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目的探讨肝X受体(liver X receptor,LXR)激动剂T0901317对高脂饲养ApoE基因敲除(apolipoprotein E gene knockout,ApoE-/-)小鼠在动脉粥样硬化病变形成的早期动脉壁内C-反应蛋白(CRP)和CD40配体(CD40L)表达及平滑肌细胞含量的影响。方法8周龄雄性ApoE-/-小鼠12只,按随机数字表法分入LXR激动剂T0901317组和二甲基亚砜(DMSO)溶剂对照组,每组6只。均给予高脂饲养8周,在高脂饲养的后4周,分别给予LXR激动剂T090131720mg·kg-1·d-1或相当剂量的DMSO腹腔注射。麻醉处死小鼠后,取小鼠主动脉,以石蜡包埋,行主动脉根部连续切片,采用免疫组化法检测主动脉壁内CRP、CD40L和平滑肌细胞α-actin的表达,以Image Pro Plus 6.0软件进行图像分析。结果LXR激动剂组动脉壁CRP表达水平较对照组明显减少(P<0.05),LXR激动剂组动脉壁CD40L表达水平较对照组明显减少(P<0.05),动脉粥样硬化斑块内平滑肌细胞α-actin表达水平与对照组比较没有统计学差异(P>0.05)。结论LXR激动剂可能通过抑制ApoE-/-小鼠动脉壁中CRP和CD40L的表达,减轻血管壁的炎症反应,从而发挥抗动脉粥样硬化形成的作用。
Objective To investigate the effects of T0901317, a liver X receptor (LXR) agonist, on the early arterial wall C in the atherosclerotic lesions of apolipoprotein E gene knockout (ApoE - / -) mice fed with high fat diet - Reactive Protein (CRP) and CD40 Ligand (CD40L) Expression and Smooth Muscle Cell Content. Methods Twelve male ApoE - / - mice aged 8 weeks were divided into LXR agonist T0901317 group and dimethylsulfoxide (DMSO) solvent control group according to random number table. Were given high-fat feeding for 8 weeks. Four weeks after the high-fat feeding, LXR agonist T090131720 mg · kg-1 · d-1 or equivalent dose of DMSO was intraperitoneally injected respectively. Anesthetize the mice, take the aorta of mice, embedded in paraffin, the aortic roots were sectioned, the expression of CRP, CD40L and smooth muscle cells α-actin were detected by immunohistochemistry. 6.0 software for image analysis. Results The expression of CRP in arterial wall of LXR agonist group was significantly lower than that in control group (P <0.05). The expression of CD40L in arterial wall of LXR agonist group was significantly lower than that of control group (P <0.05), while the level of atherosclerosis plaque smooth muscle cells α-actin expression levels compared with the control group had no statistical difference (P> 0.05). Conclusion LXR agonists may play an anti-atherogenic role by inhibiting the expression of CRP and CD40L in the arterial wall of ApoE - / - mice and attenuating the inflammatory response in the vascular wall.