Pan Qihong, Liu Yang, Wei Shaofeng
College of Traditional Chinese Medicine, Nanchang Medical College, Nanchang, Jiangxi, China.
Organization Department of the Party Committee, Nanchang Medical College, Nanchang, Jiangxi, China.
Pak J Pharm Sci. 2025 Jan-Feb;38(1):261-268.
The incidence of inflammatory bowel diseases (IBDs) is increasing yearly and treatment options remain limited. Sishen Pill (SSP), a Chinese medicine, may aid IBD by impacting energy metabolism and immune response in memory Treg cells, though its exact mechanism remains unclear. This study was designed to investigate the SSP's mechanism in IBD treatment via regulating memory T cells based on the theory of Benefiting Source of Fire and Eliminating Yin. A spleen-kidney yang deficiency model was induced in mice using rhubarb decoction and hydrocortisone, followed by a DSS-induced IBD model. Mice were treated with SSP at varying doses. Disease activity index (DAI) scores, colonic weight index and histological injury scores were measured. Flow cytometry quantified T cell subsets and ELISA tests assessed TNF-α, IL-17 and energy metabolites (ATP, ADP and AMP). The establishment of an ulcerative colitis mouse model with spleen-kidney yang deficiency was conducted. As opposed to controls, DSS increased TEM (CCR7-CD45RA-) and Foxp3+ T-cell ratios and reduced TCM (CCR7+CD45RA-) (P<0.05). SSP dose-dependently improved colitis indicators, decreased TNF-α, IL-17 and enhanced energy metabolism by modulating ATP, ADP and AMP levels (P<0.05). SSP may alleviate DSS-induced IBDs by regulating memory T cell metabolism and energy metabolism.
炎症性肠病(IBD)的发病率逐年上升,而治疗选择仍然有限。四神丸(SSP)作为一种中药,可能通过影响记忆性调节性T细胞的能量代谢和免疫反应来辅助治疗IBD,但其确切机制尚不清楚。本研究旨在基于“益火之源,以消阴翳”理论,探讨SSP通过调节记忆性T细胞治疗IBD的机制。使用大黄水煎剂和氢化可的松诱导小鼠脾肾阳虚模型,随后建立DSS诱导的IBD模型。小鼠接受不同剂量的SSP治疗。测量疾病活动指数(DAI)评分、结肠重量指数和组织学损伤评分。流式细胞术定量T细胞亚群,ELISA试验评估TNF-α、IL-17和能量代谢产物(ATP、ADP和AMP)。建立了脾肾阳虚型溃疡性结肠炎小鼠模型。与对照组相比,DSS增加了TEM(CCR7-CD45RA-)和Foxp3+T细胞比例,降低了TCM(CCR7+CD45RA-)(P<0.05)。SSP剂量依赖性地改善了结肠炎指标,降低了TNF-α、IL-17,并通过调节ATP、ADP和AMP水平增强了能量代谢(P<0.05)。SSP可能通过调节记忆性T细胞代谢和能量代谢来减轻DSS诱导的IBD。