No abstract

The present work reports the anti-inflammatory and antinociceptive activities of the ethanol extract obtained from the stem bark of Sterculia striata A. St.-Hil. & Naudin (Ss-EtOH) in the experimental models of edema induced by carrageenan, dextran, or histamin and nociception induced by chemical stimuli, such as acetic acid, formalin, capsaicin, or glutamate. The Ss-EtOH (50 mg/kg) promoted a marked inhibition on the hind paw edema induced by carrageenan or dextran (30% and 73%, respectively). Besides, Ss-EtOH (25 mg/kg) exhibited a slight activity (30%) on the hind paw edema induced by histamin. The Ss-EtOH (12.5 and 25 mg/kg) showed the antinociceptive activity on chemical stimuli induced by acetic acid (65.59% and 38.37%, respectively), formalin, in the initial (35.08% and 31.5%, respectively) and late phases (44.09% and 83.57%, respectively), capsaicin (43.77% and 51.31%, respectively), or glutamate (36.6% and 52.12%, respectively). Regarding the possible mechanism involved in the antinociceptive effect, Ss-EtOH (12.5 mg/kg) showed a decrease in the antinociceptive effect (65.8%) in the acetic acid model after pretreatment with naloxone. Thus, opioid mechanisms might be underlying this response.

Parkia platycephala Benth. (Leguminosae -Mimosoideae), popularly known as "visgueira", fava bean tree or "fava-de-bolota", is widely found in the Northern and Northeastern regions of Brazil. Its pods are used as cattle food supplement in the drought period. Compounds with a gastroprotective activity were obtained from the genus Parkia. Therefore, this study aimed at investigating the gastroprotective effect of the ethanolic extract of Parkia platycephala Benth. leaves (Pp-EtOH), as well as evaluating its possible mechanisms of action in experimental ulcer induction models. Lesions were induced by absolute ethanol, ethanol-HCl, ischemiareperfusion and indomethacin in rodents. Pp-EtOH showed a protective effect in the lesion models (66, 48 and 52 %, respectively), but it was not able to protect gastric mucosa against indomethacin-induced lesions. Results show a possible participation of the NOsynthase pathway in the gastroprotection and an antioxidant activity, by the increase of the catalase activity. The participation of prostaglandins and potassium channels sensitive to ATP in the gastroprotective effect of Pp-EtOH seems less likely to occur. More comprehensive studies, therefore, should be carried out to elucidate the antiulcerative effects of this promising natural product against this gastrointestinal disorder.

No abstract

This study investigates the gastroprotective effect of a crude ethanolic extract of Neoglaziovia variegata (Arruda) Mez (Bromeliaceae), designated Nv-EtOH, in experimental models of gastric ulcer. In the ethanol-induced gastric ulcer model, Nv-EtOH showed gastroprotection at doses of 200 and 400 mg/kg body weight (BW) (57.0% and 79.7%, respectively). Nv-EtOH also signifi cantly reduced the formation of gastric lesions induced by ethanol/HCl (31.6% and 63.5%), ibuprofen (70.0% and 74.3%), or ischemia/reperfusion in rats (65.0% and 87.0%) at 200 and 400 mg/kg BW when compared with the vehicle group. In the antioxidant activity assessment, Nv-EtOH (400 mg/kg BW) increased the catalase activity and sulfhydryl groups (SH) levels, respectively. Moreover, gastroprotection against ethanol damage was decreased after ibuprofen pretreatment. Nv-EtOH (400 mg/kg BW) promoted a signifi cant increase in the content of gastric wall mucus. The Nv-EtOH effect was signifi cantly reduced in mice pretreated with N G -nitro-L-arginine (L-NOARG) or glibenclamide, inhibitors of nitric oxide synthase and K ATP channel activation, respectively, suggesting the involvement of these mechanisms in the Nv-EtOH-induced gastroprotective effect. Nv-EtOH decreased the total acidity, but did not modify other gastric juice parameters. Nv-EtOH was also effective in promoting the healing process in chronic gastric ulcer induced by acetic acid in rats.

The Sterculia striata ethanolic extract (Ss-EtOH) inhibited gastric lesions induced by ethanol, HCl/ethanol, and ischemia/reperfusion, but not those induced by indomethacin, and did not alter the gastric secretion. Ss-EtOH restored the catalase activity and content of nonprotein sulfhydryl groups in the stomach of mice treated with ethanol. The gastroprotection induced by Ss-EtOH in the ethanol-induced gastric lesion model was abolished by NG-nitro- L-arginine methyl ester (L-NAME) pretreatment, suggesting the involvement of nitric oxide and antioxidant compounds, but not prostaglandins, in this activity. Lupeol obtained from Ss-EtOH promoted gastroprotection as well as the extract at the same dose, and it must therefore contribute to the observed effects

Carvacrol (CARV) is a phenolic monoterpene present in the essential oil of several aromatic spices. The purpose of the present study was to evaluate the antinociceptive effect of CARV on formalin-, capsaicin-, and glutamate-induced orofacial nociception in mice. Male mice were pretreated with CARV [25, 50, and 100 mg/kg body weight (BW), intraperitoneal (i.p.)], morphine (5 mg/kg BW, i.p.), or vehicle (distilled water + one drop of 0.3% cremophor in distilled water), before formalin (20 μl, 2%), capsaicin (20 μl, 2.5 μg), or glutamate (40 μl, 25 μM) was injected into the right upper lip. Our results revealed that i.p. pretreatment with CARV was effective in reducing the nociceptive face-rubbing behaviour in both phases of the formalin test and also produced a signifi cant antinociceptive effect at all doses in the capsaicin and glutamate tests. Further, we showed that the action of CARV on the central nervous system (CNS) did not affect these results, since this compound did not exert a significant CNS-depressant effect, as shown by the pentobarbital-induced hypnosis. Our results suggest that CARV might represent an important tool for the treatment of orofacial pain

This study investigates the gastroprotective effect of a crude ethanolic extract of Neoglaziovia variegata (Arruda) Mez (Bromeliaceae), designated Nv-EtOH, in experimental models of gastric ulcer. In the ethanol-induced gastric ulcer model, Nv-EtOH showed gastroprotection at doses of 200 and 400 mg/kg body weight (BW) (57.0% and 79.7%, respectively). Nv-EtOH also significantly reduced the formation of gastric lesions induced by ethanol/HCl (31.6% and 63.5%), ibuprofen (70.0% and 74.3%), or ischemia/reperfusion in rats (65.0% and 87.0%) at 200 and 400 mg/kg BW when compared with the vehicle group. In the antioxidant activity assessment, Nv-EtOH (400 mg/kg BW) increased the catalase activity and sulfhydryl groups (SH) levels, respectively. Moreover, gastroprotection against ethanol damage was decreased after ibuprofen pretreatment. Nv-EtOH (400 mg/kg BW) promoted a significant increase in the content of gastric wall mucus. The Nv-EtOH effect was significantly reduced in mice pretreated with N(G)-nitro-L-arginine (L-NOARG) or glibenclamide, inhibitors of nitric oxide synthase and K(ATP) channel activation, respectively, suggesting the involvement of these mechanisms in the Nv-EtOH-induced gastroprotective effect. Nv-EtOH decreased the total acidity, but did not modify other gastric juice parameters. Nv-EtOH was also effective in promoting the healing process in chronic gastric ulcer induced by acetic acid in rats.