Objective: To investigate the anti-diabetic activity of Azadirachta Indica using IDDM and NIDDM animal models . Methods: Streptozotocin induced models of IDDM (65 mg/kg, iv) as well as NIDDM model (90 mg/kg, i.p in neonates) were given neem leaf extract (NLE, 1 g/kg, po) for 6 weeks and their anti-diabetic activity was assessed. Result: The treatment with insulin, aqueous NLE, aqueous NLE with insulin and insulin with aminoguanidine showed a fall in blood glucose levels of 80, 45.4, 38.02 and 77-65% whereas in NIDDM model, a fall of 53.95 and 60.50% were observed with glibenclamide and NLE. Conclusion: Aqueous extract of NLE has a good therapeutic potential as anti-hyperglycaemic agent in IDDM and NIDDM.

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Objective: To investigate the antistress activity of water soluble part of ethanolic extract of Butea monosperma on water immersion stress-induced ulceration, elevation of serotonin (5-HT) in brain and corticosterone in plasma in rats. Methods: Stress was induced by forcing rats (n = 5) to swim in water for 2 hours and brain 5-HT and plasma corticosterone were estimated using a fluorimetric method. The rats received the extract (100, 200 or 400 mg/kg) or diazepam (0.2 mg/kg) i.p. 30 min before stress. Results: Water soluble part of ethanolic extract of flowers of Butea monosperma (100-400 mg/kg i.p.) attenuated water immersion stress induced elevation of brain serotonin and plasma corticosterone levels. The ulcer index also decreased in dose dependent manner. Diazepam (0.2 mg/kg i.p.) which was used as a reference standard exhibited similar effects.

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Objective: To evaluate the antiasthmatic and antianaphylactic activity of E-721B in various experimental models. Methods: The antiasthmatic and antianaphylactic activity of E-721B was studied on the active and passive anaphylaxis in rats, acetyl choline-induced bronchospasm in guinea pigs, anaphylactic shock-induced bronchospasm in guinea pigs and rats and on degranulation of mast cells by Compound 48/80. Results: Treatment with E-721B showed a dose dependent (at 50, 100, 250 and 500 mg/kg p.o.) beneficial effect on degranulation rate of actively and passively sensitized mesenteric mast cells of albino rats when challenged with antigen (horse serum). E-721B treatment for 7 days resulted in significant protection against acetylcholine aerosol-induced bronchospasm in guinea pigs. E-721B treatment for 10 and 14 days, in guinea pigs and rats respectively, offered marked protection against anaphylactic shock-induced bronchospasm. E 721B treatment also protected the mast cell disruption induced by Compound 48/80. Conclusion: Antiasthmatic and antianaphylactic activity of E-721B may be possibly due to the membrane stabilising potential, suppression of antibody production and inhibition of antigen induced histamine release.

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Objective: To compare the effect of finasteride with that of epristeride on 5(-reductase kinetics in vitro to explain the increase in serum testosterone level by finasteride but not by epristeride when treated for benign prostatic hyperplasia. Methods: Sprague-Dawley rat liver microsomal crude suspension served as the source of steroid ?(?-reductase. The enzyme, Tris-HCl buffer, [3H] testosterone and epristeride or finasteride were incubated together at 37oC for 20 min. The substrate, [3H] testosterone, and its product, [3H] dihydrotestosterone (DHT) were isolated by thin-layer chromatography. To measure the initial velocity of [3H] DHT (the activity of 5(-reductase), the radioactivity of [3H] DHT, scrapped off thin-layer plate was determined with isotope scintillation counter. The enzyme activity was expressed as (M/min of [3H] DHT. Results: Epristeride was an uncompetitive inhibitor, but finasteride was a competitive one to steroid 5(- reductase and their inhibition constants were 67 ( 19 and 25 ( 3 nM, respectively. Conclusion: The inhibition mechanism of finasteride different from epristeride perhaps was the reason for increase in serum testosterone levels in patients with benign prostatic hyperplasia treated by finasteride.

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Objective: To see the effect of anti-stress agents like Panax ginseng and diazepam on stress-induced elevation of norepinephrine (NE) in brain and hypothalamus of rats. Methods: NE was estimated in brain and hypothalamus of rats by spectrophotofluorimetry. Plasma corticosterone was measured by fluorimetry. Results: Panax ginseng and diazepam both per se did not modify NE levels of brain and hypothalamus in unstressed rats. But both the drugs attenuated stress-induced elevation of NE of brain and hypothalamus and simultaneously attenuated stress-induced elevation of plasma corticosterone. Conclusion: Anti-stress effect of Panax ginseng and diazepam seems to be mediated through attenuation of levels of NE in brain and hypothalamus.

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Objective: To investigate the antidepressant effect of NMDA receptor (NMDAR) antagonists (MK 801 and ketamine) using forced swimmming test, and to study their interaction with established antidepressants. Methods: The study was conducted in albino mice of either sex weighing 25 ( 5g. They were subjected to forced swimming test. The duration of immobility of mice in the last 4 min of a 6min test was recorded. A mouse was considered immobile when floating motionless, or making only those movements necessary to keep its head above water. All the drugs were dissolved in 0.9% saline and were administered intraperitoneally. The data was analysed using ANOVA followed by either Dunnett's test or Tukey's multiple range test, wherever applicable. Results: Imipramine (8-32 mg/kg), MK 801 (0.05-0.2 mg/kg) and ketamine (2.5-10 mg/kg) reduced duration of immobility in a dose dependent fashion. The immobility reducing effect of imipramine (16 mg/ kg) was potentiated by concomitant administration of either MK 801 (0.1 mg/kg) or ketamine (5 mg/kg). Fluvoxamine (5-20 mg/kg) failed to modify the duration of immobility. However, fluvoxamine (20 mg/kg) potentiated the immobility reducing action of MK 801 (0.1 mg/kg) and ketamine (5 mg/kg). The positive response of imipramine was antagonised by prazosin (3 mg/kg), whereas that of MK 801 and ketamine was abolished by haloperidol (0.1 mg/kg). Haloperidol could also antagonise the effect of the combination of fluvoxamine with NMDA antagonists. Both prazosin and haloperidol pretreatment attenuated the effect of the combination of NMDA antagonists with imipramine. Conclusion: MK 801 and ketamine reduced the duration of immobility which was antagonised by haloperidol pretreatment. This suggests that antidepressant action of these agents is mediated through dopaminergic pathway. Both these agents also potentiated the actions of imipramine and fluvoxamine.

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Objective: To investigate the ulcer-protective effect of Rhinax (a herbal formulation) in rats. Methods: The study was done in male albino rats. Gastric ulcers were induced by exposing rats to cold restraint stress or by oral administration of aspirin / alcohol. The stomach was incised along the greater curvature and examined for ulcers. Duodenal ulcers were induced by injecting (s.c.) cysteamine hydrochloride. Duodenum was examined for the presence or absence of ulcers. Effect of Rhinax on volume, pH, free and total acid content of gastric juice in pylorus ligated rats was also determined. In addition, effect of Rhinax on gastric mucus barrier in rats was determined and histological examination of gastric glandular mucosa carried out employing alcian blue stain. In this study, each group in each experiment consisted of 8 animals. Results: Oral administration of Rhinax resulted in promotion of gastric mucus secretion in normal as well as in cold restraint stress, drug and alcohol - induced ulceration in rats. The volume and acidity of gastric juice in pyloric ligated rats was also reduced by Rhinax administration. Conclusion: All the results suggest that Rhinax possessess ulcer - protective activity which is evoked mainly by the modulation of defensive factors by improvement in gastric cytoprotection and partly by acid inhibition and free radical scavenging properties.

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Antiretroviral drugs directed at various targets in the replication cycle of HIV are now in clinical use. The earliest drugs available were the nucleoside analogue reverse transcriptase (RT) inhibitors. Subsequently non-nucleoside RT inhibitors were also introduced into clinical use. The newly developed HIV protease inhibitors have shown excellent efficacy, leading to optimistic attempts at "virus eradication". The trend in HIV antiretroviral therapy has shifted in recent years from monotherapy to combination therapy with even 3 drugs used simultaneously, and from treatment late in disease to early in infection. These approaches are based on the replication characteristics of the virus. A large number of clinical trials have been carried out and are ongoing for the evaluation of the various antiretroviral drugs in different treatment regimens. This review presents information on the antiretroviral drugs currently available for clinical use against HIV, along with the rationale and evolution of the strategies of anti-HIV therapy.

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Objective: To study calcined arsenic preparations Kushta Sammul Far Qawi (KS-Q) and Aatishaki (KS-A) varieties for effects on animal models of epilepsy and acute toxicity. Methods: The investigations were carried out on pentylene tetrazole and maximal electroshock induced seizures in mice. Approximate LD50 values were also determined. Results: KS-A (5 mg/kg p.o.) caused significant reduction in onset time for various phases of convulsions and mortality vs vehicle treated mice. KS-Q showed a similar proconvulsive tendency but the effects were not significant. The oral LD50 values for KS-A and KS-Q were 750 and 490 mg/kg respectively. Conclusion: The test drugs showed no acute toxicity and apparantly had a wide therapeutic index but KS-A exhibited proconvulsant activity necessitating caution in its use in epilepsy prone subjects.

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Objective: To study the effect of ramiprilat on experimentally induced acute and chronic glaucoma in rabbits. Methods : Acute glaucoma was produced by i.v. infusion of 5% glucose in rabbits. Injection of alpha-chymotrypsin into posterior chamber of rabbit eye produced sustained elevation of intra ocular pressure (IOP) which lasted for almost 3 months. The effect of ramiprilat(0.1%) and ramipril(0.1%) was studied in these models of glaucoma. The interaction of ramiprilat with acetylcholine was studied on isolated rat ileum . Effect of ramiprilat on the enzyme cholinesterase and angiotensin converting enzyme (ACE) was studied biochemically. Results : Ramiprilat produced significant fall in IOP in normotensive rabbit eyes and also in rabbits with alpha-chymotrypsin induced glaucoma. It prevented the acute rise in IOP due to infusion of 5% glucose. It caused significant potentiation of responses to acetylcholine in isolated rat ileum preparation. True as well as pseudo cholinesterase enzymes of human blood and ACE in aqueous humor were found to be significantly inhibited by ramiprilat. Conclusion: Our data suggest a potential ocular hypotensive activity of ramiprilat which may be due to inhibition of ACE (Kininase-II) and cholinesterase.

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Objectives: To characterize the changes in intestinal transit induced by diabetes and the implication of nitric oxide in such changes. Methods: Diabetes was induced in mice by single injection of streptozotocin (STZ 160 mg/kg, ip). One, four and six weeks later, intestinal transit was measured after pretreatment with saline or drug, using charcoal meal method. Results: Intestinal transit was significantly reduced in 1, 4 and 6 weeks STZ diabetic mice as compared with normal mice. Treatment with N(-nitro-L-arginine (10,20and 25 mg/kg, ip ) dose dependently increased the intestinal transit in STZ-diabetic mice. Increased intestinal transit effect of N(-nitro-L-arginine (20 mg/kg) was dose dependently reversed by L-arginine (300, 600 and 900 mg/kg ) but not by D-arginine (600 mg/kg ). Conclusion: In the early stages of STZ diabetes, there may be an enhanced production of nitric oxide, which could account for reduced intestinal transit in diabetes.

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Objectives: To study the functional characteristics of ca2+ channels in rat vas deferens following cyclophosphamide treatment. Methods: The study was conducted on vas deferens isolated from cyclophosphamide-treated (40 mg/kg s.c., once on alternate day for 5 times) albino rats. The following parameters were assessed: IC50 values of verapamil against 1 m mol BaCl 2 -induced rhythmic contractions, maximum absolute tension (g) generated by norepinephrine (NE) in the presence of verapamil 10-6 mol and EC 50 value of NE in inducing contractile responses in the presence of verapamil 10-6 mol. Results: The mean IC50 value of verapamil against BaCl2 -induced rhythmic contractions was significantly decreased, the maximum absolute tension generated by NE did not change significantly and the EC50 value of NE in the presence of verapamil was significantly increased in the cyclophosphamide-treated group as compared to the control. Conclusion: The study revealed decreased functional activity of Ca2+ channels of rat vas deferens following cyclophosphamide treatment.

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Objective: To examine the involvement of K ATP channels in inhibition of single pulse induced responses in rat detrusor muscle. Methods: The rat bladder strips were stimulated with square wave single pulse of 1ms duration at 80V. The effect of pinacidil and cromakalim on responses to single pulse stimulation either in absence or presence of glibenclamide was evaluated. Results: The single pulse stimulation of bladder strips elicited a biphasic neurogenic response having noncholinergic (fast) and cholinergic (slow) components. Pinacidil and cromakalim(10 -6 M) caused significant inhibition of the cholinergic component. Glibenclamide (10 -6 M) pretreatment prevented the inhibition of slow component. Conclusion: K ATP channels primarily involved in inhibition of cholinergic component of single pulse induced neurogenic response in rat urinary bladder.

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