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Aim:To investigate the effect of geranylgeranylacetone (GGA) on the progres-sion of atrophic gastritis in rats and its potential mechanism.Methods:Atrophicgastritis was induced in Sprague-Dawley rats with 0.1% ammonia solution,60%ethanol,and 20 mmol/L deoxycholic acid for 24 weeks.Accompanied by theinduction of atrophic gastritis,200 mg/kg GGA was administered by oral gavagefor 8 weeks (weeks 17-24).The histological changes in gastric mucosa werequantitated by the index of inflammation,the gastric mucosal thickness,and theamount of glands of 1 mm horizontal length in antrum.Endogenous heat shockprotein (HSP)70 levels and distribution were determined by immunoblotting andimmunohistochemistry in gastric mucosa.Results:GGA alleviated the pathologi-cal progression of atrophic gastritis with inflammation relief (inflammation index:1.40 in the GGA group and 1.65 in the atrophic gastritis group) and glandularrestoration (mucosal thickness and quantity of glands:194.3 μm and 38.7 mm inthe GGA group;123.3 μm and 32.7 mm in the atrophic gastritis group;P<0.05).GGA significantly induced HSP70 synthesis (P<0.05).Moreover,quercetin,aninhibitor of HSP70 expression,aggravated the infiltration of inflammatory cellsand glandular loss in the antrum.Conclusion:GGA prevented the progression ofatrophic gastritis in rats via the induction of HSP70 expression.
Aim: To investigate the effect of geranylgeranylacetone (GGA) on the progres-sion of atrophic gastritis in rats and its potential mechanism. Methods: Atrophic gastritis was induced in Sprague-Dawley rats with 0.1% ammonia solution, 60% The deoxycholic acid for 24 weeks. A compcompanied by the induction of atrophic gastritis, 200 mg / kg GGA was administered by oral gavage for 8 weeks (weeks 17-24). The histological changes in gastric mucosa were quantitated by the index of inflammation, the gastric mucosal thickness , and the thickness of 1 mm horizontal length in antrum. Endogenous heat shock protein 70 (HSP) 70 levels and distribution were determined by immunoblotting and immunohistochemistry in gastric mucosa. Results: GGA alleviated the pathologi-cal progression of atrophic gastritis with inflammation relief : 1.40 in the GGA group and 1.65 in the atrophic gastritis group) and glandular restoration (mucosal thickness and quantity of glands: 194.3 μm and 38.7 mm inthe GGA group; 123.3 μm and 32.7 mm in the atrophic gastritis group; P <0.05) .GGA significantly induced HSP70 synthesis (P <0.05) .Moreover, quercetin, an inhibitor of HSP70 expression, aggravated the infiltration of inflammatory cells and glandular loss in the antrum. Conclusion: GGA prevented the progression of atrophic gastritis in rats via the induction of HSP70 expression.