Peptic ulcer disease (PUD) is a serious gastrointestinal disorder that requires a well targeted therapeutic strategy. A number of drugs including proton pump inhibitors and H2 receptor antagonists are available for the treatment of peptic ulcer, but clinical evaluation of these drugs has shown incidence of relapses, side effects, and drug interactions. This has been the rationale for the development of new antiulcer drugs and the search for novel molecules has been extended to herbal drugs that offer better protection and decreased relapse. Drugs of plant origin are gaining popularity and are being investigated for a number of disorders, including peptic ulcer. The present article reviews the antiulcerogenic and ulcer healing property of Ocimum sanctum , Allophylus serratus , Desmodium gagenticum, Azadirachta indica , Hemidesmus racemosus , Asparagus racemosus, and Musa sapientum. We have highlighted some of the important plants reported for their anti-ulcer and ulcer healing properties, in our laboratory and elsewhere during the last few years. Ayurvedic knowledge supported by modern science is necessary to isolate, characterise, and standardise the active constituents from herbal sources for antiulcer activity.

New agents are being added to the armamentarium of drugs used for the treatment of diabetes mellitus. Today, extensive research is being conducted on incretin hormones. Important among them are, Glucagon like peptide-1 (GLP-1) and Glucose dependent insulinotropic peptide (GIP). The gastrointestinal tract secretes these hormones in response to the ingestion of nutrients. These hormones increase secretion of insulin, decrease secretion of glucagon, decrease gastric emptying time (only by GLP-1). In addition, they decrease body weight and prevent development of resistance to insulin. They are rapidly degraded by dipeptidyl peptidase (DPP-IV) enzyme. Analogs of GLP-1 and GIP and inhibitors of DPP-IV are being synthesised. Exenatide, a synthetic analog of GLP-1, has recently been approved by the FDA, USA for use in patients with type 2 diabetes who have sub optimal control despite treatment with metformin and / or a sulfonylurea. Other GLP-1 analogs under clinical trial are: NN2211, CJC1131, and Albugon. No analog of GIP and inhibitor of DPP-IV have been approved by the FDA for clinical use till now. Vildagliptin, an inhibitor of DPP-IV, is under phase 2 clinical trials. The incidence of hypoglycemia is less with these incretin mimetics and inhibitors of DPP-IV. Minimal gastrointestinal side effects are seen. Analogs of GLP-1 have to be given subcutaneously, while inhibitors of DPP-IV can be given orally. There is a need to synthesise long acting analogs of GLP-1 and selective inhibitors of DPP-IV.

Objectives: To study, the anticataract activity of lisinopril and enalapril on cataract induced by glucose, in goat lenses. Materials and Methods: Goat lenses were incubated in artificial aqueous humor containing 55 mM glucose (cataractogenesis) with lisinopril or enalapril in different concentrations at room temperature for 72 h. Biochemical parameters studied in the lens were electrolytes (Na+, K+), Na+-K+-ATPase activity, malondialdehyde (MDA) and proteins. Results: Glucose induced opacification of goat lens began 8-10 hrs after incubation and was complete in 72-80 hrs. Cataractous lenses showed higher Na+, MDA (P<0.001), lower Na+-K+-ATPase activity, and water-soluble protein content. Lenses treated with lisinopril or enalapril in concentrations of 1, 5, and 10 ng/ml showed higher protein (total and water soluble proteins) content and prevented formation and progress of cataract by glucose, as evidenced by biochemical parameters. Conclusion: The anticataract activity of lisinopril and enalapril may be because of the antioxidant and free radical scavenging activity, as evidenced by a decrease in MDA in treated lenses. Further in-vitro and in-vivo studies in various experimental models and long term clinical trials are required to validate the anticataract activity of ACE-inhibitors.

Objective: To study the antiovulatory and abortifacient activity of the ethanolic extract of roots of Momordica cymbalaria Fenzl. Materials and Methods: Female Wistar albino rats (150 to 200 g) with at least three regular estrous cycles were administered ethanolic extracts of roots of Momordica cymbalaria Fenzl. at two doses 250 and 500 mg/kg orally for 15 days. Control group received vehicle (tween 80 1%, p.o. daily). Animals were sacrificed on 16th day. One ovary was subjected to histopathological studies and the other for biochemical studies. Abortifacient study was done in another set of three groups of animals. The extracts at doses of 250 and 500 mg/kg were administered orally through gastric gavage from the day 6 to day15 of pregnancy (the period of organogenesis). The animals were laparotomised under light ether anesthesia and semi- sterile conditions on day 19th of pregnancy. Both horns of the uterus were observed for the number of implantation sites, resorptions, dead and alive foetus. Results: Highly significant (P<.001) decrease in the duration of estrous cycle and metaestrous phase and increase in proestrous phase was seen, but diestrous phase was unchanged in both 250 and 500 mg treated group when compared to untreated group. Significant decrease in the ovarian weight and a highly significant increase in serum cholesterol with 250 mg/kg dose were seen. Histology of ovary showed an increase in preovulatory and atretic follicles. Ethanolic extract showed a dose dependent abortifacient effect in pregnant rats during organogenesis period. At 250 mg/kg ethanolic extract did not show any abortifacient activity but reduced the number of viable foetus and resorptions with no change in the foetal weight when compared with control group. At 500 mg/kg ethanolic extract showed highly significant (P< 0.001) abortifacient activity. Conclusion: The ethanolic extract at both doses (250 and 500 mg/kg) showed antiovulatory activity. It is abortifacient at 500 mg/kg but not at 250 mg/kg.

Objective: To evaluate the acute and chronic antiinflammatory properties of leaf extracts of Kalanchoe crenata in rats. Material and methods: The methylene chloride/methanol extract of K. crenata was extracted by using hexane, methylene chloride, ethyl acetate, and n-butanol. The antiinflammatory profile of these extracts was investigated on the basis of paw edema induced by carrageenan. The n-butanol fraction (most potent) was further assessed through acute inflammatory models induced by histamine, serotonin, and formalin. The chronic antiinflammatory and the ulcerogenic activities of the n-butanol fraction were also examined. Results: The oral administration of n-butanol fraction (600 mg/kg) caused a maximum inhibition of about 45% in paw edema induced by carrageenan. The n-butanol fraction also exhibited acute antiinflammatory activity on paw edema induced by histamine (47.51%), serotonin (54.71%), and formalin-(40.00%) . In the chronic inflammation model, this extract showed maximum inhibition of 61.26% on the ninth day of treatment. The ulcerogenic assessment showed that ulcer indices after oral treatment with n-butanol fraction were zero and 0.4±0.2, for the 300 and 600 mg/kg doses, respectively. Conclusion: On the basis of these findings, it may be inferred that K. crenata is an antiinflammatory and antiarthritic agent that blocks histamine and serotonin pathways. The results are in agreement with the traditional use of the plant in inflammatory conditions.

Objective : Several medicinal plants have been evaluated for their antidiarrhoeal activity. Most studies evaluated their effect on intestinal motility and antimicrobial activity and, therefore, did not take into account the pathogenesis of infectious diarrhoea. Features of infectious diarrhoea like abdominal pain, cramps, inflammation, and passage of blood/mucus in the stools are the combined effect of one or more virulence factors of the infecting organism. The effect of medicinal plants on the microbial virulent features can serve as marker(s) for testing their efficacy. In this study, we evaluated the effect of a decoction of dried leaves of Dalbergia sissoo on aspects of pathogenicity, that is, colonisation to intestinal epithelial cells and production/action of enterotoxins. This was done to define its possible mechanism(s) of action in infectious diarrhoea. Materials and Methods : Antibacterial, antiprotozoal, and antiviral activities of the plant decoction were checked by agar dilution method, tube dilution method, and neutral red uptake assay, respectively. Cholera toxin (CT) and Escherichia coli labile toxin (LT) were assayed by ganglioside monosialic acid receptor ELISA. Suckling mouse assay was used to assess E. coli stable toxin (ST). As a measure of colonisation, the effect against adherence of E. coli and invasion of E. coli and Shigella flexneri to HEp-2 cells were studied. Results: The decoction had no antibacterial, antiprotozoal, and antiviral activity. It reduced the production and the binding of CT and bacterial adherence and invasion. Conclusion : This study showed that D . sissoo is antidiarrhoeal as it affects bacterial virulence. However, it has no antimicrobial activity.

Objective: To study the redox regulation of vascular responses to endogenous nitric oxide (NO) and NO derived from nitrovasodilator sodium nitroprusside (SNP) in isolated rat aorta. Materials and Methods: To determine the influence of reducing [ascorbic acid (1 mM) and reduced glutathione (GSH) (1 mM)] and oxidizing agents [oxidized glutathione (GSSG) (1 mM) and CuSO4 (1 and 5 µM)] on the vasodilation caused by acetylcholine (ACh; 10-11-10-5 M) and SNP (10-9-10-4 M). Isometric tensions were measured in isolated aorta by a force transducer and recorded in a computer, using Chart V4.1.2 software. Results: ACh and SNP produced relaxation of rat aortic rings that was dependent on concentration. The rings were preconstricted with L-phenylephrine (1 µM). It was observed that oxidizing and reducing agents caused opposite effects on vasodilation induced by NO in rat aorta. Ascorbic acid and GSH potentiated the responses to NO, causing a leftward shift in the concentration-response curve of ACh with significant increase in the pD2 and the Emax. GSSG and CuSO4 inhibited relaxation caused by ACh and shifted the concentration-response curve to the right. In concentration-responses induced by SNP, ascorbic acid significantly increased the pD2 and Emax values from 5.85 ± 0.08 to 6.24 ± 0.05 and 80.83 ± 1.37% to 89.26 ± 1.49%, respectively. However, CuSO4 significantly decreased these values from 5.85 ± 0.02 to 4.56 ± 0.10 and 77.18 ± 0.82% to 53.52 ± 1.60%, respectively. Potentiation of NO response by reducing agents may be related to either increased availability of nitroxyl anion (NO-) or reduction in superoxide anion radical (O2·-). The opposite could be true for the oxidizing agents. Conclusion: The findings of this study suggest that reducing agents like ascorbic acid can improve the vascular responses to NO under oxidative stress.