Background Lutein has been of great interest to the food processing and pharmaconutrient industries owing to its beneficial effects on human health. However, lutein is very sensitive to heat, light, pH and oxidative conditions, which limits its application in food systems. The present study aimed to prepare lutein–alginate microspheres by a calcium chloride gelation method with the purpose of improving the stability and antioxidant abilities of lutein. Results The loading capacity of lutein in the microspheres was approximately 5.3% (w/w) and the entrapment efficiency was about 63%. The loaded microspheres were nearly spherical with an average size of 150 μm. They exhibited a crimped surface by scanning electron microscopy. The lutein was in amorphous state by X‐ray powder diffraction. Analysis by Fourier transform infrared spectroscopy and molecular docking revealed an intermolecular hydrogen bond interaction between lutein and sodium alginate. In vitro release experiments showed that the microspheres presented slower release at acidic conditions than at neutral intestinal conditions. The 2,2‐diphenyl‐1‐picrylhydrazyl radical scavenging activity of the microencapsulated lutein was higher than that of free lutein. The stability of lutein in the microspheres was improved significantly when compared with that of free lutein at various temperatures. Conclusion The present work successfully developed well‐protected lutein–alginate microspheres. This indicates that it is feasible to use microspheres loaded with lutein as antioxidant functional ingredients in food products. © 2019 Society of Chemical Industry

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The mechanisms underlying neurodegenerative diseases are not fully understood yet. However, an increasing amount of evidence has suggested that these disorders are related to oxidative stress. We reported herein that lipoamide (LM), a neutral amide derivative of lipoic acid (LA), could resist oxidative stress-mediated neuronal cell damage. LM is more potent than LA in alleviating hydrogen peroxide- or 6-hydroxydopamine-induced PC12 cell injury. Our results reveal that LM promotes the nuclear accumulation of NFE2-related factor 2 (Nrf2), following with the activation of expression of Nrf2-governed antioxidant and detoxifying enzymes. Notably, silencing Nrf2 gene annuls the protection of LM, which demonstrates that Nrf2 is engaged in this cytoprotection. Our findings suggest that LM might be used as a potential therapeutic candidate for oxidative stress-related neurological disorders.

Oxidative stress is implicated in the pathogenesis of a wide variety of neurodegenerative disorders, and accordingly, dietary supplement of exogenous antioxidants or/and upregulation of the endogenous antioxidant defense system are promising for therapeutic intervention or chemoprevention of neurodegenerative diseases. Nrf2, a master regulator of the cellular antioxidant machinery, cardinally participates in the transcription of cytoprotective genes against oxidative/electrophilic stresses. Herein, we report the synthesis of 59 structurally diverse dithiolethiones and evaluation of their neuroprotection against 6-hydroxydopamine- or H2O2-induced oxidative damages in PC12 cells, a neuron-like rat pheochromocytoma cell line. Initial screening identified compounds 10 and 11 having low cytotoxicity but conferring remarkable protection on PC12 cells from oxidative-mediated damages. Further studies demonstrated that both compounds upregulated a battery of antioxidant genes as well as corresponding genes’ products. Significantly, silence of Nrf2 expression abolishes cytoprotection of 10 and 11, indicating targeting Nrf2 activation is pivotal for their cellular functions. Taken together, the two lead compounds discovered here with potent neuroprotective functions against oxidative stress via Nrf2 activation merit further development as therapeutic or chemopreventive candidates for neurodegenerative disorders.

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