基质硬化及其信号通路是肌成纤维细胞（MFB）活化成熟的必需条件。抑制基质硬化及其信号通路，不仅阻止MFB活化，且为保存肺正常结构及功能所必需，因此是抗放射性肺纤维化（RILF）的关键。前期研究显示，减少MFB的活化是雷公藤内酯醇（TPL）抗RILF的重要途径，但TPL对基质硬化及其信号通路的作用尚不清楚。本研究通过应用体外基质硬化模型及体内小鼠RILF模型，探讨TPL对RILF中基质硬化及其信号通路的影响，以及此影响与MFB活化、肺组织结构与功能的相关性，以期阐明TPL抗RILF的关键机制，为TPL的抗RILF应用提供有力支撑。同时本研究将揭示基质硬化及其信号通路在RILF中的关键地位，为抗纤维化药物的研究提供新的思路。

Matrix stiffness and its signaling pathway are the conditions necessary to activate myofibroblasts (MFB). Inhibition of matrix stiffness and its signaling pathways, not only prevented the activation of MFB, but also for the preservation of normal lung structure and function, and therefore play a key role in anti-radiation-induced pulmonary fibrosis (RILF). Previous studies have shown that reducing the activation of MFB is an important way in anti-RILF effect of triptolide (TPL), but TPL's effect on matrix stiffness and its signaling pathway are unclear. In this study, through the application of in vitro matrix stiffess model and in vivo RILF mouse model, we explore the effects of TPL on matrix stiffess and its signaling pathway , and the relevance of this impact on MFB activation, lung tissue structure and function, so to clarify the key mechanism of anti RILF of TPL. Meanwhile, the study will reveal the key role of matrix stiffness and its signaling pathway in RILF , and provide new ideas for the study of anti-fibrotic drugs.