Suryakanth Dattatraya Anturlikar

The objective of this study was to evaluate the synergistic activity of Bacopa monniera with Rivastigmine against aluminum-chloride (AlCl3)-induced cognitive impairment in rats. Adult male Wistar rats were divided into ten groups (n = 10) and subjected to their assigned treatments for 42 days. On the 20(th) day of the respective drug treatments, all the animals were trained in the Morris water maze (retention latency) and the elevated plus maze (transfer latency). After the initial training, the retention latency (RL) and the transfer latency (TL) were evaluated on the 21(st) and the 42(nd) days of the study. Chronic administration of AlCl3 caused significant memory impairment associated with increased RL in the Morris water maze task and increased TL in the elevated plus maze test. Interestingly, animals treated with oral administration of B. monniera (100 and 200 mg/kg), Rivastigmine (5 mg/kg) or a combination of B. monniera (100 mg/kg) with Rivastigmine (5 mg/kg) showed significant protection against AlCl3-induced memory impairment compared to animal treated with AlCl3per se. Additionally, the neuroprotective effect of B. monniera (100 and 200 mg/kg) was significantly improved when supplemented with Rivastigmine (5 mg/kg). These findings suggest that treatment with a combination of B. monniera with Rivastigmine may be highly beneficial compared to their per-se treatment.

The present study was conducted to evaluate the efficacy of Abana(®) (a poly-ingredient formulation with natural constituents) on in vitro platelet aggregation and occlusion-induced deep venous thrombosis in rats.Anti-platelet property of Abana(®) was evaluated using ADP (Adenosin 5-diphosphate) and adrenaline-induced platelet aggregation models, and anti-thrombotic activity was evaluated against occlusion-induced deep venous thrombosis model in wistar rats.Under the in vitro conditions, Abana® (250, 500 and 1000 µg/ml) alleviated ADP and adrenaline-induced platelet aggregation in a dose-dependent manner. Abana® (1000 µg/ml) inhibited ADP and adrenaline-induced platelet aggregation by as much as 50.69% and 64.83% respectively. Furthermore, 6 days pre-treatment with Abana® (250 and 500 mg/kg, p.o.) in an in vivo study showed significant and dose-dependent protection against occlusion-induced deep venous thrombosis in rats.These findings suggest that Abana(®), a polyherbal formulation possesses anti-platelet and anti-thrombotic activities in the experimental models of in vitro platelet aggregation and in vivo deep venous thrombosis in rats.

SJ-200 (Himcospaz), an herbal preparation, was investigated for antispasmodic activity on gastrointestinal smooth muscles of guinea pig, rats, rabbits and mice. SJ-200 dosedependently inhibited acetylcholine, histamine and barium chloride-induced contraction of guinea pig ileum. It inhibited spontaneous contraction of rabbit and rat colon. Oxytocin-induced contraction of rat uterus was also inhibited. Oral administration of SJ-200 dose-dependently reduced gastric emptying in rats and intestinal transit in mice. All these findings suggest the non-specific antispasmodic activity of SJ-200 in experimental models.

The liver is a major parenchymal organ involved in many functional activities in the body. Hepatic encephalopathy is a syndrome characterized by increased blood ammonia level and is one of the major complications of cirrhosis. In the present study the protective effect of HD‐03, a poly‐herbal formulation, was evaluated against CCl₄‐induced hepatic encephalopathy in rats. Hepatic encephalopathy was induced in Wistar rats by administration of CCl₄ at a dose of 1 mL/kg orally in liquid paraffin (1:1) twice a week for 90 days. The liver enzymes (SGPT and SGOT) and blood ammonia levels were significantly (p < 0.001) higher in the CCl₄‐intoxicated group compared with the untreated control group. Administration of HD‐03 at a dose of 750 mg/kg orally as an aqueous suspension significantly prevented the elevation of SGPT, SGOT and blood ammonia levels. Histomorphometric evaluation of liver and brain showed a protective effect of the HD‐03 treatment, thus correlating with the changes in biochemical profiles. The protective effect of HD‐03 against CCl₄‐induced encephalopathy may be due to the improved hepatocellular function, which in turn helps in regulating the metabolism of ammonia. However, further studies are required to measure the activity of enzymes involved in the urea cycle and brain aromatic amino acids in order to elucidate the exact mechanism of action of HD‐03. Copyright © 2001 John Wiley & Sons, Ltd.

To investigate the protective effect of HD-03 in experimental cirrhosis following chronic intoxication with thioacetamide (TAA). The effect of HD-03 (750 mg/kg p.o.) was studied in rats following TAA-induced intoxication (50 mg/kg p.o.) for a period of 90 d. HD-03 was administered as an aqueous suspension. Levels of biochemical markers indicative of hepatotoxicity were assessed in serum and liver. Histopathological evaluation of liver was also carried out to find out the protective effect of HD-03 following TAA-induced chronic intoxication. Administration of TAA at a dose of 50 mg/kg p.o. for 90 d resulted in a significant derangement of serum [serum glutamic pyruvate transaminase (SGPT), serum glutamic oxaloacetate transaminase (SGOT), alkaline phosphatase (ALP), albumin and bilirubin] and hepatic (triglycerides, protein, hydroxyproline, collagen and glycogen) biochemical parameters. Histopathological evaluation of liver sections following TAA-intoxication showed necrosis and proliferative changes characteristic of cirrhosis. Simultaneous treatment of TAA-intoxicated rats with HD-03 at a dose of 750 mg/kg p.o. for the same duration significantly prevented the changes in both serum and hepatic biochemical parameters. The reversal of serum and hepatic biochemical parameters also correlated with the preservation of liver histoarchitecture in HD-03 treated rats. The responses such as membrane stabilization, hepatocellular regeneration, and inhibition of collagen formation are the contributing factors in the correction of TAA-induced cirrhosis by HD-03.

Prostane, a polyherbal formulation, was evaluated for its efficacy on 5alpha-reductase inhibition, alpha-adrenergic antagonistic activity and testosterone-induced prostatic hyperplasia. 5alpha-reductase inhibition was evaluated using rat prostate homogenate as an enzyme source. Adrenergic antagonistic activity was evaluated using isolated rat vas deferens. Experimental prostatic hyperplasia was induced in rats by giving testosterone 3 mg/kg sc for 21 days. Prostane dose-dependently inhibited 5alpha-reductase activity and exhibited alpha-adrenergic antagonistic activity. Treatment with Prostane at 250, 500 and 750 mg/kg body wt, po for 21 days significantly reduced the prostatic weight, the epithelial height and the stromal proliferation in experimental prostatic hypertrophy. Prostane is effective in the treatment of experimental prostatic hypertrophy in rats and may be passed on to clinical trials on benign prostatic hypertrophy after necessary toxicological evaluations.