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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 effect of DXR on the expression of phosphatase and tensin homolog (PTEN) on chromosome 10 in ApoE-knockout (ApoE ~ (-) -) mice and the effect of DXR on AS Possible mechanism. Methods: 50 ApoE ~ (- / -) mice were randomly divided into model group, simvastatin group, DXR low, medium and high dose groups, and another 10 C57 / BL6J mice as normal group. DXR solutions were administered to DXR low, medium and high groups at dosage of 9.25, 18.59 and 37.18 g · kg-1 · d ~ (-1) ig, respectively. Simvastatin group was treated with 0.005 g · kg-1 · d ~ (-1) 1) ig simvastatin, high-fat diet were sacrificed 16 weeks after feeding, the aortic plaque area was observed by hematoxylin-eosin (HE) staining, serum lipid and malondialdehyde (MDA), total superoxide dismutase (T-SOD), glutathione peroxidase (GSH-Px) and total antioxidant capacity (T-AOC). The protein expression of PTEN in thoracic aorta was detected by Western blot. Results: Compared with normal group, the levels of serum lipids and MDA in model group were significantly increased (P <0.05), the levels of T-SOD, GSH-Px and T-AOC were decreased and the expression of PTEN protein in thoracic aorta was significantly decreased ; Compared with the model group, DXR medium and high dose groups could significantly decrease the level of serum lipids, raise the level of T-SOD, GSH-Px, T-AOC and decrease the level of MDA in ApoE ~ (- ), And upregulated the expression of PTEN protein in ApoE ~ (- / -) mice aorta (P <0.05). Compared with the model group, the plaque area of each dose group of DXR was significantly reduced (P <0.05). CONCLUSION: DXR can inhibit the occurrence and development of AS in ApoE ~ (- / -) mice by regulating lipid metabolism, inhibiting oxidative stress and up-regulating the expression of PTEN in ApoE ~ (- / -) mice.