摘要
目的:探讨定心方(DXR)对Apo E基因敲除(ApoE^(-/-))小鼠人第十号染色体缺失磷酸酶及张力蛋白同系物(PTEN)的影响,以及DXR抗AS的可能机制。方法:将50只ApoE^(-/-)小鼠随机分为模型组,辛伐他汀组,DXR低、中、高剂量组,另取10只C57/BL6J小鼠作为正常组。分别给予DXR低、中、高组按剂量9.25,18.59,37.18 g·kg-1·d^(-1)DXR药液ig,辛伐他汀组按剂量0.005 g·kg-1·d^(-1)ig辛伐他汀,高脂饲料喂养16周后处死,苏木素-伊红(HE)染色观察主动脉斑块面积,检测小鼠血脂以及血清中丙二醛(MDA),总超氧化物歧化酶(T-SOD),谷胱甘肽过氧化物酶(GSH-Px),总抗氧化能力(T-AOC)水平。蛋白质免疫印迹(Western blot)法检测胸主动脉PTEN蛋白表达。结果:与正常组比较,模型组小鼠血脂及MDA明显升高(P<0.05),T-SOD,GSH-Px,T-AOC水平降低,胸主动脉PTEN蛋白表达明显降低(P<0.05);与模型组比较,DXR中、高剂量组能明显降低ApoE^(-/-)小鼠血脂水平,升高T-SOD,GSH-Px,T-AOC水平,并降低MDA水平(P<0.05),且能上调ApoE^(-/-)小鼠主动脉PTEN蛋白表达水平(P<0.05)。DXR各剂量组斑块面积较模型组明显缩小(P<0.05)。结论:DXR可通过调节ApoE^(-/-)小鼠血脂代谢,抑制氧化应激,上调PTEN蛋白表达,进而抑制ApoE^(-/-)小鼠AS的发生发展。
Objective： To investigate the effects of Dingxin recipe（ DXR） on phosphatase and tensin homologue deleted on chromosome 10（ PTEN） and the possible anti-atherosclerotic mechanism of DXR in Apo E knockout（ ApoE^（-/-）） mice. Method： Totally 50 ApoE^（-/-）mice were randomly divided into model group,lowdose DXR group（ 9. 25 g·kg^（-1）·d^（-1））,medium-dose DXR group（ 18. 59 g·kg^（-1）·d^（-1））,high-dose DXR group（ 37. 18 g·kg^（-1）·d^（-1））,and simvastatin group（ 0. 005 g·kg^（-1）·d^（-1））,n = 10 in each group. Another 10 C57 /BL6 J mice were selected as normal group. After feeding with high-fat diet for 16 weeks,all the mice were sacrificed and the atherosclerotic lesions in aortas were examined by HE staining. The levels of blood lipid and malondialdehyde（ MDA）,total superoxide dismutase（ T-SOD）,glutathione peroxidase（ GSH-Px） and total antioxidant capacciyt（ T-AOC） were detected. PTEN protein expression in the aorta was identified by Western blot. Result： As compared with the normal group,the levels of blood lipid and MDA were increased in model group,while the levels of T-SOD,GSH-Px,T-AOC were reduced,and the protein expression of PTEN was significantly reduced（ P〈0. 05）. As compared with the model group,blood lipid level was significantly reduced,while the levels of TSOD,GSH-Px,and T-AOC were increased,and MDA level was reduced in medium and high-dose DXR groups（ P〈0. 05）; in addition,the medium and high-dose groups could up-regulate the expression level of PTEN in ApoE^（-/-）mice（ P〈0. 05）. As compared with the model group,plaque size was significantly reduced in all DXR groups.（ P〈0. 05）. Conclusion： DXR can attenuate atherosclerosis in ApoE^（-/-）miceby regulating blood lipids,suppressingoxidative stress,and up-regulating the protein expression of PTEN.
出处
《中国实验方剂学杂志》
CAS
CSCD
北大核心
2016年第24期111-115,共5页
Chinese Journal of Experimental Traditional Medical Formulae
基金
国家自然科学基金项目(81373574)
广东省自然科学基金项目(2014A030313354
2014A030310150)
广州市海珠区科技计划项目(2013-cg-35)
