论文部分内容阅读
目的:探讨重组融合蛋白蜱抗凝血肽(TAP)-金黄色葡萄球菌超抗原样蛋白5(SSL5)对Apo E基因敲除(Apo E~(-/-))小鼠动脉粥样硬化病变形成的影响。方法:选取12周龄雄性Apo E~(-/-)小鼠21只,随机分为3组:TAP-SSL5组(3 mg·kg~(-1)·d~(-1))、SSL5组(2 mg·kg~(-1)·d~(-1))、空白对照组(p H 7.4磷酸盐缓冲液),ip,qd,连续给药12周,观察小鼠体质量变化。高脂饮食饲养12周后取材,检测血浆总胆固醇(TC)、三酰甘油(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)水平;对小鼠主动脉血管进行石蜡切片,常规HE染色,分析小鼠主动脉根部血管动脉粥样硬化斑块的形成情况,小鼠主动脉内膜面采用油红O染色,比较动脉粥样硬化斑块的分布情况。结果:高脂饲养12周后,与空白对照组比较,TAP-SSL5组小鼠体质量增长和TC水平明显降低(P<0.001),而TG、HDL-C、LDL-C水平无明显变化。HE染色结果表明,TAP-SSL5组主动脉根部切片斑块面积明显降低(P<0.05);主动脉大体标本斑块油红O染色提示TAP-SSL5干预组主动脉动脉粥样硬化斑块形成明显小于空白对照组。结论:TAP-SSL5可显著抑制Apo E~(-/-)小鼠动脉血管粥样硬化斑块的形成。
Objective: To investigate the effect of recombinant fusion protein Tsp - Staphylococcus aureus super antigen - like protein 5 (SSL5) on the atherosclerotic lesions in Apo E knock - out (Apo E - / -) mice The formation of the impact. Methods: Twenty-one male 12-week-old Apo E ~ (-) mice were randomly divided into 3 groups: TAP-SSL5 group (3 mg · kg -1 d -1) (2 mg · kg -1 · d -1), blank control group (p H 7.4 phosphate buffer), ip and qd for 12 weeks. The body weight of mice was observed. The rats in the high-fat diet were fed for 12 weeks and the levels of total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C) and low density lipoprotein cholesterol (LDL- Aortic blood vessels were paraffin sections, routine HE staining, analysis of mouse aortic root atherosclerotic plaque formation, the aortic intima with oil red O staining, atherosclerotic plaque distribution comparison Happening. Results: After 12 weeks of high-fat diet, the body weight and TC level in TAP-SSL5 group were significantly lower than those in control group (P <0.001), while TG, HDL-C and LDL-C levels did not change significantly. The results of HE staining showed that the plaque area of the aorta root in TAP-SSL5 group was significantly reduced (P <0.05). The staining of aorta plaque oil red O suggested that the formation of atherosclerotic plaque in TAP-SSL5 group was significant Less than the blank control group. Conclusion: TAP-SSL5 can significantly inhibit the formation of atherosclerotic plaque in ApoE ~ (- / -) mice.