Background Zeaxanthin, a carotenoid commonly found in plants, has a variety of biological functions including anti-cancer activity. Purpose This study aimed to investigate the potential mechanisms of zeaxanthin in human gastric cancer cells. Methods CCK-8 assay was used to examine the cytotoxic effect of zeaxanthin on human gastric cancer cells. Flow cytometry was used to analyse AGS cell cycle distribution and apoptosis status. Western blot analysis was used to detect the expression levels of cycle-related proteins (Cyclin A, Cyclin B1, CDK1/2, p21, and p27), apoptosis-related proteins (Bcl-2, Bad, caspase-3, PARP), MAPK, AKT, STAT3, and NF-κB. Results CCK-8 assay showed that zeaxanthin has obvious cytotoxic effects on 12 types of human gastric cancer cells, but no obvious toxic effect on normal cells. In addition, flow cytometry and Western blotting results showed that zeaxanthin induces apoptosis by reducing mitochondrial membrane potential; increasing Cytochrome C, Bax, cleaved-caspase-3 (cle-cas-3), and cleaved-PARP (cle-PARP) expression levels; and decreasing Bcl-2, pro-caspase-3 (pro-cas-3), and pro-PARP expression levels. Additionally, zeaxanthin caused cell cycle arrest at the G2/M phase by increasing the levels of p21 and p27 and reduced the levels of AKT, Cyclin A, Cyclin B1, and Cyclin-dependent kinase 1/2 (CDK1/2). Furthermore, after zeaxanthin treatment, the expression levels of reactive oxygen species (ROS), p-JNK, p-p38, and I-κB increased, and the expression levels of p-ERK, p-AKT, STAT3, and NF-κB decreased. However, the ROS scavenger N-acetylcysteine (NAC) and MAPK inhibitors inhibited zeaxanthin-induced apoptosis, and under the action of zeaxanthin, MAPK regulated NF-κB and STAT3, and reduced their protein expression levels. Conclusion Zeaxanthin has a potential effect against gastric cancer cells through the ROS-mediated MAPK, AKT, NF-κB, and STAT3 signaling pathways, and it is expected to become a new drug for the treatment of human gastric cancer.

Summary In this study, mung bean was used as raw material to reveal the interaction mechanism between mung bean protein and polyphenols in the water solution system of heat treatment and to speculate the binding form of the two. Structural and functional changes of globulin–polyphenol complexes in mung bean under different interaction ratios and heat treatment conditions (70, 85 and 100 °C) were analysed using 2D and 3D fluorescence, Fourier transform infrared spectroscopy, particle size and ζ potential. The results showed that mung bean globulin–polyphenol binding was a static quenching mechanism, with mainly hydrophobic interactions. Heat treatment had little effect on binding sites and may induce partial covalent binding. Antioxidant activity of the interaction improved; however, heat treatment reduced the antioxidant capacity of the complexes. Before and after heat treatment, globulin–polyphenol complexes had poor solubility, but its emulsification and foaming ability are significantly improved. Polyphenol addition improved mung bean globulin secondary structure, and the thermal stability of the complex was greater than that of mung bean globulin. This study provides a theoretical reference for clarifying the binding mechanism of mung bean protein and polyphenols, which is significant for mung bean food processing and production.

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Quinalizarin has been demonstrated to exhibit potent antitumor activities in lung cancer and gastric cancer cells, but currently, little is known regarding its anticancer mechanisms in human breast cancer cells. The aim of the present study was to investigate the apoptotic effects of quinalizarin in MCF-7 cells and to analyze its molecular mechanisms. The MTT assay was used to evaluate the viability of human breast cancer cells that had been treated with quinalizarin and 5-fluorouracil. Flow cytometric analyses and western blotting were used to investigate the effects of quinalizarin on apoptosis and cycle arrest in MCF-7 cells with focus on reactive oxygen species (ROS) production. The results demonstrated that quinalizarin exhibited significant cytotoxic effects on human breast cancer cells in a dose-dependent manner. Accompanying ROS, quinalizarin induced MCF-7 cell mitochondrial-associated apoptosis by regulating mitochondrial-associated apoptosis, and caused cell cycle arrest at the G2/M phase in a time-dependent manner. Furthermore, quinalizarin can activate p38 kinase and JNK, and inhibit the extracellular signal-regulated kinase, signal transducer and activator of transcription 3 (STAT3) and NF-κB signaling pathways. These effects were blocked by mitogen-activated protein kinase (MAPK) inhibitor and N-acetyl-L-cysteine. The results from the present study suggested that quinalizarin induced G2/M phase cell cycle arrest and apoptosis in MCF-7 cells through ROS-mediated MAPK, STAT3 and NF-κB signaling pathways. Thus, quinalizarin may be useful for human breast cancer treatment, as well as the treatment of other cancer types.

BackgroundStorage is an essential part of brown rice circulation. During the storage process, the metabolic activity of brown rice is still ongoing, and long‐term storage leads to the deterioration of brown rice. Metabolomics analysis was performed using gas chromatography–mass spectrometry to investigate the changes in metabolites of brown rice after storage at 18 °C for 12 months.ResultsIn terms of quantity, sugar, fatty acids, and other metabolites in brown rice decreased after storage, and alcohols, aldehydes, phenols, and amines increased. A total of 34 differential metabolites were screened. In terms of contents, carbohydrates, amino acids, and fatty acids of brown rice decreased after storage, while those of sugar alcohol, amines, and aldehydes increased after storage. Cluster analysis of the samples at zero storage time revealed that the metabolites expressed least became highly expressed after storage and those expressed highly became low after storage. Metabolic pathway analysis showed that storage significantly influenced the lipid metabolism in brown rice. Palmitoleic acid, cholesterol, linoleic acid, and lauric acid are four key metabolites in lipid metabolism during storage of brown rice.ConclusionSignificant changes occurred in quantity and type of brown rice metabolites after storage. Storage has the greatest effect on lipids. Storage caused a ‘reverse change’ in the metabolites content of brown rice. The results obtained may help in understanding the changes in metabolites profile and delaying of the quality deterioration of brown rice during storage.