| Objective:To investigate the cardioproective effect and mechanism of vitexin on myocardialischemia/reperfusion (I/R) injury in the rat in vivo, in order to provide proof for clinic tofacilitate work.Methods:By occluding the anterior descending artery for30min with60min reperfusionfollowed, the injury of rat myocardial I/R can be established. The elevation of the STsegment of Electrocardiograph (ECG) was observed. The infarct size of rat heart wasassessed by triphenyltetrazolium chloride staining (TTC). After the treatment, LDH, CK,SOD activities and MDA contents would be determined. The Immunohistochemicalanalysis was applied to measure the expression of myocardial NF-κB and TNF-a.ERK/phospho-ERK and c-Jun/phospho-c-Jun protein expression were examined byusing Western Blotting. Establish rat blood stasis model, we detect hemodynamicindexes. Establish rat thrombosis model, we measure the dry weight and wet weight ofthrombus.Results:The elevation of the ST segment was significantly enhanced in I/R group30minafter ischemia,30and60min after reperfusion compared with sham group, vitexin6mg/kg and puerarin have significant inhibiting effect against the elevation of the ST segment30and60min after reperfusion compared with I/R group.Compared with sham group, the myocardial infarct size of I/R group significantlyenhanced which proved the injury induced by ischemia/reperfusion in vivo.Administration of vitexin reduced the infarct size in different extent; treatment with6mg/kg of vitexin was most effective, reducing infarct size by40%compared with I/Rgroup treatment.There were significant increases in LDH and CK in I/R group compared to shamgroup, these parameters decreased significantly in those groups treated with vitexin andpuerarin in comparison with I/R group. Compared with sham group, the content ofserum SOD was significantly decreased in I/R group, while SOD levels increasedsignificantly in vitexin and puerarin groups compared with I/R group. In addition, thecontent of MDA was increased in I/R group compared with sham group, and decreasedin the vitexin6,3mg/kg and puerarin groups compared with I/R group.A very small amount of NF-κBp65and TNF-α were detected in myocardial tissueof the sham group, which significantly increased in I/R group. Vitexin and puerarinsignificantly reduced the expression of NF-κBp65and TNF-α protein, when comparedwith I/R group.Treatment with puerarin and vitexin6,3mg/kg increased phospho-ERKexpression significantly compared with I/R group. While the expression ofphospho-c-Jun was significantly increased in I/R group, and administration of puerarinand vitexin inhibited the increase of phospho-c-Jun.Vitexin6,3,1.5mg/kg attenuated the viscosity of blood and plasma, increasederythrocyte deformation ability; vitexin6,3mg/kg markedly reduced the dry weight ofthrombus, thus inhibited thrombosis.ConclusionThe significant protective effect against myocardial ischemical/reperfusion injury in rat heart in vivo which exhibited by vitexin may related to its antioxidation andanti-inflammatory effect via regulating inflammatory cytokines and MAPK pathway, aswell as related to its reducing the blood and plasma viscosity, improving the ability ofRBC deformation, inhibiting thrombosis, etc. |
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