Objective: To study the effect of β-sitosterol on gastric mucosal injury induced by aspirin and its possible mechanism

and explore the effect of β-sitosterol on pharmacological functions of aspirin. Method: Gastric mucosa injury modelsinduced by aspirinin SD rats was established by intragastric administration of different dosesof β-sitosterol(50

150

250 mg·kg-1) for seven days

and ulcer area was assessed to analyze the effect of β-sitosterol on gastric mucosal injury induced by aspirin in rats. Serum superoxide dismutase(SOD)

tumor necrosis factor-α(TNF-α)

prostaglandin E2(PGE2)

malondialdehyde(MDA) and nitric oxide(NO) were measured to analyze the possible mechanism. Rat paw edema test

mouse ear swelling

rat yeast-induced fever test and mouse hot plate test

and platelet aggregation in rats were used to examine the pharmacological effect of different doses of β-sitosterol on anti-inflammatory

antipyretic

analgesic

and inhibition of platelet aggregation induced by aspirin. Result: Compared with aspirin-treated group

gastric ulcer area of β-sitosterol group rats was significantly reduced(P<0.05);gastric ulcer area in the high and middle dose β-sitosterol group rats was significantly smaller than that in β-sitosterol low dose group(P<0.05). Compared with aspirin-treated group

NO and SOD in serum of β-sitosterol rats increased significantly(P<0.05)

TNF-α

MDA significantly decreased(P<0.05)

and PGE2 level was not significantly different. Compared with the model group

toe swelling of rats and ear swelling of micein various treatment groups were significantly reduced(P<0.05);compared with the aspirin-treated group

toe swelling of rats and ear swelling of mice in β-sitosterol group were significantly reduced(P<0.05)

but there is no significant differences between the β-sitosterol groups. Compared with aspirin-treated group

the change in the value of the rectal temperature and pain threshold in mice and platelet aggregation rate in rat of the corresponding β-sitosterol group were no significant difference. Conclusion: β-sitosterol can reduce the aspirin-mediated gastric mucosal injury

and its mechanism may be related to enhancing the clearance capacity of oxygen free radicals(OFR) of body

improving levels of NO

inhibiting aggregation and release of inflammatory cytokines TNF-α;β-sitosterol can enhance the anti-inflammatory effects of aspirin and have no significant effect on antipyretic

analgesic

and inhibition of platelet aggregation.