Mechanism Of Apigenin Improvement On Endothelial Injury In Rats With High Fructose-Induced Metabolic Syndrome

Objective:The purpose of the study was to investigate whether apigenin could protect the vascular damage with metabolic disorders induced by drinking 10% fructose freely.The potential mechanisms were explored in the experiment.Methods:Rats were randomly into three groups: Control,Model and Apigenin groups.Model and apigenin groups were freely provided enough water with 10% fructose consistently for twelve weeks.At the same time,the apigenin group were savaged apigenin at the concentration of 50 mg/kg every day.We used non-invasive blood pressure measurement in rats at twelve weeks.We detected the important markers of glycometabolism,lipid metabolism and uric acid to evaluate the extent of abnormal metabolism.Additionally,HE and EVG staining were used to show the pathological damage in tissues.In the study,v WF level was detected to evaluate the endothelial dysfunction.IGF-1 and the expression of GLUT1 protein was detected to explore whether the activity of apigenin was associated with the absorption of carbohydrate.Moreover,e NOS protein and its natural inhibitor ADMA were detected;levels of NO and c GMP were detected to confirm whether NO signaling pathway was associated with the model.Results:Data show that the body fat rate is lower in the apigenin group than that in the 10% fructose model group.In terms of hypertension,fructose significantly increase the systolic pressure and mean pressure,which were improved by apigenin.Additionally,fructose could induce the insulin resistant in rats and apigenin could improve the tendency.In terms of lipid metabolism,fructose could affect the levels of TG and TC,and apigenin could ameliorates these indexes.Additionally,we find that apigenin could ameliorate high-fructose induced hyperuricemia in rats.These results show that apigenin could improve metabolic abnormalities caused by 10% fructose.Apigenin could protect the damage in the liver,kidney and thoracic aorta tissues in rats with metabolic disorders.The increased level of v WF demonstrates that high fructose could induce serious endothelial injury.The increased level of IGF-1 and down-regulated expression of GLUT1 protein indicate that apigenin may inhibit the uptake of glucose to reduce the injury in the thoracic aorta.Moreover,the increased ADMA and downregulation of p-e NOS show that apigenin may influence the NO signaling pathway.Therefore we find that the levels of NO and c GMP were both decreased.Apigenin may promote NO signaling to protect the endothelial injury induced by excessive fructose.Conclusion:Apigenin could protect and ameliorate the vascular injury with metabolic disorders in rats induced by high fructose.Apigenin may regulate the activity of GLUT1 and IGF-1 to affect the glycometabolism and protect the endothelial injury by promoting p-e NOS to promote NO signaling pathway.