文献类型：期刊文献

中文题名：敦煌大宝胶囊对衰老大鼠及肾阳虚小鼠肝脏代谢能力的影响

英文题名：Influence of Dunhuang Dabao Capsule on metabolism functions in the liver of aging model rats and the kidney-yang deficiency mice

作者：梁玉杰[1];段永强[1];成映霞[1];程容[1];朱立鸣[1];虎峻瑞[1]

第一作者：梁玉杰

机构：[1]甘肃中医学院基础课部,甘肃兰州730000

第一机构：甘肃中医药大学

年份：2011

卷号：31

期号：1

起止页码：75

中文期刊名：中国老年学杂志

外文期刊名：Chinese Journal of Gerontology

收录：CSTPCD;;北大核心:【北大核心2008】；CSCD:【CSCD2011_2012】；

基金：甘肃省科技攻关计划项目(2GS064-A43-020-22);兰州市科技局计划项目(06-2-87)

语种：中文

中文关键词：衰老;SDH;LDH;肾阳虚证;肝糖原;血清乳酸;敦煌大宝胶囊

外文关键词：Aging model; Succinic acid dehydrogenase（SDH）; Lactic dehydrogenase（LDH）; Syndrome of kidney-yang sufficiency; Glycogen; Liver; Lactic acid; Dunhuang Dabao Capsule（DHDB）

摘要：目的研究敦煌大宝胶囊对衰老大鼠及肾阳虚小鼠肝脏代谢能力的影响。方法采用D-半乳糖颈部大鼠皮下注射造成亚急性衰老动物模型,采用泼尼松小鼠皮下注射,造成肾阳虚动物模型。观察敦煌大宝胶囊对衰老模型大鼠肝组织琥珀酸脱氢酶(SDH)、乳酸脱氢酶(LDH)水平以及肾阳虚小鼠负重游泳后肝糖原和血清乳酸(LA)含量的影响。结果与模型组比较,敦煌大宝胶囊可显著提高衰老模型大鼠肝组织SDH水平(P<0.01),显著降低肝组织LDH水平(P<0.05);敦煌大宝胶囊能明显提高肾阳虚小鼠负重游泳后肝糖原(P<0.05),降低运动后血清LA含量(P<0.05)。结论敦煌大宝胶囊能够改善肝细胞能量代谢,增强细胞有氧呼吸,使细胞处于功能活跃状态,提高衰老大鼠及肾阳虚小鼠肝脏代谢能力。
Objective To observe influence of Dunhuang Dabao capsule（DHDB） on metabolism functions in the liver of aging model rats and the kidney-yang deficiency mice.Methods Sub-acute aging animal models were made by D-galactose hypodermic injection from the neck and the model mice with deficiency of kidney-yang by subcutaneouly injecting hydrocortisone.The activity of succinic acid dehydrogenase（SDH） and lactic dehydrogenase（LDH） in aging rats′ liver,and the content of glycogen and lactic acid of model mice with deficiency of kidney-yang after loaded-swimming were observed.Results Compared with model group,DHDB could enhance the level of SDH（P0.01）,decrease the level of LDH（P0.05）, increase the level of glycogen（P0.05）,also decrease content of lactic acid obviously（P0.05）.Conclusions DHDB can improve energy of cells metabolism,enhance aerobic respiration of cells and cause the cell to be active in its function.So DHDB plays a significant role in keeping metabolism in the liver of the aging model rats and the kidney-yang deficiency mice.