普洱茶调节apoE基因敲除小鼠血脂水平的研究
The Regulation of Pu-erh Tea onBlood Lipids in apoE-Gene Knocked Mice
DOI: 10.12677/ACRG.2013.11001, PDF, HTML, XML, 下载: 3,653  浏览: 14,853  国家科技经费支持
作者: 江新凤, 刘彩霞:江西省蚕桑茶叶研究所;邵苑芳*:云南农业大学龙润普洱茶学院;程春华, 杨继红:云南省天然药物药理重点实验室
关键词: 普洱茶动脉粥样硬化apoE基因敲除小鼠Pu-erh Tea; Atherosclerosis; The Mice of apoE-Gene Knocked
摘要: 为了验证普洱茶对apoE基因敲除小鼠动脉粥样硬化的作用;本研究选取了404周龄雄性apoE基因敲除小鼠,按照体重随机分成降脂药组、模型组、生茶组、熟茶组4组外加10只正常对照组。用普洱茶汤进行干预性试验90天后,空腹12小时,摘眼球采血,采用全自动生化仪测血清中的总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白(LDL-C)、高密度脂蛋白(HDL-C)等血脂指标;试验结果显示:普洱茶(生、熟)均可显著控制小鼠体重增长(P < 0.05);普洱生茶可显著降低小鼠血清中TGLDL-C的含量,升高HDL-C的含量(P < 0.05),可显著降低AI系数;因此可判定,普洱茶对apoE基因敲除小鼠的抗动脉粥样硬化有一定的调节作用。 This study aimed to investigate the effects of Pu-erh tea on blood lipids in apoE-knockout mice. So we selected 4-week-old male apoE-gene knocked mice, and they were randomly divided into four groups: atherosclerosis group, fermenting Pu-erh Tea group, fermented Pu-erh Tea group and drug group. The all mice were used as the control. All mice were fed with normal chow diet. After 90 days, Vessels blood was collected for serum lipid, using automatic biochemical analyzed measuring serum the total clesterol (TC), triglycerides (TG), low-density lipoprotein (LDL-C), high-density lipoprotein (HDL-C), and other hyperlipidemia indicators. The result is that Pu-erh Health (cooked) tea cansignificantly increase control of body weight (P < 0.05); reduce the high fat mice serum TG, LDL-C content, increased HDL-C in (P < 0.05); And cooked Pu-erh tea can significantly reduce the high fat rat serum TC, TG, LDL-C in (P < 0.05). These results suggested that Pu-erh tea may play a role in anti-atherosclerosis in apoE-knockout mice.
文章引用:江新凤, 邵苑芳, 刘彩霞, 程春华, 杨继红. 普洱茶调节apoE基因敲除小鼠血脂水平的研究[J]. 亚洲遗传病病例研究, 2013, 1(1): 1-5. http://dx.doi.org/10.12677/ACRG.2013.11001

参考文献

[1] 张新波, 王绿娅, 陈保生. 载脂蛋白AI的抗动脉粥样硬化功能研究的进展[J]. 中国动脉粥样杂志, 2007, 15(3): 233-236.
[2] 彭旷. 载脂蛋白E及基因敲除小鼠的研究进展[J]. 心血管病学进展, 2006, 27: 74-78.
[3] 刘勤晋, 陈文品, 白文祥. 普洱茶急性毒性安全性评价研究报告[J]. 茶叶科学, 2003, 23(2): 141-145.
[4] 孙敬修. 实验动物方法学[M]. 北京: 人民卫生出版社, 2001.
[5] A. S. Plum, Jonathan D. Smith, Tony Hayek, et al. Severe hyPereholesterolemia and atheroslerosis in apolipoprotein E-deficient mice created by homologous recombination in EC cells. CELL, 1992, 71(10): 343-353.
[6] L. Park, K. G. Raman, K. J. Lee, et al. Suppression of accelerated diabetic atherosclerosis by the soluble receptor for advanced glycation endpro-ducts. Nature Medicine, 1998, 4(9): 1025-1031.