早有报道阴虚证本质是白介素 1 (IL-1)等细胞因子的生物学活性相对升高所致，但我们在 973 项目中药药性相关基础问题研究中发现虚热证及虚寒证均出现 IL-1 不同程度的表达降低，虚热证脂素 1(Lipin-1)基因表达增强。IL-1、Lipin-1 在虚热、虚寒证发生中作用如何？本研究拟建立虚寒与虚热证动物模型，采用寒热偏好测定、基础代谢测定、酶联免疫、定量 PCR、Western blot 等方法，观察虚寒、虚热证模型动物寒热趋向、能量及糖脂代谢、细胞因子网络的改变，特别是 IL-1、IL-1 受体及调节蛋白的改变及 Lipin-1 变化。并给予IL-1 及 IL-1 受体拮抗剂、Lipin-1 激活及抑制剂，进一步阐释其作用。论证 IL-1 信号通路降低是虚寒、虚热证产生的共同分子基础，Lipin-1 表达的高低，是产生虚寒、虚热差异的假说。阐释虚寒、虚热证的生物学机制。

It has long been reported that interleukin 1 (IL-1) increasing with othercytokines play a pivot role in Yin Deficiency state. However, in our study in 973projects “study on fundamental issue related with the properties of traditionalChinese medicine”, the expression of IL-1 was found decreased and that of Lipin-1increased. What role the IL-1 and Lipin-1 really played in deficiency warm and coldsyndrome? In this study, deficiency warm syndrome and deficiency cold syndrome willbe induced, cold and warm tends, energy and glucose and lipid metabolism, cytokinenetwork of animals will be measured with cold and heat preference analyzer, basalmetabolic analyzer, ELISA, quantitative PCR, Western blot, etc. To active andinactive the signal transduction, IL-1 and IL-1Ra will be given to the animals, andalso Lipin-1 activator and inhibitor, and then observing the signs and indicatorsmentioned above in order to further explain the role of the IL-1 and Lipin-1. Todemonstrated the hypothesis that the active decreasing of IL-1 signaling pathwayas a common molecular basis, when the active and inactive of Lipin-1 as basis ofwarm and cold, and then Interpreting the molecular mechanism of deficiency warm and cold syndromes.