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目的本文旨在研究黄芪多糖(Astragalus Polysaccharide,AP)对CVB3病毒感染的乳鼠心肌细胞和小鼠的保护作用,为进一步作用机制研究提供理论依据。方法使用AP对CVB3病毒介导的病毒性心肌炎病理模型进行治疗,通过对MTT染色和小鼠病毒性心肌炎模型治疗前、后心肌病理切片的观察,检测小鼠外周血液中乳酸脱氢酶和磷酸肌酸激酶的含量,判断AP对CVB3病毒感染后小鼠心肌的保护作用。结果 MTT染色结果表明,给药组的OD值均明显高于病毒对照组(P<0.05),与病毒对照组比较,AP能够减轻由CVB3介导的心肌细胞炎症和病理改变的程度;AP能够显著的降低小鼠外周血中的心肌酶含量(P<0.05);心肌病理切片表明,给药组心肌早期钙化面积减少,与阳性对照组比较仅有少量的炎性细胞浸润,说明其能防止感染的心肌细胞溶解,对心肌具有保护作用;给药组细胞上清液中病毒的TCID50比病毒对照组小一个数量级,说明AP对病毒繁殖有抑制作用。结论 AP对CVB3病毒感染后的心肌细胞和心肌有一定的保护作用,该结果为AP的更深入研究提供了理论依据。
Objective To study the protective effect of Astragalus Polysaccharide (AP) on neonatal rat cardiomyocytes and mice infected with CVB3 virus, and to provide a theoretical basis for the further study of its mechanism. Methods APB was used to treat CVB3-induced viral myocarditis. The changes of lactate dehydrogenase and phosphoric acid in peripheral blood were detected by MTT staining and mouse myocarditis model before and after treatment. Creatine kinase, to determine the AP of CVB3 virus infection in mice after myocardial protection. Results The results of MTT assay showed that the OD value of the treated group was significantly higher than that of the virus control group (P <0.05). Compared with the virus control group, AP could reduce the extent of CVB3-mediated cardiomyocyte inflammation and pathological changes. AP could (P <0.05). The pathological sections of myocardium showed that the area of myocardial calcification in the administration group decreased and there was only a small amount of inflammatory cell infiltration compared with the positive control group, indicating that it can prevent The infected cardiomyocytes dissolved and had a protective effect on the myocardium. The TCID50 of the virus in the supernatant of the drug-treated group was one order of magnitude smaller than that of the virus control group, indicating that AP has an inhibitory effect on virus multiplication. Conclusion AP has a protective effect on CVB3-infected cardiomyocytes and myocardium. This result provides a theoretical basis for further study of AP.