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作 者:黄自通 杨伟韬 黄晓霞 王红刚 周敏华 罗兰 HUANG Zitong;YANG Weitao;HUANG Xiaoxia;WANG Honggang;ZHOU Minhua;LUO Lan(Qingyuan Polytechnic,Qingyuan 511510,China;Guangdong Pharmaceutical University,Guangzhou 510006,China;Guangdong Hospital of Integrated Chinese and Western Medicine,Foshan 528200,China)
机构地区:[1]清远职业技术学院,广东清远511510 [2]广东药科大学中药学院,广东广州510006 [3]广东省中西医结合医院,广东佛山528200
出 处:《广东药科大学学报》2022年第6期74-79,共6页Journal of Guangdong Pharmaceutical University
基 金:广东省高水平专业群建设项目(490201);广东省中医药局科研项目(20202033);广东省省级科技计划项目(2016A070712021)。
摘 要:目的 探究强舒降压方(QJF)对高血压大鼠干预效果及其作用机制。方法 采用L-NAME诱导高血压大鼠模型,设立空白组、模型组、卡托普利组、QJF低剂量组和高剂量组;连续灌胃给药4周,每周测量大鼠血压1次,并于末次给药1 h后测量大鼠血压;腹腔注射麻醉,取材。HE染色观察胸主动脉病理变化;测量血浆NO含量,血清ET-1、vWF、TNF-α、eNOS含量,心脏匀浆MMP-9含量。结果 与模型组相比,QJF低剂量组与高剂量组收缩压、舒张压与血清ET-1、vWF、TNF-α含量显著降低(P<0.05或P<0.01),血浆NO、血清eNOS及心脏匀浆MMP-9显著升高(P<0.01);组织病理学检查显示,QJF低剂量组和高剂量组的胸主动脉病理改善明显。结论 QJF对L-NAME诱导的大鼠高血压具有明显的干预效果,其机制与升高血浆NO、血清eNOS及心脏匀浆MMP-9含量,同时降低血清中ET-1、vWF、TNF-α含量有关。Objective To study the preventive effect and mechanism of Qiangshujiangya formula(QJF) on hypertension in rats. Methods The hypertension model was induced by L-NAME administration. Rats were divided into the blank group, the model group, captopril group, and low and high dose of QJF groups. The rats were treated by gavage for 4 weeks, and their blood pressures were measured once a week and at 1 h after the last treatment. After intraperitoneal anesthesia, tissue samples were taken. HE staining was used to observe the pathological changes of thoracic aorta. The content of plasma NO, serum ET-1, v WF, TNF-α, eNOS, and heart homogenate MMP-9 were measured. Results Compared with the model group, the systolic blood pressure, diastolic blood pressure and the content of serum ET-1, v WF, TNF-α were significantly decreased in low and high dose of QJF groups(P < 0.05 or P <0.01). Meantime, the content of plasma NO, serum eNOS and MMP-9 were increased obviously(P < 0.01), and the pathological injury of thoracic aorta was improved in both QJF groups. Conclusion QJF has obvious intervention effect on L-NAME-induced hypertension in rats. Its mechanism is related to the increase of plasma NO, serum eNOS and cardiac homogenate MMP-9, and the decrease of serum ET-1, v WF and TNF-α.
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