脾虚证衰老大鼠心肌和脑组织线粒体DNA损伤的实验研究

Experimental Study on the Damage of Mitochondrial DNA in Myocardium and Encephalon Tissue of Aging Rats Model with Deficiency in Spleen

目的:探讨脾虚证和衰老大鼠心肌和脑组织线粒体DNA(mtDNA)损伤的变化,进一步揭示脾虚证衰老的病理机制。方法:采用饮食不节和劳倦过度结合法建立脾气虚证模型,然后分别采用苦寒法和辛热法建立脾阳虚和脾阴虚证模型。分别提取心肌和脑组织的mtDNA,用PCR法检测mtDNA缺失情况。结果:与青年正常对照组相比,老年各组缺失突变均显著增强,P<0.01;与老年正常对照组相比,各老年脾虚证组缺失突变均显著增强,P<0.01;与脾虚证模型组相比,治疗组缺失突变均显著减轻,P<0.01,但未达到正常水平。脾阴虚与脾阳虚证相应组之间无显著差异。结论:脾虚证衰老状态下,大鼠心肌和脑组织mtDNA发生缺失突变,说明脾虚证与衰老、脾虚证衰老与mtDNA缺失突变之间有着内在的联系。

Objective ：To study the change of damage of mtDNA in myoeardium and eneephalon tissue of aging rats defieieney in spleen; to reveal the pathological mechanism of senescence which was caused by deficiency in spleen. Methods ： Deficiency of spleen-Qi models were established by the combined methods of no-controlling diet and over-fatigue, then, the methods of bitter cold and pungent warm were used to found deficiency of spleen-yin and deficiency of spleen-yang models. PCR was used to detect the deletion of mtDNA by respectively extract mtDNA in myocardium and encephalon tissue. Results ： Compared with young normal control group, the deletion mutation of respective aging group strengthened obviously,P 〈 0. 01 ;Compared with aging normal control group, the deletion mutation of respective aging deficiency in spleen model group strengthened obviously,P 〈 0. 01 ;Compared with deficiency in spleen model group, the deletion mutation of therapy group weakened obviously, P 〈 0.01, but which was not come up to the normal level. Differents between deficiency of spleen-yin and deficiency of spleen-yang were not very obviously. Conclusion： In the state of senescence of deficiency in spleen,deletion mutation of mtDNA in myoeardium and eneephalon tissue of rats demonstrate the interior relationship between deficiency in spleen and senescence and between senescence of deficiency in spleen and deletion mutation of mtDNA.