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作 者:罗银利[1] 黄晓松[1] 谭李红[1] 刘柳青[1] 袁波[1]
机构地区:[1]湖南省第二人民医院,湖南中医药大学临床医学院,湖南长沙410007
出 处:《中医药导报》2015年第9期26-28,共3页Guiding Journal of Traditional Chinese Medicine and Pharmacy
基 金:湖南省中医药管理局重点资助项目(No.201329);湖南省中医药管理局一般资助项目(No.2013126)
摘 要:目的:观察红景天苷对大鼠脑缺血-再灌注损伤后PI3-K、p-Akt及Caspase-3表达的影响。方法:将60只SD雄性大鼠随机分为假手术组12只、脑缺血-再灌注组(模型组)及红景天苷组(10 mg/kg)各24只。采用线栓法制备大鼠右侧大脑中动脉缺血-再灌注模型,观察缺血2 h再灌注6 h、12 h、24 h、48 h 4个不同时间点,采用Western Blotting法检测PI3-K、p-Akt及Caspase-3的蛋白表达。结果:与假手术组比较,模型组及红景天苷组4个不同时间点PI3-K、p-Akt、Caspase-3蛋白表达量均显著升高,差异均有统计学意义(P<0.01)。与模型组比较,红景天苷组4个不同时间点PI3-K、p-Akt蛋白表达量均升高,Caspase-3蛋白表达量均减少,差异均有统计学意义(P<0.05)。模型组及红景天苷组PI3-K、p-AKT蛋白表达趋势均从再灌注6 h开始逐渐升高,24 h达高峰,48 h较24 h下降,但高于12 h;Caspase-3蛋白表达趋势均从再灌注6 h开始逐渐升高,48 h达高峰。结论:红景天苷可能通过激活PI3-K/Akt信号转导通路,上调PI3-K、p-Akt的蛋白表达,抑制Caspase-3的蛋白表达,从而发挥对大鼠脑缺血-再灌注损伤抗凋亡的神经保护作用。Objective: To observe the changes on the protein expressions of PI3-K,p-Akt and Caspase-3 in rats with cerebral ischemia/reperfusion injury. Methods: The 60 SD rats were randomly divided into three groups, the sham-operation group, the I/R group (the model group), the rhodioloside treatment group (10mg/kg). The model of middle cerebral artery occlusion was established by thread ligation method. Adult SD rats were observed cerebral ischemia for 2 h, and reperfusion at 6 h, 12 h, 24 h and 48 h respectively. The protein expressions of PI3-K,p-Akt and Caspase-3 were evaluated by Western Blotting at the four different time points.Results: The protein expressions of PI3-K,p-Akt and Caspase-3 in hippocampus at four different time points in model group and rhodioloside treatment group were significantly higher than that of the sham group(P〈0.01). The pro- tein expressions of PI3-K and p-Akt in hippocampus at the four different time points in rhodioloside treatment group were higher than that of the model group (P〈0.05).The protein expression of Caspase-3 in rhodioloside treatment group were less than that of the model group (P〈0.05).The protein expressions of PI3-K and p-Akt in model group and rhodioloside treatment group were gradually increased at 6h after the reperfusion, reached the peak at 24 h, and declined at 48 h. The protein expression of Caspase-3 in model group and rhodioloside treatment group were gradually increased in 6 h after the reperfusion, and reached the peak in 48 h. Conclusion: The neuroprotective mechanism of rhodioloside in cerebral ischemia/reperfusion injury rats might be associated with the increased protein expressions of PI3-K and p-Akt and the inhibited expression of Caspase-3 by activating the PI3-K/Akt signaling pathway.
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