Grossamide

J Agric Food Chem. 2010 Apr 28;58(8):4779-85.

Lignans from the tuber-barks of Colocasia antiquorum var. esculenta and their antimelanogenic Activity.[Pubmed: 20359228]

Colocasia antiquorum var. esculenta , a variant of C. antiquorum , commonly known as "Imperial Taro", is an edible vegetable in many tropical and subtropical regions of the world.
METHODS AND RESULTS:
This study with the aim of evaluating the potential of C. antiquorum var. esculenta as a functional food with a depigmenting effect resulted in the identification of a new sesquilignan, named colocasinol A (1), and a new acyclic phenylpropane lignanamide, named cis-Grossamide K (2), together with 10 known compounds (3-12). The identification and structural elucidation of these compounds were based on 1D and 2D nuclear magnetic resonance (NMR) spectroscopic data analysis as well as high-resolution fast atom bombardment mass spectrometry (FABMS) and electron impact mass spectrometry (EIMS). Quantitation of the melanin contents and cell viability in murine melanocyte melan-a cells was used to assess the antimelanogenic activities of the isolated compounds. Among them, cis-Grossamide K (2), isoamericanol A (3), americanol A (4), 2-hydroxy-3,2'-dimethoxy-4'-(2,3-epoxy-1-hydroxypropyl)-5-(3-hydroxy-1-propenyl)biphenyl (5), and (-)-pinoresinol (6) showed inhibitory effects on melanin production. Compounds 2, 5, and 6 exerted a particularly strong antimelanogenic activity on the cells without high cell toxicity (IC(50) = 54.24, 53.49, and 56.26 microM, and LD(50) = 163.60, 110.23, and >500 microM, respectively).

Mol Cell Biochem. 2017 Apr;428(1-2):129-137.

Anti-neuroinflammatory effects of grossamide from hemp seed via suppression of TLR-4-mediated NF-κB signaling pathways in lipopolysaccharide-stimulated BV2 microglia cells.[Pubmed: 28224333 ]

Grossamide, a representative lignanamide in hemp seed, has been reported to possess potential anti-inflammatory effects. However, the potential anti-neuroinflammatory effects and underlying mechanisms of action of Grossamide are still unclear. Therefore, the present study investigated the possible effects and underlying mechanisms of Grossamide against lipopolysaccharide (LPS)-induced inflammatory response in BV2 microglia cells.
METHODS AND RESULTS:
BV2 microglia cells were pre-treated with various concentrations of Grossamide before being stimulated with LPS to induce inflammation. The levels of pro-inflammatory cytokines were determined using the enzyme-linked immunoassay (ELISA) and mRNA expression levels were measured by real-time PCR. The translocation of nuclear factor-kappa B (NF-κB) and contribution of TLR4-mediated NF-κB activation on inflammatory effects were evaluated by immunostaining and Western blot analysis. This study demonstrated that Grossamide significantly inhibited the secretion of pro-inflammatory mediators such as interleukin 6 (IL-6) and tumor necrosis factor α (TNF-α), and decreased the level of LPS-mediated IL-6 and TNF-α mRNA. In addition, it significantly reduced the phosphorylation levels of NF-κB subunit p65 in a concentration-dependent manner and suppressed translocation of NF-κB p65 into the nucleus. Furthermore, Grossamide markedly attenuated the LPS-induced expression of Toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 (MyD88).
CONCLUSIONS:
Taken together, these data suggest that Grossamide could be a potential therapeutic candidate for inhibiting neuroinflammation in neurodegenerative diseases.