本研究基于慢性复发性UC脏腑病机规律及临床实践基础，结合p38 MAPK介导相关信号通路诱发肠黏膜稳态失衡而导致炎性病变发生的理论背景以及前期工作基础，建立“p38 MAPK介导MSK1/2-CREB通路关键分子在UC病程中结肠黏膜微环境中的响应及温补脾肾法干预效应的可能机制”工作假说，以脾肾阳虚型UC大鼠为研究对象，在评估结肠黏膜病理损伤基础上，采用qPCR、免疫组化和蛋白免疫印迹技术检测p38 MAPK介导MSK1/2-CREB信号通路上p38 MAPK、MSK1/2、CREB以及下游c-jun，c-fos、cox-2、IL-10、IL-17、IL-33基因蛋白在结肠组织中的表达规律；并应用以温补脾肾法为指导的久泻灵进行干预，通过相关性分析，拟从p38 MAPK介导MSK1/2-CREB信号通路关键分子角度揭示UC的病理机制以及温补脾肾法的干预效应，为该制剂的临床应用提供理论支撑。

Based on chronic recurrent UC viscera pathogenesis regularity and clinical practice, combined with the theoretical background of inflammatory lesions related to the imbalance of intestinal mucosal homeostasis caused by p38 MAPK-mediated signaling pathways and previous basis, the study hypothesis of the response of p38 MAPK-mediated Key Molecules of MSK1/2-CREB signaling pathway in the colonic mucosal microenvironment of ulcerative colitis and the possible mechanism of intervention by warming and tonifying the spleen and kidney were established. UC rats with spleen and kidney yang deficiency were used as research objects. On the basis of evaluating the pathological damage of colonicmucosa, immunohistochemistry, qPCR and western blotting were adopted to determine protein and mRNA expression of p38 MAPK, MSK1/2, CREB in p38 MAPK-mediated MSK1 / 2-CREB signaling pathway and c-jun, c-fos, cox-2, IL-10, IL-17 and IL-33 in the downstream of the signaling pathway in UC colonic mucosal tissue. At the same time, through the intervention of Jiuxieling Decoction by warming and tonifying the spleen and kidney and through the correlation analysis, the pathological mechanism of UC and intervention effect of warming and tonifying the spleen and kidney were revealed from the perspective of p38 MAPK-mediated Key Molecules of MSK1/2-CREB signaling pathway, providing theoretical support for the clinical application of the preparation and the development of the key technologies for the prevention and treatment of UC proprietary Chinese medicinals.