肺虚络瘀与细胞凋亡在IPF发病过程中相关性探讨

Study on the Correlation Between Lung Deficiency and Collateral Blood Stasis and Apoptosis in the Pathogenesis of IPF

深入研究肺络理论,将特发性肺纤维化归属于肺络病范畴,结合导师经验,提出特发性肺纤维化"肺虚络瘀"病机观,并从结构、发病机制与治疗原则三方面,探究"肺虚络瘀"病机观与肺纤维化细胞凋亡机制的相关性。结果证实:(1)肺之络脉乃三维立体网状结构,其气血运行特点为"运行缓慢、双向流动、并呈面性弥散",这与细胞凋亡信号通路立体、多维的网状信息传递及正负反馈、双向调节的特性具有高度相似性。(2)肺泡上皮细胞及支气管上皮细胞过度凋亡及成纤维细胞的凋亡抑制致细胞外基质的沉积加重肺纤维化的病理过程与肺虚日久,肺络运行不畅,痰热毒瘀阻于络脉的病机演变具有相似性。(3)基于"肺虚络瘀"病机观提出益气养阴活血通络法为治疗IPF基本原则,经临床证实可以通络调控细胞凋亡,延缓IPF的进程。故文章认为"肺虚络瘀"与细胞凋亡学说在IPF的发病中具有相关性,意在进一步解释、明确从络论治疗IPF的作用机制及靶点,为IPF的治疗提供新的研究思路与科学依据。

This paper studies the theory of lung collaterals, idiopathic pulmonary fibrosis attributable to pulmonary collateral disease category, combined with the tutor＇s experience, the idiopathic pulmonary fibrosis, lung deficiency and collateral blood stasis pathogenesis concept, and from the structure, pathogenesis and treatment principles of the three aspects, explore ＂lung deficiency and collateral blood stasis＂ pathogenesis and correlation the mechanisms of apoptosis of pulmonary fibrosis. The results： ①The lung meridian is the three-dimensional reticular structure, its blood running characteristics as ＂slow, two-way flow, and a surface diffusion＂, and characteristics of the signal pathway of apoptosis three-dimensional and multi-dimensional network information transmission and the positive and negative feedback and bidirectional regulation with high similarity. ②The excessive apoptosis of alveolar epithelial cells and bronchial epithelial ceils and fibroblast apoptosis induced by inhibiting the deposition of extracellular matrix increased pulmonary fibrosis and pathological process of lung deficiency with lung collaterals running sluggish, phlegm heat and blood stasis in the pathogenesis of collaterals evolution is similar. ③Based on the concept of ＂deficiency of lung and collateral blood stasis＂, this paper proposes the basic principle of supplementing Qi, nourishing Yin, promoting blood circulation and dredging collaterals, which can be used to regulate and control the apoptosis of cells and delay the process of IPF through clinical verification. The author thinks that the theory of ＂lung deficiency and collateral blood stasis＂ is associated with apoptosis in the pathogenesis of IPF, to further explain and clear on the mechanism and target for treatment of IPF from the network, to provide new research ideas and scientific basis for the treatment of IPF.