4.7 Article

Efficacy of Eisenia bicyclis phlorotannins in the treatment of diabetes and reducing inflammation

Journal

FOOD BIOSCIENCE
Volume 52, Issue -, Pages -

Publisher

ELSEVIER
DOI: 10.1016/j.fbio.2023.102381

Keywords

Seaweeds; Eisenia bicyclis; Antioxidant; Antidiabetic; Anti-inflammatory

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Crude phlorotannins from Eisenia bicyclis (CPEb), a common perennial brown seaweed, were found to have anti-inflammatory, antioxidant, and antidiabetic effects. The composition of CPEb was analyzed and it was discovered to contain dieckol, 8, 8'bieckol, fucofuroeckol, and the carotenoid zeaxanthin. In experiments, CPEb was found to reduce the production of cytokines induced by LPS in THP1 macrophage cells and promote glucose absorption in C2C12 myotubes.
Crude phlorotannins from Eisenia bicyclis (CPEb), a common perennial brown seaweed were screened for pharmacological activities such as anti-inflammatory, antioxidant, and antidiabetic effects. Crude Phlorotannins (CPEb) studied by FT-IR, LC-MS, UHPLC, and UV chromatography showed the occurrence of dieckol, 8, 8'bieckol, fucofuroeckol, and the carotenoid, zeaxanthin (0.5 mg/kg). LPS, an inflammatory mediator, enhanced the production of cytokines such IL-1 (interleukin-1), IL-6 (interleukin-6), IL-8 (interleukin-8), IL-10 (interleukin10), TNF-alpha (tumour necrosis factor-alpha), chemokine CXCL10, and NF-kappa B (nuclear factor kappa-light-chainenhancer of activated B cells) in differentiated THP1 macrophage cells. On differentiated human monocytic cell line LPS-induced THP1 cells, CPEb was found to have anti-inflammatory effects by reducing the expression of IL-1, IL-6, IL-8 (1.2 fold), CXCL10, NF-kappa B, and TNF-alpha. CPEb promoted 2-NBDG absorption in differentiated C2C12 myotubes under both basal (16.08%) and insulin-stimulated (51.09%) conditions. CPEb increased IRS/ AKT-dependent glucose absorption and also activates the AMPK pathway. Anti-alpha-glucosidase, antiinflammatory and antioxidant activity of CPEb indicate their role in treating hyperglycemia by scavenging ROS and inflammatory responses.

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