Pigeon pea (Cajanus cajan L.) is one of the most important legume crops grown in subtropical and tropical regions with high nutritional quality. However, the consumption of pigeon pea is very limited worldwide owing to its high level of anti‐nutrients, hard texture, and unpleasant characteristic taste. The present review summarized the nutritional profile and health benefit of pigeon pea with special attention to its bioactive phytochemicals (e.g., cajanin, cajanol, and cajaninstilbene acid). Furthermore, some aspects that can help promote the application of pigeon pea in foods were highlighted from the perspectives of physical (i.e., thermal, extrusion, and ultrasound‐assisted), chemical (i.e., chemical modification and enzymatic hydrolysis), and biological treatment (i.e., sprouting and fermentation). The primary impact of physical methods was confined to the mitigation of anti‐nutrients. Chemical approaches were less explored and mainly targeted on the modification of starch and protein in pigeon pea. In contrast, the biological methods were found to decrease the level of anti‐nutritional factors, increase the production of bioactive phytochemicals, and improve the sensory properties of pigeon pea. Therefore, biological methods, especially sprouting techniques, are considered to be more promising.
15 April 2020 in Journal of Translational Medicine
Background: 17AAG has been extensively studied for its antitumor effects that protect cells from lethal stress by maintaining protein stability. The role of 17AAG in sevoflurane-induced neuronal injury has never been studied. We aim to investigate the effect of 17AAG on sevoflurane-induced neurotoxicity in vivo and in vitro. Methods: Sevoflurane-induced hippocampal neuron injury model was established in aged Sprague–Dawley rats. Pretreatment of vehicle or 17AAG was administered prior to sevoflurane inhalation. H4 neuroglioma cells were pretreated with vehicle or 17AAG and exposed to sevoflurane. Apoptosis, oxidative stress, expression of interleukin-6 (IL-6), and activation of the nuclear factor-κB (NF-κB) signaling pathway in H4 cells were examined by Hoechst assay, flow cytometry, Western blot, and immunofluorescent staining. RNA interference against HSPA1A was performed to test the function of HSP70 in neuroprotection. Results: Exogenous 17AAG reduced sevoflurane-induced apoptosis and oxidative stress in rat hippocampal neurons and in H4 cells. In H4 cells, 17AAG suppressed sevoflurane-induced upregulation of IL-6 and activation of NF-κB signaling. 17AAG enhanced sevoflurane-induced upregulation of HSP70 in rat hippocampal neurons and in H4 cells. Conversely, silencing of HSPA1A in H4 cells blocked the cytoprotective effect of 17AAG against sevoflurane-induced apoptosis and oxidative stress, and prevented upregulation of IL-6 and activation of NF-κB signaling. Conclusions: 17AAG protects against sevoflurane-induced neurotoxicity in vivo and in vitro via HSP70-dependent inhibition of apoptosis, oxidative stress, and pro-inflammatory signaling pathway.
The formation of advanced glycation end products (AGEs) in daily diets poses a great threat to human health, since AGEs are closely related to some chronic metabolic diseases. In this study, we investigated the antiglycative capabilities of some popular microgreens in chemical model. Our data indicated that baby spinach (Spinacia oleracea) had the highest antiglycative activity during 4-wks incubation, with antioxidation being the main action route. Moreover, a bread model was set up to evaluate its antiglycative potential in real food model. The results showed that the fortification of baby spinach in bread significantly inhibited AGEs formation, with acceptable taste and food quality. Further study revealed that the antiglycative components were mainly distributed in leaves, which were separated via column chromatography and tentatively identified as chlorophyll derivatives. In summary, this study highlighted the antiglycative benefits of baby spinach which can be developed into healthy functional foods.