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Article | IMSEAR | ID: sea-215602

ABSTRACT

Background: Prolonged administration of neurolepticdrugs cause disrupted D dopamine receptor which 2leads to increased prolactin level, causesgyanaecomastia. Presently, dopamine receptor agonistis the choice of treatment for hyperprolactinemia. Aimand Objectives: The study aims to determine the antihyperprolactinemic effect of methanolic extract ofButea monosperma (MEBM) against haloperidol(HPL) and sulpiride (SPD) induced hyperprolactinemiaand to correlate with its active constituents. Materialand Methods: To induce hyperprolactinemia HPL 5mg/kg for 16 continuous days and SPD 20 mg/kg for 28continuous days was administred. MEBM 200mg/kg/day and 400 mg/kg/day were administered for16 and 28 days respectively half an hour beforeadministration of HPL and SPD. The serum prolactin(PRL) level, dopamine (DA) level and antioxidantstatus in the rat brain, hematological parameters weremeasured and histological examination of the anteriorpituitary gland, adrenal gland and spleen were done. Inaddition, antioxidant enzymes like superoxidedismutase (SOD) and catalase (CAT) were alsoestimated. Results: MEBM decreases serum PRL leveland increased DA level in brain significantly. Further,MEBM also restored SOD and CATstatus significantly.The inflammatory markers induced by HPL and SPDwere suppressed by MEBM. Discussion: Neuronal DAinhibition by neuroleptic drugs decreases the release ofDAwhich leads to hyperprolactinemia. MEBM (butrin)may activate DA neurones to ameliorate hyperprolactinaemia. The dopaminergic, anti-oxidant andanti-inflammatory effect of MEBM may be attributed toits anti-hyperprolactinemic effect. Conclusion: Buteamonosperma possesses anti-hyperprolactinemic effectwhich may be attributed to its marker constituent likeButrin.

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