Several new and promising antiviral drugs have been approved which allow better options to control infections caused by herpes virus. Vidarabine has been the earliest available drug against herpes simplex (HSV) and varicella zoster (VZV), but is an agent that is rarely used at present. Acyclovir has replaced vidarabine in treating herpes infections in immunocompetent and immuno compromised patients. The low oral bioavailability of acyclovir, as well as emergence of drug resistant strains have stimulated efforts towards development of newer compounds for treatment of herpes infection. These include penciclovir and its oral prodrug famciclovir and the oral prodrug form of acyclovir, valacyclovir. These drugs are dependent on virus encoded thymidine kinase (TK) for their intracellular activation (phosphorylation) and, upon conversion to their triphosphate form which act as inhibitors/alternative substrate of viral DNA polymerase. Therefore resistance of these drugs may occur for virus mutants that are TK-deificient. Newer drugs as Sorivudine which is a nucleoside analogue has been pursued in treating herpes infections. Foscarnet, which does not require any previous metabolism to interact with viral DNA polymerase is useful in clinical settings when TK deficient mutant strains emerge. Cidofovir, an acyclic nucleoside phosphonate is yet another available drug to which TK deficient strains are sensitive. This review describes these currently available antiviral drugs against herpes virus, some approved and others under clinical evaluation for approval.

Objectives: To study traditional gold preparations for anti-cataleptic, anti-anxiety and anti-depressant effects. Methods: Swarna Bhasma used in Ayurveda, Kushta Tila Kalan used in Unani-Tibb and Auranofin used in modern medicine were subjected to videopath analyzer, vogel conflict/anxiometer, elevated plus maze, and social behavioural deficit tests for anxiolytic activity, behavioural despair and learned helplessness tests for antidepressant activity, haloperidol-induced catalepsy tests for neuroleptic activity, and maximum tolerated dose, gross behavioural observations and hematological parameters for safety evaluation in rats and mice. Results: The test drugs caused significant increase in punished drinking episodes in anxiometer and open arm entries and time in elevated plus maze and decrease in behavioural deficit. A decrease in immobility time in forced swimming test, normalization of shock induced escape failures in learned helplessness test, and reduction of haloperidol-induced catalepsy scores were also noted in treated animals. The maximum tolerated doses were found to be more than 80 times the effective doses and no weight loss or untoward effects were observed on gross behaviour and hematological parameters. Conclusions: Traditional gold preparations used in Ayurveda and Unani-Tibb exhibited anxiolytic, antidepressant and anticataleptic actions with wide margin of safety.

Objectives : To investigate the effect of nifedipine and nimodipine on acute [maximal electroshock and pentylenetetrazol (PTZ) induced convulsions in rats] and chronic (pentylenetetrazol induced kindling in rats and mice) models of epilepsy. Methods: The maximal seizure pattern was induced in animals by giving an alternating current of 150 mA for 0.2 secs, while tonic clonic seizures were seen with 50 mg/kg i.p. dose of PTZ. Test drugs were administered 30 min before electrical or chemical induction. The ability of test drug to abolish/reduce tonic hind limb extensor component in MES group and jerky movements and clonic seizures in PTZ group was selected as antiepileptic criteria. Kindling was established in mice with PTZ in subconvulsive dose (30 mg/kg i.p.) thrice a week for nine weeks and effect observed for 15 min using 4 point scoring system. Rechallenge with same dose on 3rd and 10th day showed that kindling was established. Calcium channel blockers were then administered prior to convulsions and effects observed. Results : In acute studies, both nifedipine and nimodipine decreased the duration of tonic hind limb extensor phase in maximal electroshock seizures while in PTZ (50 mg/kg) treated animals, both drugs significantly decreased the duration of clonic convulsions, only nifedipine increased the latent period while nimodipine did not affect the latent period. The protective effect with nifedipine was significant (p<0.05) at 10 mg/kg while with nimodipine at 5 mg/kg dose. In chronic studies, nifedipine (2 mg/kg) given prophylactically in PTZ (30 mg/kg thrice weekly for 9 weeks) kindled rats and mice significantly (p<0.05) reduced the convulsive score in both the animals, however, the pattern of response was different. No significant effect on kindling was observed with nimodipine. Conclusions :The results with acute studies suggest that both nifedipine and nimodipine, the calcium channel blockers, possess anticonvulsant activity. Chronic studies showed anticonvulsant profile only with nifedipine and better response observed in mice as compared to rats.

Objective: To study the role of nitric oxide in cocaine and amphetamine induced increased locomotor activity and reverse tolerance. Methods: Locomotor activity was measured using a hole board. Increased locomotor activity was induced by administration of cocaine (15mg/kg, s.c.,) and amphetamine (0.7mg/kg, s.c.) once daily for 6 days. ?(-nitro-L-arginine (NOARG), a nitric oxide synthase inhibitor (8mg/kg, i.p.) was administered 30 min before the administration of cocaine or amphetamine as single injection or once daily for 6 days. Results: NOARG (8 mg/kg) inhibited the cocaine and amphetamine induced increased locomotor activity. NOARG administered before and during chronic injection of cocaine and amphetamine in rats blocked the development of reverse tolerance to the increased locomotor activity. Conclusion: Dopaminergic mediated behaviours of cocaine and amphetamine are partially mediated via the activation of the nitric oxide system and the enhancement of postsynaptic dopamine receptor sensitivity may be an underlying common mechanism that mediates this reverse tolerance.

Objective: To evaluate the analgesic and antipyretic activities of alcoholic extract of Dalbergia sissoo leaves. Methods: The peripheral analgesic activity of Dalbergia sissoo leaves (SLE; 100, 300 and 1000 mg/kg) was studied using acetic acid induced writhing in mice and by Randall-Selitto assay. The central analgesic activity of SLE was studied using hot-plate method and tail clip test in mice. The antipyretic activity of SLE was studied in Brewer's yeast-induced pyrexia in rats. Results: SLE significantly decreased the writhing movements in mice in acetic acid-induced writhing test. SLE (1000 mg/kg) significantly increased the pain threshold capacity in rats in Randall-Selitto assay and the reaction time in hot-plate test but not in tail-clip test. It also showed significant antipyretic activity in Brewer's yeast-induced pyrexia in rats throughout the observation period of 6 h. Conclusion: SLE may have analgesic and antipyretic activities.

Objective: To review the evidence for a role of HD-03, a polyherbal formulation in regulating the sodium pump in hepatic injury induced by paracetamol. Methods: Alterations in sodium pump was induced by chronic administration of paracetamol at the dose of 500 and 1000 mg/kg, b. wt. for 28 days. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), liver glutathione, glycogen and Na+ -K+ ATPase activity estimation and histology of liver were studied in rats. Results: Chronic administration of paracetamol for 4 weeks to rats produced dose dependent increase in ALT, AST and reduction in liver Na+ -K+ -ATPase activity, glycogen and glutathione levels, indicating the hepatocellular damage. Histological evaluation supported this change with evidence of swelling, hydropic degeneration and necrosis of the hepatocytes. These changes were reversed with simultaneous administration of paracetamol and HD-03 at 750 mg/kg, for 28 days. Conclusion: Reversal of Na+ -K+-ATPase, glycogen, glutathione levels and restricted hepatic damage in HD-03 treated animals confirms the hepatoprotective effect of HD-03. Thus, Na+ -K+ -ATPase may be considered as a marker to evaluate the hepatoprotective effects of various herbs.

Objective : To study the role of NO in the modulation of extracellular and intracellular Ca++ in vasodilator mechanism. Methods: Goat hearts were collected from local abattoirs within 20-30 min. of slaughter in cold aerated modified Kreb's Henseleit solution. Both the left anterior and circumflex coronary artery branches were dissected out, cut into rings of 3-4 mm length and 2-3 mm external diameter and mounted in a 20 ml organ bath through triangular stainless steel hook. The tissues were equilibrated for 90 min. under a resting tension of 1.5 g. Responses were recorded isometrically with a force displacement transducer connected to a polygraph. Role of extracellular Ca++ was studied in Ca++ - induced contractile tissues and that of intracellular Ca++ was studied in U- 46619 - contracted tissues either in the absence or presence of NO donors. Results: SIN-1 inhibited the contractions induced by Ca++ with a rightward shift of concentration-response curve and with corresponding, but not concentration- dependent increase in EC50 . SNP caused concentration-dependent rightward shift of concentration -response curve of Ca++ . Both SIN-1 and SNP had a bimodal effect with significant inhibition at low concentration of Ca++ and a potentiating effect at high Ca++ concentration. In addition, SNP and SIN -1 inhibited U- 46619 - induced contraction dose dependently. Conclusion: Both SIN-1 and SNP inhibited influx of extracellular Ca++ as well as release of intracellular Ca++ .

Objectives: Toxicological and pharmacological studies of "Navbal Rasayan" a metal based Ayurvedic formulation used for the treatment of multiple sclerosis, have been carried out. Methods: Acute and chronic toxicities studies were conducted in rats with oral graded doses (0.37 to 3.0 g/kg) of Navbal Rasayan (NR). In-vitro study was carried out on isolated guinea pig ileum obtained from control or animal pretreated with oral NR, 1.5 g/kg for 3 days. Dose responses with acetylcholine, histamine and 5-HT were obtained. The analgesic activity of oral NR 1.5 g/kg for 3 days was evaluated in albino mice against acetic acid induced writhings. The hypnotic activity was measured with pentobarbital after oral pretreatment with 1.5 and 3.0 g/kg NR for 3 days. The anti-convulsant activity was observed in rats against i.p. pentylenetetrazol induced seizures. Results: Oral administration of graded doses of NR (upto 3.0 g/kg) did not produce any acute or chronic toxicities in rats. Oral pretreatment of guinea pigs with NR (1.5 g/kg for 3 days) increased 36.43 time the histamine dose while the agonistic effect of acetylcholine and 5-hydroxytryptamine was completely attenuated. Further, NR neither exhibited any analgesic, sedative effect or anticonvulsant effect in rodents. Conclusion: Toxicological and pharmacological study with NR in animals does not show any toxic effect. However, decrease or attenuation of agonistic activities of histamine, acetylcholine and serotonin needs further exploration.

Objective: To study the antinociceptive effect of A.indica in rats. Methods: Analgesia was evaluated using tail flick reaction time to thermal stimulus and glacial acetic acid (GAA) induced writhing. A. indica leaf extract (500mg/kg) and A. indica seed oil (2ml/kg) were given orally by an intragastric tube. Naloxone was given to study the mechanism of antinociceptive effect. Results: Tail flick reaction time was significantly increased in rats with both leaf extract and seed oil. Naloxone pretreatment partially reversed the antinociceptive effect of leaf extract and seed oil. GAA induced writhing was reduced with both leaf extract and seed oil. Pretreatment with naloxone partially reversed the inhibitory effect of leaf extract and seed oil on GAA induced writhing. Leaf extract was more potent than seed oil. Conclusion: The results indicate that both the preparations of A. indica (leaf extract and seed oil) possess antinociceptive activity in rats, leaf extract being more potent.

Objectives: To study the antiinflammatory activity of Curcuma amada rhizome extract in albino rats. Methods: Rhizomes of Curcuma amada were extracted and subjected to spectroscopic studies. The extract was screened for antiinflammatory activity in albino rats using acute carrageenan paw oedema and chronic granuloma pouch model. Results: The extract showed presence of chemical compounds with hydroxyl, ester, carbonyl and olefin funtionalities and exhibited dose dependant antiinflammatory activity in acute and chronic models. Conclusions: The extract of Curcuma amada rhizomes showed antiinflammatory activity in acute and chronic administration in albino rats.

Objective: To investigate the anti-peptic ulcer effect of Shankha bhasma (conch shell ash) in rats. Methods: Gastric ulcers were induced in rats by indomethacin and cold restraint stress, and the effect of two different doses of Shankha bhasma was studied. The response of the bhasma on ulcer index, lipid peroxidation (thiobarbituric acid reacting substances TBARS) in gastric tissue and serum calcium was determined. Results: Shankha bhasma caused significant reduction in ulcer index (P<0.001) in both the indomethacin and cold restraint models. TBARS of stomach in indomethacin treated rat was also reduced (P<0.001) by Shankha bhasma but serum calcium level was not altered. Conclusion: Shankha bhasma induced dose dependent protection against experimental gastric ulcers.

Objective: The antiulcerogenic activity of flavonoid (A) and alkaloid (B) fractions of the S. scabrida and their effect on alkaline phosphatase activity were studied. Methods: The ethanol extract of S. scabrida was subjected to a column and preparative thin layer chromatography to obtain partially pure fractions of A and B which were subjected to antiulcerogenic screening and effects on alkaline phosphatase activity using aspirin and 0.6N NaOH ulcer models. Results: The results showed that fractions A and B significantly (P<0.05) reduced both the ulcer index and alkaline phosphatase activity when compared with aspirin or 0.6N NaOH only. Conclusion: This study seems to implicate alkaline phosphatase as a biochemical evidence of the antiulceroragenic activity of S. scabrida.