load various biomolecules is crucial to fully harnessing its potential in food applications.
Assuntos
Ferritinas , Ferro , Ferritinas/química , Ferro/metabolismo , Minerais/metabolismo , Polifenóis/químicaRESUMO
In a previous study by our group memory impairment in rats with minimal hepatic encephalopathy (MHE) was associated with the inhibition of the glutamatenitric oxidecyclic guanosine monophosphate (GluNOcGMP) pathway due to elevated dopamine (DA). However, the effects of DA on the GluNOcGMP pathway localized in primary cortical astrocytes (PCAs) had not been elucidated in rats with MHE. In the present study, it was identified that when the levels of DA in the cerebral cortex of rats with MHE and highdose DA (3 mg/kg)treated rats were increased, the colocalization of Nmethyldaspartate receptors subunit 1 (NMDAR1), calmodulin (CaM), nitric oxide synthase (nNOS), soluble guanylyl cyclase (sGC) and cyclic guanine monophosphate (cGMP) with the glial fibrillary acidic protein (GFAP), a marker protein of astrocytes, all significantly decreased, in both the MHE and highdose DAtreated rats (P<0.01). Furthermore, NMDAinduced augmentation of the expression of NMDAR1, CaM, nNOS, sGC and cGMP localized in PCAs was decreased in MHE and DAtreated rats, as compared with the controls. Chronic exposure of cultured cerebral cortex PCAs to DA treatment induced a dosedependent decrease in the concentration of intracellular calcium, nitrites and nitrates, the formation of cGMP and the expression of NMDAR1, CaM, nNOS and sGC/cGMP. High doses of DA (50 µM) significantly reduced NMDAinduced augmentation of the formation of cGMP and the contents of NMDAR1, CaM, nNOS, sGC and cGMP (P<0.01). These results suggest that the suppression of DA on the GluNOcGMP pathway localized in PCAs contributes to memory impairment in rats with MHE.