Anti-inflammatory and anti-melanogenic proanthocyanidin oligomers from peanut skin.

Peanut skin (Arachis hypogaea L., Fabaceae) is an abundant source for polyphenols, such as proanthocyanidin oligomers. To determine whether proanthocyanidin has beneficial effects on skin, we tested for inhibitory activity of proanthocyanidins isolated from peanut skin on inflammatory cytokine production and melanin synthesis in cultured cell lines. Administration of peanut skin extract (PSE, 200 µg/mL) decreased melanogenesis in cultured human melanoma HMV-II co-stimulated with phorbol-12-myristate-13-acetate. It also decreased production of inflammatory cytokines (PSE at 100 µg/mL), tumor necrosis factor-α and interleukin-6, in cultured human monocytic THP-1 cells in response to lipopolysaccharide. We isolated ten known proanthocyanidins and one new proanthocyanidin trimer from the PSE. The structure of the new compound (5) was determined by 1D- and 2D-NMR and mass spectrometry analyses, and was determined as epicatechin-(2ß→O→7,4ß→6)-epicatechin-(4ß→6)-epicatechin. The other known proanthocyanidins were identified as proanthocyanidin monomers (1), dimers (6-9), trimers (3-5) and tetramers (2, 10, 11). They showed suppressive activities against melanogenesis and cytokine production at concentrations ranging from 0.1-10 µg/mL. Among the tested compounds, suppressive activities of proanthocyanidin dimers or trimers in two assay systems were stronger than those obtained with monomer or tetramers. These data indicate that proanthocyanidin oligomers from peanut skin have the potential to reduce dermatological conditions such as inflammation and melanogenesis.

Aqueous extract of peanut skin and its main constituent procyanidin A1 suppress serum IgE and IgG1 levels in mice-immunized with ovalbumin.

In this study, we investigated the effects of an aqueous extract of peanut (Arachis hypogaea L.) seed skin (PSE) and its main constituent procyanidin A1 (PA) on the allergic response to allergen ovalbumin (OVA) in a mouse model. Mice immunized interaperitoneally with OVA dramatically increased anti-OVA IgE and total IgG1 levels in serum compared with non-treated control mice. Oral injection of PSE at doses ranging from 10 to 100 mg/kg/d (for 21 consecutive days) decreased anti-OVA IgE and IgG1 levels 21 d after OVA-immunization. OVA-induced increments in spleen weight and peripheral white blood cell count were also suppressed by this PSE administration. Polyphenol-enriched fractions from apple (30 mg/kg) and grape seed (30 mg/kg) also decreased anti-OVA IgE level but did not affect total IgG1 levels. Oral injection of PA (1 to 10 mg/kg/d) purified from PSE resulted in a suppression of IgE and total IgG1 levels in serum. An increment of serum interleukin-4 level in mice that were immunized with OVA was reduced by all tested samples, whereas PSE and PA were the only compounds that could reverse the reduced interferon-gamma level by OVA. These findings suggest that intake of PSE or its main active constituent PA may prevent an allergic reaction by inhibiting immunoglobulin synthesis, and the mechanism of this action of PSE and PA is in part due to their regulation of T helper cytokine production.