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Sheng-Mai-San attenuates contractile dysfunction and structural damage induced by chronic intermittent hypoxia in mice 被引量:4
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作者 MO Wei-Lan CHAI Cheng-Zhi +2 位作者 KOU Jun-Ping YAN Yong-Qing YU Bo-Yang 《Chinese Journal of Natural Medicines》 SCIE CAS CSCD 2015年第10期743-750,共8页
Sheng-Mai-San(SMS), a well-known Chinese medicinal plant formula, is widely used for the treatment of cardiac diseases characterized by deficiency of Qi and Yin syndrome. A mouse chronic intermittent hypoxia(CIH) mode... Sheng-Mai-San(SMS), a well-known Chinese medicinal plant formula, is widely used for the treatment of cardiac diseases characterized by deficiency of Qi and Yin syndrome. A mouse chronic intermittent hypoxia(CIH) model was established to mimic the primary clinical features of deficiency of Qi and Yin syndrome. Mice experienced CIH for 28 days(nadir 7% to peak 8% oxygen, 20 min per day), resulting in left ventricle(LV) dysfunction and structure abnormalities. After administration of SMS(0.55, 1.1, and 5.5 g·kg-1·d-1) for four weeks, improved cardiac function was observed, as indicated by the increase in the ejection fraction from the LV on echocardiography. SMS also preserved the structural integrity of the LV against eccentric hypotrophy, tissue vacuolization, and mitochondrial injury as measured by histology, electron microscopy, and ultrasound assessments. Mechanistically, the antioxidant effects of SMS were demonstrated; SMS was able to suppress mitochondrial apoptosis as indicated by the reduction of several pro-apoptotic factors(Bax, cytochrome c, and cleaved caspase-3) and up-regulation of the anti-apoptosis factor Bcl-2. In conclusion, these results demonstrate that SMS treatment can protect the structure and function of the LV and that the protective effects of this formula are associated with the regulation of the mitochondrial apoptosis pathway. 展开更多
关键词 sheng-mai-san Chronic intermittent hypoxia Contractile dysfunction Left ventricle Mitochondrial apoptosis
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加味生脉散对大鼠缺血再灌注肾脏损伤的保护作用
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作者 李静 阙海萍 +2 位作者 林秋霞 吕双红 高俊钰 《军事医学科学院院刊》 CSCD 北大核心 2005年第4期346-348,共3页
目的:观察加味生脉散对大鼠缺血再灌注肾脏损伤的保护作用。方法:双侧肾动脉夹闭45min,再灌注24h,造成大鼠缺血再灌注肾脏损伤模型。分别测定加味生脉散治疗组、病理模型组、假手术组大鼠血尿素氮(BUN)、血肌酐(Cr)、组织中髓过氧物酶(M... 目的:观察加味生脉散对大鼠缺血再灌注肾脏损伤的保护作用。方法:双侧肾动脉夹闭45min,再灌注24h,造成大鼠缺血再灌注肾脏损伤模型。分别测定加味生脉散治疗组、病理模型组、假手术组大鼠血尿素氮(BUN)、血肌酐(Cr)、组织中髓过氧物酶(MPO)和丙二醛(MDA)浓度,并进行组织病理学检查。结果:与病理模型组相比,加味生脉散治疗组的缺血再灌注大鼠血尿素氮下降42.8%(P=0.024),血清肌酐下降55.9%(P=0.011);肾脏组织MPO及MDA含量明显降低(P<0.01);组织病理学改变明显减轻(P<0.05)。结论:加味生脉散可减轻缺血再灌注引起的肾脏损伤,其机制与降低缺血再灌注有关的自由基损伤和炎性损伤有关。 展开更多
关键词 急性肾小管坏死 缺血再灌注损伤 加味生脉散 大鼠
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