CONICET | Buscador de Institutos y Recursos Humanos

Gastric ulcers are caused by an imbalance between protective and aggressive factors on the mucosa. Current pharmacological treatment of peptic ulcer focuses on the inhibition of the acid secretion and eradication of Helicobacter pylori. However, enhanced cytoprotection was found to be an interesting therapeutic approach. Atamisqui, Capparis atamisquea Kuntze, is an autochthonous plant from northwestern Argentina with many beneficial properties. Our previously studies showed that 5% infusion (I) and 10% hidroalcoholic extract (E) from the atamisqui leaves present a significant gastroprotective effect. For the assessment of the participation of nitric oxide (NO), prostaglandins (PG) and non-protein sulfhydryl compounds (NP-SH) the ethanol-induced ulceration model was developed in Wistar rats (n=6 animals/group). The inhibitors L-nitroargininemethyl ester (L-NAME) (70 mg/kg, intraperitoneally) and indomethacin (10 mg/kg, intraperitoneally) were used to evaluate the participation of NO and PG respectively in the gastroprotection. To determine the intervention of the NP-SH in the gastroprotective effect, the blocker N-methylmaleimide (NEM) (10 mg/kg, intraperitoneally) was used. The experimental groups were ulcer control group (NaCl 0.9%), positive control group (sucralfate 100 mg/kg, orally) and two treated groups (I 150 mg/kg and E 150 mg/kg, both orally). The ulceration area in the stomachs of each group was determined. Pretreatment with indomethacin and L-NAME but not with NEM significantly blocked the atamisqui extracts gastroprotection. This indicates that the gastroprotective effect of both atamisqui leaf extracts is mediated in part by the PG and NO synthesis but not by NP-SH production in gastric mucosa. More studies will be necessary to define the active compound/s and the molecular mechanisms involved in this effect