• Indian J Med Res · Sep 2011

    In vitro & in vivo estrogenic activity of glycoside fractions of Solanum nigrum fruit.

    • S Jisha, S Sreeja, and S Manjula.
    • Division of Plant Molecular Biology, Rajiv Gandhi Centre for Biotechnology, Thiruvananthapuram, India.
    • Indian J Med Res. 2011 Sep 1; 134 (3): 369374369-74.

    Background & ObjectivesThe mature fruits of Solanum nigrum contains steroidal glycosides. These are often used as vegetable and there are evidences on tribal use of these fruits as an oral contraceptive. The present study was carried out to evaluate the estrogenic potential of S. nigrum fruits by in vitro and in vivo assays.MethodsDefatted methanol extract of dried S. nigrum fruits was column fractionated and the glycoside positive fractions pooled. Definite concentrations of the fraction were used for in vitro and in vivo assays. The effect on cell viability was analyzed in MCF-7 cell lines by MTT assay followed by in vitro evaluation of estrogenicity by hydroxy apatite (HAP) binding assay. The results were further evaluated in vivo by performing uterotrophic assay in ovariectomized mouse models.ResultsAt low concentration (40 μg/ml), SNGF induced a dose-dependent increase in MCF-7 cell proliferation, while higher extract concentrations (80-320 μg/ml) caused progressive cell growth inhibition. The competitive binding assay using ³H-E₂ suggests that this effect is mediated by estrogen receptor. Mouse uterotrophic assay revealed a classical uterotrophic response in ovariectomized mice in response to S. nigrum glycoside fraction (SNGF). SNGF at a dose of 100 mg/kg of body wt induced the maximum height of luminal epithelial cells which indicated an increase of 30.8 per cent over control (P<0.01) with a correlated increase in uterine wet wt (150% increase over control). Higher doses (250 and 500 mg/kg body wt) of SNGF did not induce any uterotrophic effect.Interpretation & ConclusionsOur preliminary data demonstrate the hormone like activity of Solanum glycosides both in vitro and in vivo in mouse, which needs to be further explored to evaluate the possible mechanism and clinical implications.

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