Résumé
Objective: To investigate the influence of Taxus polysaccharide on myocardial NADPH oxidase mRNA, SOD, and MDA in myocardial ischemia-reperfusion injury (MIRI) model of Beagle's dogs. Methods: Beagle's dogs (30) were randomly divided into Sham operation, model, low-dose Taxol polysaccharide, high-dose Taxol polysaccharide, and Carvedilol groups, six in each group, and MIRI model was established after 7 d administration. Stained with HE, pathological changes in myocardial tissue were observed with light microscopy; NADPH oxidase p47phox (NCF-47K) mRNA expression was detected with in situ hybridization; Myocardial SOD and MDA contents were detected with colorimetry. Results: Under light microscope, serious cardiac cells disorders, fracture, karyopyknosis, and significant eosinophilic cytoplasm existed, mild to moderate hyperemia and edema and inflammatory cell infiltration appeared in the model group. However, in the high-dose group, myocardial cells disorders and destruction existed in a lesser extent, karyopyknosis and eosinophilic cytoplasm decreased significantly, and some organizations were still mild hyperemia and edem. Myocardial NCF-47K mRNA expression of Beagle's dogs in the model group and low-dose group were significantly higher than that in the Sham-operated group (P<0.01), NCF-47K mRNA expression of Beagle's dogs in the high-dose group was significantly lower than that in the model group (P<0.05). And SOD content in myocardial tissue of the model group and the treatment group was significantly lower than that in the Sham-operated group (F<0.01). SOD content in the high dose group was significantly higher than that in the model group (P<0.01). MDA contents in myocardial tissue in the model and low-dose groups were significantly higher than those in the Sham-operated group (P<0.05). MDA content in high-dose group was significantly lower than that in the model group (P<0.05). Conclusion The Taxus polysaccharide may reduce ischemia-reperfusion myocardial injury by reducing the expression of NADPH oxidase, increasing SOD activity, and reducing injury of O2.- and other oxygen free radicals in myocardial cell.