Role of Prostaglandins, Nitric oxide, Sulfhydryls and Capsaicin-sensitive Neurons in Gastroprotection of Stigmasterol and β-Sitosterol

In this investigation the gastroprotective activity of stigmasterol and β-sitosterol was evaluated. Gastric mucosal damage was induced in rats by intragastric ethanol (1 mL/rat). Rats treated orally with stigmasterol suspended in Tween 80 at 10, 30, 100 and 300 mg kg−1 showed 26.2, 39.6, 58.3 and 70.7% gastroprotection, respectively. β-Sitosterol at 10, 30,100 and 300 mg kg−1 showed 21.6, 42.5, 48.5 and 71.2% gastroprotection, correspondingly. The gastroprotection observed at 30 mg kg−1 for stigmasterol and β-sitosterol was attenuated in rats pretreated with indomethacin, (10 mg kg−1, s. c.), NG-nitro-L-arginine methyl ester (L-NAME, 70 mg kg−1, i. p.) and capsaicin (125 mg kg−1, s. c), suggesting that the gastroprotective mechanism of these sterols involves, at least in part, the participation of prostaglandins, nitric oxide (NO) and capsaicin-sensitive sensory neurons (CPSN). The gastroprotection of β-sitosterol was also attenuated by the pretreatment with N-ethylmaleimide (NEM, 10 mg kg−1, s. c.) indicating that endogenous sulfrydryls may be involved in the gastrorpotection of this compound. Carbenoxolone was used as a gastroprotective model drug and showed a dose-dependent gastroprotective effect (25.7, 33.6 and 88.3% of gastroprotection, at 3, 10 and 30 mg kg−1, respectively). The partial participation of PGs, sulfhydryls and NO was observed in the gastroprotective mechanism of carbenoxolone.