Fucosterol Research Articles

In silico andnetwork pharmacologyanalysis of fucosterol: a potent anticancer bioactive compound against HCC.

The Fucaceae family of marine brown algae includes Ascophyllum nodosum. Fucosterol (FSL) is a unique bioactive component that was identified through GC-MS analysis of the hydroalcoholic extract of A. nodosum. Fucosterol's mechanism of action towards hepatocellular cancer was clarified using network pharmacology and docking study techniques. The probable target gene of FSL has been predicted using the TargetNet and SwissTargetPred databases. GeneCards and the DisGNet database were used to check the targeted genes of FSL. By using the web programme Venny 2.1, the overlaps of FSL and HCC disease demonstrated that 18 genes (1.3%) were obtained as targeted genes Via the STRING database, a protein-protein interaction (PPI) network with 18 common target genes was constructed. With the aid of CytoNCA, hub genes were screened using the Cytoscape software, and the targets' hub genes were exported into the ShinyGo online tool for study of KEGG and gene ontology enrichment. Using the software AutoDock, a hub gene molecular docking study was performed. Ten genes, including AR, CYP19A1, ESR1, ESR2, TNF, PPARA, PPARG, HMGCR, SRC, and IGF1R, were obtained. The 10 targeted hubs docked with FSL successfully. The active components FSL of ASD, the FSL, are engaged in fatty liver disease, cancer pathways, and other signalling pathways, which could prove beneficial for the management of HCC.

Fucosterol isolated from Sargassum horneri attenuates allergic responses in immunoglobulin E/bovine serum albumin-stimulated mast cells and passive cutaneous anaphylaxis in mice

Allergic diseases have become a serious problem worldwide and occur when the immune system overreacts to stimuli. Sargassum horneri is an edible marine brown alga with pharmacological relevance in treating various allergy-related conditions. Therefore, this study aimed to investigate the effect of fucosterol (FST) isolated from S. horneri on immunoglobulin E(IgE)/bovine serum albumin (BSA)-stimulated allergic reactions in mouse bone marrow-derived cultured mast cells (BMCMCs) and passive cutaneous anaphylaxis (PCA) in BALB/c mice. The in silico analysis results revealed the binding site modulatory potential of FST on the IgE and IgE-FcεRI complex. The findings of the study revealed that FST significantly suppressed the degranulation of IgE/BSA-stimulated BMCMCs by inhibiting the release of β-hexosaminidase and histamine in a dose-dependent manner. In addition, FST effectively decreased the expression of FcεRI on the surface of BMCMCs and its IgE binding. FST dose-dependently downregulated the expression of allergy-related cytokines (interleukin (IL)-4, -5, -6, -13, tumor necrosis factor (TNF)-α, and a chemokine (thymus and activation-regulated chemokine (TARC)) by suppressing the activation of nuclear factor-κB (NF-κB) and Syk-LAT-ERK-Gab2 signaling in IgE/BSA-stimulated BMCMCs. As per the histological analysis results of the in vivo studies with IgE-mediated PCA in BALB/c mice, FST treatment effectively attenuated the PCA reactions. These findings suggest that FST has an immunopharmacological potential as a naturally available bioactive compound for treating allergic reactions.

Fucosterol improves palmitic acid-induced oxidative stress, lipid droplet formation and insulin resistance in liver cells by mediating Keap1-Nrf2-lipocalin 13 axis

Purpose: To determine the possible effects of fucosterol (FST) on non-alcoholic fatty liver disease (NAFLD), and the mechanisms involved.
 Methods: The NAFLD model was constructed using palmitic acid (PA) induction, and the expression of NF-E2-related factor 2 (Nrf2), lipocalin 13 (LCN13) and Keap1 were analyzed by immunoblot. The oxidative stress of hepatocytes was determined via ELISA assay. In addition, the role of FST on lipid content and metabolism were evaluated by Oil Red O staining and immunoblot, while the levels of p-AKT, p-IRS1, and p-PI3K were evaluated by immunoblot assay.
 Results: The data revealed that FST significantly increased the viability of PA-induced hepatocytes, and the expression levels of Nrf2 and LCN13 (p < 0.05). Fucosterol enhanced Keap1-Nrf2 mediated LCN13 expression, and alleviated PA-induced oxidative stress by contributing to Keap1-Nrf2-LCN13 axis. In addition, it significantly reduced (p < 0.05) lipid droplet formation, promoted lipid metabolism, and lowered insulin resistance by enhancing Keap1- Nrf2-LCN13 axis.
 Conclusion: Fucosterol regulates Keap1-Nrf2-mediated LCN13 to aid the ameliorate palmitic acid-induced oxidative stress, lipid droplet formation and insulin resistance in liver cells.

Fucosterol Isolated from Dietary Brown Alga Sargassum horneri Protects TNF-α/IFN-γ-Stimulated Human Dermal Fibroblasts via Regulating Nrf2/HO-1 and NF-κB/MAPK Pathways.

Sargassum horneri is a well-known edible brown alga that is widely abundant in the sea near China, Korea, and Japan and has a wide range of bioactive compounds. Fucosterol (FST), which is a renowned secondary metabolite in brown algae, was extracted from S. horneri to 70% ethanol, isolated via high-performance liquid chromatography (HPLC), followed by the immiscible liquid-liquid separation, and its structure was confirmed by NMR spectroscopy. The present study was undertaken to investigate the effects of FST against oxidative stress, inflammation, and its mechanism of action in tumor necrosis factor (TNF)-α/interferon (IFN)-γ-stimulated human dermal fibroblast (HDF). FST was biocompatible with HDF cells up to the 120 μM dosage. TNF-α/IFN-γ stimulation significantly decreased HDF viability by notably increasing reactive oxygen species (ROS) production. FST dose-dependently decreased the intracellular ROS production in HDFs. Western blot analysis confirmed a significant increment of nuclear factor erythroid 2-related factor 2 (Nrf2)/ heme oxygenase-1 (HO-1) involvement in FST-treated HDF cells. In addition, the downregulation of inflammatory mediators, molecules related to connective tissue degradation, and tissue inhibitors of metalloproteinases were identified. TNF-α/IFN-γ stimulation in HDF cells increased the phosphorylation of nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK) mediators, and its phosphorylation was reduced with the treatment of FST in a dose-dependent manner. Results obtained from western blot analysis of the NF-κB nuclear translocation were supported by immunocytochemistry results. Collectively, the outcomes suggested that FST significantly upregulates the Nrf2/HO-1 signaling and regulates NF-κB/MAPK signaling pathways to minimize the inflammatory responses in TNF-α/IFN-γ-stimulated HDF cells.

Phycochemistry of some Sargassum spp. and their cytotoxic and antimicrobial activities

Purpose A comparative study on the chemical composition as well as cytotoxic and antimicrobial activities of the brown algae Sargassum asperifolium, Sargassum dentifolium, and Sargassum linifolium (family: Sargassaceae) from the Red Sea, Hurghada, Egypt, is carried out. Methods The volatile constituents obtained by hydrodistillation as well as the isolated unsaponifiable matter and the fatty acids were analyzed using the gas chromatography/mass spectrometry technique. Antitumorigenic activities of the crude extracts of the three algae have been evaluated in vitro on different human cell lines. Furthermore, the antimicrobial activities of the volatile constituents, successive extractives, unsaponifiable matter, and fatty acids have been tested on 11 different microorganisms. Results The analysis of the volatile fraction led to the identification of sexual pheromones, terpenes, phenolic compounds, free fatty acids, and esters. The most abundant sterols of unsaponifiable matter were fucosterol and cholesterol in all algae. Palmitic acid was found in all investigated algae as a major fatty acid. Biological screening proved that the tested algae have various cytotoxic and antimicrobial activities. Conclusion S. asperifolium, S. dentifolium, and S. linifolium are rich in cytotoxic and antimicrobial bioactive metabolites.

Synthesis of (24R,28R)- and (24S,28S)-fucosterol epoxides. Revision of C-24,28 configurations

Synthesis of (24R,28R)- and (24S,28S)-fucosterol epoxides. Revision of C-24,28 configurations