Protective Effect of Polydatin on Experimental Acute Gastric Mucosal Lesion and Its Mechanisms

Acute gastric mucosal lesions occur in a variety of pathological processes, their injury involves gastric acid, pepsin, Helicobacter pylori, drugs, stress, ethanol, surgery. In recent years ischemia-reperfusion important role in the pathogenesis of acute gastric mucosal lesion has attracted extensive attention. The Polydatin (Polydatin, PD), piceid is one of the active ingredients of Polygonum cuspidatum has to protect myocardial cells, improve microcirculation, inhibition of platelet aggregation, the endotoxin shock resistance, lowering blood pressure, relieving cough, asthma, variety of pharmacological effects against pathogenic microorganisms. PD acute gastric mucosal protective effect and mechanism has not been reported. This study will examine the effect and mechanism of gastric mucosal injury caused by ethanol in mice, rats, frozen - restraint stress, ischemic reperfusion Polydatin provide experimental basis for the further development and utilization of Polydatin . The main content summarized as follows: PD anhydrous ethanol-induced acute gastric mucosal lesion in mice ethanol (0.1ml/10g) orally induced acute gastric mucosal injury model in mice. PD (120,60,30 mg / kg) in modeling intragastrically administered for 5 days, can effectively reduce acute gastric mucosal injury model mice gastric mucosal damage index (P lt; 0.01 or P lt; 0.05). Prompted PD has a protective effect on ethanol-induced acute gastric mucosal injury. 2. PD pylorus ligation induced rat gastric juice volume, free acidity, total acidity and pepsin activity PD (80,40 mg / kg, ig) juice volume, free acidity of gastric juice of pylorus ligated rats, total acidity, and gastric juice pepsin activity statistically test differences no significant sex (P gt; 0.05). Prompted PD gastric mucosal injury protection mechanism, not primarily by influencing the activity of gastric acid and pepsin play a role. PD (80,40,20 mg / kg, ig) PD frozen - restraint stress (CRS) induced acute gastric mucosal injury in rats intragastrically administered for 5 days, can significantly reduce gastric mucosal damage area, lower serum MDA content, SOD levels rebound increase of PGE2 OD value (P lt; 0.01 or P lt; 0.05). Prompted PD CRS induced acute gastric mucosal damage protective effect and its mechanism of oxygen free radicals and the increase of the expression levels of PGE2 (P lt; 0.01 or P lt; 0.05). 4. PD gastric ischemia-reperfusion induced gastric mucosal damage in rats affect PD (80,40,20 mg / kg, ig) intragastrically administered for 5 days, compared with the model group, can reduce gastric mucosal damage area; reduce stomach tissue infiltration of inflammatory cells, significantly change the histopathological changes of the gastric mucosa. PD (80,40 mg / kg, ig) can still reduce gastric juice after intravenous injection of Evans Blue Evans Blue exudation. PD (80,40,20 mg / kg, ig) may be elevated rat gastric tissue SOD, GSH-Px, NO and NOS level, to reduce the content of MDA, MPO organization; radioimmunoassay and RT-PCR detection results, PD can reduce plasma TNF-α and IL-1β content, inhibition of TNF-α and IL-1β mRNA expression in the tissue (P lt; 0.01 or P lt; 0.05). Prompted PD on gastric ischemia-reperfusion induced gastric mucosal injury has a protective effect and its mechanism may reduce gastric vascular permeability, resistance to oxidative stress, reduce the inflammatory cytokines TNF-α and IL-1β levels and inhibition of both mRNA expression related (P lt; 0.01 or P lt; 0.05). Conclusion: PD has a protective effect on experimental acute gastric mucosal injury. Possibly through anti-oxidative stress, anti-ischemic reperfusion, the inhibition of inflammatory cell infiltration, reduce gastric vascular permeability and anti-injury role; their molecular mechanisms of PGE2 may be related to oxygen free radicals, improve the level of NO and NOS, inhibition inflammatory cytokines TNF-α and IL-1β expression.