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目的探讨过氧化物酶体增殖物激活受体-γ(PPAR-γ)在兔动脉粥样硬化模型中的表达,以及阿托伐他汀的干预作用。方法2005年1月至2006年12月,在吉林大学中日联谊医院心内科将24只雄性日本大耳白兔随机分为高脂饮食组(A组)、高脂饮食+阿托伐他汀组(B组)和正常饮食组(C组)3组,每组8只。各组分别在喂养16周末处死,免疫组化法检测PPAR-γ,全自动生化分析仪检测血脂的表达水平。结果PPAR-γ的表达分别为A组(11·23±1·21)%,B组(11·05±1·02)%,C组(7·68±1·04)%,A、B2组比较差异无显著性意义(P>0·05),A、B2组与C组相比差异均有显著性意义(均P<0·01)。总胆固醇(TC)在A、B、C3组的表达分别为(23·51±10·58)mmol/L,(14·27±3·51)mmol/L,(1·36±0·33)mmol/L,各组间比较差异有显著性意义;低密度脂蛋白(LDL)在A、B、C3组的表达分别为(21·39±10·00)mmol/L,(14·23±4·01)mmol/L,(0·72±0·35)mmol/L,各组间比较差异亦有显著性意义;甘油三酯(TG)在3组间比较差异无显著性意义(P>0·05)。结论在兔动脉粥样硬化模型中PPAR-γ表达增高;阿托伐他汀可促进PPAR-γ的表达。
Objective To investigate the expression of peroxisome proliferator-activated receptor-γ (PPAR-γ) in atherosclerotic rabbit model and the intervention of atorvastatin. Methods From January 2005 to December 2006, 24 male Japanese white rabbits were randomly divided into high fat diet group (group A), high fat diet + atorvastatin group (B group) and normal diet group (C group) 3 groups, 8 in each group. The rats in each group were sacrificed at 16 weeks of feeding, PPAR-γ was detected by immunohistochemistry, and the level of lipids was detected by automatic biochemical analyzer. Results The expression of PPAR-γ was significantly higher in group A than in group A (11 · 23 ± 1 · 21)%, group B (11.05 ± 1.02)%, group C (7 · 68 ± 1.04)%, There was no significant difference between the two groups (P> 0.05). There was significant difference between group A and group B2 and group C (all P <0.01). The levels of total cholesterol (TC) in A, B and C3 groups were (23.51 ± 10.58) mmol / L, (14.27 ± 3.51) mmol / L, (1.36 ± 0.33 ) mmol / L, the differences among the groups were significant. The expressions of LDL in group A, B and C3 were (21.39 ± 10.00) mmol / L, (14.23 ± 4.01 mmol / L and (0.72 ± 0.35) mmol / L, respectively. There was also significant difference among the three groups. There was no significant difference in triglyceride between the three groups P> 0.05). Conclusion The expression of PPAR-γ is increased in atherosclerosis model of rabbits. Atorvastatin can promote the expression of PPAR-γ.