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机构地区:[1]辽宁医学院附属第一医院中医科,辽宁锦州121001 [2]辽宁医学院附属第三医院肿瘤科,辽宁锦州121001
出 处:《中国药房》2015年第16期2192-2195,共4页China Pharmacy
摘 要:目的:研究淫羊藿苷对心肌缺血再灌注损伤(IR)模型大鼠心肌组织的保护作用。方法:取SD大鼠随机分为假手术(等容生理盐水)组、模型(等容生理盐水)组和淫羊藿苷低、中、高剂量(5、10、20 mg/kg)组,除假手术组6只外其余每组12只。各组大鼠ig给予相应药物,每日1次,连续14 d,末次给药1 h后行冠状动脉结扎术复制IR模型。采用2,3,5-氯化三苯基四氮唑(TTC)染色法考察各组大鼠心肌梗死比例;原位末端标记法检测各组大鼠心肌细胞凋亡率;western blot法检测各组大鼠心肌组织中p38和JNK磷酸化(p-p38、p-JNK)蛋白水平。结果:与假手术组比较,模型组大鼠心肌梗死比例、心肌细胞凋亡率、心肌组织中p-p38和p-JNK蛋白水平均增加,差异具有统计学意义(P<0.01或P<0.05)。与模型组比较,淫羊藿苷各剂量组大鼠上述指标均降低,差异具有统计学意义(P<0.01或P<0.05),其中高、中剂量组效果较低剂量组更明显(P<0.05)。结论:淫羊藿苷预处理对IR模型大鼠的心肌组织具有保护作用,并呈浓度依赖性。其作用机制可能与降低心肌细胞凋亡,下调p-p38和p-JNK蛋白水平有关。OBJECTIVE: To study the protective effects of icariin on the myocardial tissue of model rats with myocardial isch- emic-reperfusion (IR) injury. METHODS: SD rats were randomly divided into sham-operation group (isovolumetric saline) (n= 6), model group (isovolumetric saline) (n=12) and icariin low, medium and high dose groups (5, 10, 20 mg/kg) (n=12). Rats in all groups were given related drugs, ig, once a day for 14 d. After 1 h of the last administration, coronary artery ligation was conducted to reproduce IR model. TTC staining method was used to detect the cardiac infarction proportion, western blot was used to determine the myocardial cell apoptosis rate and western blot was used to determine the protein level of p38 and JNK phosphory- lation (p-p38 and p-JNK) in myocardial tissue of rats. RESULTS: Compared with sham-operation group, the cardiac infarction pro- portion, myocardial cell apoptosis rate and the protein level of p-p38 and p-JNK in model group were all increased, with signifi- cant difference (P〈0.01 or P〈0.05). Compared with model group, the above-mentioned indicators in icariin dose groups were all decreased, with significant difference (P〈0.01 or P〈0.05) ; and the effects in high and medium dose groups were more obvious than low dose group (P〈0.05). CONCLUSIONS: The pretreatment of icariin has protective effect on myocardial tissue of IR rats with concentration dependent. The mechanism of the action may be associated with reducing the myocardial cell apoptosis and de- creasing the protein level of p-p38 and p-JNK.
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