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Astaxanthin is increasingly attracting commercial interest for its application in the nutraceutical and pharmaceutical industries. This study aimed to produce astaxanthin from molasses with our newly mutated strain of Rhodosporidium toruloides G17 and to evaluate biological activities of the produced astaxanthin. To maximize the astaxanthin yield, the response surface methodology was used so as to optimize the culture conditions. A maximum astaxanthin yield of 1262.08 ± 14.58 µg/L was achieved by growing R. toruloides G17 in a molasses-based medium containing 49.39 g/L reducing sugar, 1.00 g/L urea, 4.15 g/L MgSO4·7H2O, and 10.05% inoculum ratio. The produced astaxanthin was then purified and studied for its antioxidant and anticancer activities. This compound exhibited 123-fold higher antioxidant activity than α-tocopherol, with an IC50 value of 0.97 ± 0.01 µg/mL. The astaxanthin also showed a potent inhibitory ability against the following three cancer cell lines: HeLa, A549, and MCF7, with IC50 values of 69.07 ± 2.4 µg/mL, 55.60 ± 2.64 µg/mL, and 56.38 ± 4.1 µg/mL, respectively. This study indicates that astaxanthin derived from our newly mutated R. toruloides G17 is a promising anticancer and antioxidant agent for further pharmaceutical applications. [ABSTRACT FROM AUTHOR]

The present study evaluated the effects of Sophora flavescens Ait. root extract on the proliferation of human hepatoma cell line HepG2. HPLC-UV analysis showed that the highest matrine and oxymatrine contents were obtained in the chloroform extract, compared to ethanol extract and ethyl acetate extract. The morphological analysis revealed that the chloroform extract of Sophora flavescens Ait. (SFA-CHCl3 extract) induced alterations of HepG2 cell morphology, resulting in the shrinkage of cells, the formation of debris, and cell detachment. The proliferation of HepG2 cells was inhibited by SFA-CHCl3 extract treatment. Cell cycle analysis exhibited that the cell proportion of the G0/G1 phase of HepG2 cells with SFA-CHCl3 extract treatment was decreased, while the cell proportion of the G2/M phase was increased. Flow cytometry analysis indicated a dramatic increase in the apoptotic percentage of HepG2 cells over the time of SFA-CHCl3 extract treatment. The SFA-CHCl3 extract also caused morphological changes in HepG2 nuclear, including chromatin condensation and DNA fragmentation. SFA-CHCl3 extract treatment induced the bax up-regulation and the bcl-2 down-regulation in HepG2 cells. These results revealed that SFA-CHCl3 extract could be a potential apoptosis inducer in HepG2 cells. [ABSTRACT FROM AUTHOR]

UV light, especially UVB, is known as a trigger of allergic reaction, leading to mast cell degranulation and histamine release. In this study, phlorotannin Fucofuroeckol-A (F-A) derived from brown algal Ecklonia stolonifera Okamura was evaluated for its protective capability against UVB-induced allergic reaction in RBL-2H3 mast cells. It was revealed that F-A significantly suppress mast cell degranulation via decreasing histamine release as well as intracellular Ca2+ elevation at the concentration of 50 μM. Moreover, the inhibitory effect of F-A on IL-1β and TNF-α productions was also evidenced. Notably, the protective activity of F-A against mast cell degranulation was found due to scavenging ROS production. Accordingly, F-A from brown algal E. stolonifera was suggested to be promising candidate for its protective capability against UVB-induced allergic reaction. [ABSTRACT FROM AUTHOR]

Astaxanthin is a valuable carotenoid, which has been approved as a food coloring by the US Food and Drug Administration and is considered as a food dye by the European Union (European Commission). This work aimed to attain Rhodosporidium toruloides mutants for enhanced astaxanthin accumulation using ultraviolet (UV) and gamma irradiation mutagenesis. Gamma irradiation was shown to be more efficient than UV for producing astaxanthin-overproducer. Among the screened mutants, G17, a gamma-induced mutant, exhibited the highest astaxanthin production, which was significantly higher than that of the wild strain. Response surface methodology was then applied to optimize the medium compositions for maximizing astaxanthin production by the mutant G17. The optimal medium compositions for the cultivation of G17 were determined as a peptone concentration of 19.75 g/L, malt extract concentration of 13.56 g/L, and glucose concentration of 19.92 g/L, with the maximum astaxanthin yield of 3021.34 µg/L ± 16.49 µg/L. This study suggests that the R. toruloides mutant (G17) is a potential candidate for astaxanthin production. [ABSTRACT FROM AUTHOR]

Wild bitter melon (Momordica charantia L. var. Abbreviata Ser.) is a wild edible variety of M. charantia, often used in folk medicine. In this study, the biological activities of its extract and fractions were investigated in vitro. It was found that ethyl acetate (EA) fraction exhibited high 1,1-diphenyl-2-picryl-hydrazyl (DPPH) scavenging activity with a half maximal inhibitory concentration (IC50) value of 0.43 ± 0.04 mg/mL, while the chloroform (CF), EA, and n-butanol (Bu) fractions had strong 2,2-azinobis-3-ethyl benzothiazoline-6-sulfonic acid (ABTS)+ scavenging ability with IC50 values of 0.36 ± 0.04 mg/mL, 0.35 ± 0.02 mg/mL, and 0.35 ± 0.05 mg/mL, respectively. Moreover, the EA and Bu fractions exhibited the highest protective effect against H2O2-induced DNA damage in a concentration-dependent manner. Furthermore, the EA fraction was effective in the inhibition of enzyme α-amylase activity with an IC50 value of 0.27 ± 0.029 mg/mL. Finally, it was observed that the production of nitric oxide (NO), a pro-inflammatory mediator, was significantly reduced from LPS-stimulated murine macrophage RAW 264.7 cells by the ethanol extract (ET) and the EA fraction. Therefore, wild bitter melon could be considered as a promising biomaterial for the development of pharmaceutical products. [ABSTRACT FROM AUTHOR]

The aminoethyl–chitooligosaccharide (AE-COS) was reported to inhibit human gastric cancer cell proliferation and human fibrosarcoma cell invasion. In this study, the role of AE-COS in down-regulation of proliferation of human lung A549 cancer cells was evaluated. It was found that AE-COS was able to reduce A549 cell proliferation to (32 ± 1.3)% at a concentration of 500 µg/mL. Moreover, AE-COS treatment caused suppression on COX-2 expression in a dose-dependent manner. Notably, the role of AE-COS in induction of cell apoptosis was observed via decreasing Bcl-2 expression and increasing caspase-3 and -9 activation. Accordingly, the antiproliferative effect of AE-COS was indicated due to suppression of cell proliferation and induction of cell apoptosis, suggesting AE-COS as a promising chemotherapy agent for treatment of lung cancer. [ABSTRACT FROM AUTHOR]