目的: 最近的证据建议必要氨基酸白氨酸可以涉及全身的胆固醇新陈代谢。在这研究,我们在 apoE 0 mice.Methods 在动脉粥样硬化的发展调查了白氨酸补充的效果: ApoE 空老鼠用食物在喝水 8 星期与白氨酸(1.5% w/v ) 补充了被喂。大动脉的动脉粥样硬化患者损害用染色的油红 O 被检验。血浆脂蛋白胆固醇层次与快蛋白质液体层析被测量。肝的基因表示用即时 PCR 和西方的污点 analyses.Results 被检测: 白氨酸补充在 apoE 0 鼠标导致了大动脉的动脉粥样硬化患者损害区域的 57.6% 减小,由浆液 LDL-C 层次的 41.2% 减少和浆液高级数据链路控制层次的 40.2% 增加伴随了。身体重量,食物吸入和血葡萄糖水平没被白氨酸补充影响。而且,白氨酸补充增加了 Abcg5 和 Abcg8 的表示(那涉及肝的胆固醇流出) 分别地,由 1.28-fold, 和 0.86 褶层增加了他们的蛋白质层次。白氨酸补充也增加了 Srebf1, Scd1 和 Pgc1b 的表示(那涉及肝的 triglyceride 新陈代谢) 由 3.73- , 1.35-fold, 和 1.71 褶层分别地。因而,白氨酸补充导致了肝胆固醇内容的 51.77% 减小和肝 triglyceride 内容的 2.2 褶层增加。另外,白氨酸补充没影响 IL-6 的浆液层次, IFN-γ;, TNF-α;, IL-10 和 IL-12,但是显著地减少了 MCP-1.Conclusion 的浆液水平: 白氨酸补充有效地由改进血浆类脂化合物侧面并且减少全身的发炎在 apoE 0 老鼠稀释动脉粥样硬化。
Aim: Recent evidence suggests that the essential amino acid leucine may be involved in systemic cholesterol metabolism. In this study, we investigated the effects of leucine supplementation on the development of atherosclerosis in apoE null mice. Methods: ApoE null mice were fed with chow supplemented with leucine (1.5% w/v) in drinking water for 8 week. Aortic atherosclerotic lesions were examined using Oil Red 0 staining. Plasma lipoprotein-cholesterol levels were measured with fast protein liquid chroma- tography. Hepatic gene expression was detected using real-time PCR and Western blot analyses. Results: Leucine supplementation resulted in 57.6% reduction of aortic atherosclerotic lesion area in apoE null mice, accompanied by 41.2% decrease of serum LDL-C levels and 40.2% increase of serum HDL-C levels. The body weight, food intake and blood glucose level were not affected by leucine supplementation. Furthermore, leucine supplementation increased the expression of Abcg5 and Abcg8 (that were involved in hepatic cholesterol efflux) by 1.28- and 0.86-fold, respectively, and significantly increased their protein levels. Leucine supplementation also increased the expression of Srebfl, Scdl and Pgclb (that were involved in hepatic triglyceride metabolism) by 3.73-, 1.35- and 1.71-fold, respectively. Consequently, leucine supplementation resulted in 51.77% reduction of liver cholesterol content and 2.2-fold increase of liver triglyceride content. Additionally, leucine supplementation did not affect the serum levels of IL-6, IFN-γ, TNF-α, IL-10 and IL-12, but markedly decreased the serum level of MCP-1. Conclusion: Leucine supplementation effectively attenuates atherosclerosis in apoE null mice by improving the plasma lipid profile and reducing systemic inflammation.