Isolation of Fucoxanthin from Sargassum oligocystum Montagne, 1845 Seaweed in Vietnam and Its Neuroprotective Activity

Abstract

Fucoxanthin extracted and purified from Vietnamese Sargassum oligocystum Montagne, 1845 exhibits various biological activities. In this study, the ability of fucoxanthin to inhibit acetylcholinesterase (AChE), the antioxidant activities, and the expression of antioxidant enzymes were investigated. Fucoxanthin isolated from Vietnamese S. oligocystum showed no cytotoxic effects; moreover, it exhibited AChE inhibitory activity (with an IC₅₀ value of 130.12 ± 6.65 μg mL^-1) and antioxidant activity (with an IC₅₀ value of 3.42 ± 0.15 mg mL^-1). At concentrations of 50 and 100 µg mL^-1, fucoxanthin provided protection against amyloid β-protein fragment 25-35-induced neurotoxicity in a C6 neuronal cell line, and the survival of C6 cells was higher than 81.01% and 80.98%, respectively, compared to the control group (59%). Moreover, antioxidant enzyme activity and quantitative PCR analysis suggested that the neuroprotective effect of fucoxanthin resulted from regulation of the gene expression of antioxidant enzymes (CAT and GPx) and ER pathways (caspase-3 and Bax), as well as the promotion of expression of genes involved in PI3K/Akt signaling (GSK-3β), autophagy (p62 and ATG5), and the biosynthesis of ACh (VAChT and ChAT). Therefore, fucoxanthin extracted from the seaweed S. oligocystum in Vietnam is a potential feedstock source for the production of health foods that exert neuroprotective effects.

Keywords: Alzheimer’s; Sargassum oligocystum; acetylcholinesterase inhibitory; fucoxanthin; health food for humans; β-amyloid protein fragment.

Figure 1

Chemical structure of extracted fucoxanthin isolated from Vietnamese S. oligocystum.

Figure 2

Effect of fucoxanthin on the survival of C6 cell lines. Ethanol (EtOH) was used as the control group. The data are expressed as the mean ± SD (n = 3).

Figure 3

Neuroprotective effects of fucoxanthin against H₂O₂-induced oxidative stress in C6 cell lines. Cells were pre-incubated with fucoxanthin or ascorbic acid (20 µg mL⁻¹) at the indicated concentrations for 24 h prior to 10 mM H₂O₂ exposure for 1 h. Cell viability was assessed by a MTT assay. The data are expressed as the mean ± SD (n = 3). Significant differences in the cell damage induced by H₂O₂ are denoted by * p < 0.05. EtOH: ethanol; H₂O₂: hydrogen peroxide.

Figure 4

Neuroprotective effects of fucoxanthin against Aβ_25–35-induced neurotoxicity in C6 cell lines. Cells were pre-incubated with fucoxanthin (at 50 and 100 µg mL⁻¹) or galantamine (at 0.1 µg mL⁻¹) for 24 h prior to 20 mM Aβ_25–35 exposure for 1 h. Cell viability was assessed by MTT assay. The data are expressed as the mean ± SD (n = 3). Significant differences in the cell damage induced by Aβ_25–35 are denoted by * p < 0.05; ** p < 0.01. EtOH: ethanol; H₂O₂: hydrogen peroxide.

Figure 5

Effect of fucoxanthin on the activities of antioxidant enzymes in C6 cell lines. Cells were pre-incubated with fucoxanthin (concentrations of 50 and 100 µg mL⁻¹) or ascorbic acid (20 µg mL⁻¹) 24 h prior to 10 mM H₂O₂ exposure for 1 h. The data are expressed as the mean ± SD (n = 3). Significant differences in the cell damage induced by H₂O₂ are denoted by * p < 0.05; ** p < 0.001. SOD: superoxide dismutase; CAT: catalase; GPx: glutathione peroxidase; EtOH: ethanol; H₂O₂: hydrogen peroxide.

Figure 6

Effect of fucoxanthin on the expression of genes related to antioxidant enzymes (A), PI3K/Akt signaling (GSK-3ß) (B), the ER pathway (C), the biosynthesis of ACh (D), proteolytic processing (E), modulating protein translation (F), and autophagy (G) in C6 cell lines. The expression levels of genes were assessed with quantitative real-time PCR and normalized to β-actin in cells stimulated with fucoxanthin (concentrations of 50 and 100 µg mL⁻¹) or galantamine (concentration of 0.1 μg mL⁻¹) for 24 h prior to 20 mM Aβ_25–35 exposure for 1 h. EtOH was used as control. The data are expressed as the mean ± SD (n = 3). Significant differences in the cell damage induced by Aβ_25–35 are denoted by * p < 0.05; ** p < 0.001. EtOH: ethanol; SOD: superoxide dismutase; CAT: catalase; GPx: glutathione peroxidase; PI3K: phosphoinositide 3-kinase; Akt: protein kinase B; GSK-3β: glycogen synthase kinase 3β; CHOP: CCAAT/enhancer-binding protein homologous protein; Bax: Bcl2-associated X; CHAT: choline acetyltransferase; VAChT: vesicle acetylcholine transporter; APP: amyloid precursor protein; S6K1: S6 kinase 1; p62: sequestosome-1/A170/Zeta-interacting protein; ATG 5: autophagy-related gene 5.