ABSTRACT
Introduction: Depression belongs to the heterogeneous group of mental disorders characterized by extreme exaggerations and disturbance of mood, which adversely affect cognition and psychomotor functions. It results from abnormal brain mechanisms functionally deficient monoaminergic (noradrenaline and/or 5-hydroxytryptamine) transmission in the central nervous system. Aims and Objectives: To evaluate comparatively the Anti- depressant activity of Berberis aristata (Daru haridra) in albino rats after inducing experimental depression using different methods. Materials and methods: The antidepressant activity of aqueous extract of berberis aristata was screened by tail suspension method and the forced swimming test and compared with the control and standard drug (fluoxetine) for two weeks. Group1- were kept as control. Group 2- were treated with fluoxetine in a dose of 14mg/kg/day as standard drug for one week. Group 3, 4 and 5- were given aqueous extract of berberis aristata intraperitoneally in three graded doses 400,800 and 1600mg/kg/day respectively for two weeks. Results: berberis aristata exhibits antidepressant activity depicted by reduction in the immobility time when compared to the control group. The onset of action was after few days according to the dose of the test drugs following their administration. The effect is comparable with that of standard drug fluoxetine which may be attributed to the phytoconstituents like berberine, berbamine and palmitine, among them most probably with berberine alkaloid. The berberine alkaloid is known to inhibit the monoamine oxidase enzyme particularly monoamine oxidase- A isoform. berberine influenced either dopaminergic system by monoamine oxidase-B inhibiting property or by blocking the reuptake of dopamine by inhibiting its transporter. Conclusion: Berberis aristata has significant antidepressant activity demonstrated by tail suspension and forced swimming test compared to the test drug.
ABSTRACT
Background: Plasma Leukocytosis is known to occur in a variety of clinical conditions viz. infections, inflammations and collagen disorders. Apart from these many physiological factors like heat, solar radiation and high altitude also causes leukocytosis. It has been reported that even corticosteroids can cause leucocytosis which is usually polY morphonuclear leucocytosis. Adrenaline administered by various routes like I/M, I/V and S/C is also known to cause a rise in blood leukocytes. It has been reported that even corticosteroids can cause leukocytosis, which is usually polymorphonuclear leukocytosis. Since catecholamines have been implicated in the release of polymorphs from bone marrow into blood in the glucocorticoids induced leukocytosis, this could be a likely mechanism. If so then adrenergic receptors may be mediating this release. Attempt will be made to characterize these adrenergic receptors by studying the effect of some beta blockers on adrenaline induced Leukocytosis. Materials and Methods: The study was conducted in conscious albino rabbit. The rabbits were divided into 3 groups with 6 rabbits in each group beta blockers used in the study were propranolol (0.5mg/kg) and atenolol (0.5mg/kg). Cell counts before drug administration served as control values. Adrenaline was used in the dose of 200microgram/kg. Result: Group1- significant rise in total leukocytes count in the form of 2 peaks, first occurring at 1hr with 21.85% rise and 2nd at 4hr with 41.89 % rise, at 2hr rise was not significant. At 24hr the counts came back to normal values Group2- significant fall in TLC at 1hr +1.2% and at 4hr +5% while at 2hr +2.4%. The fall in TLC at 24hr was insignificant.Group3- significant fall in TLC at 1hr +1.5% and at 4hr +10.2% while at 2hr +7.94%. The fall in TLC at 24hr was insignificant. Conclusion: The beta-blockers Propranolol and Atenolol successfully blocked the rise in blood leukocyte counts induced by Adrenaline which shows that Adrenaline induced leukocytosis occurs through the activation of beta-adrenoreceptors.