Current Status and Evaluation Considerations of Constructing Disease-syndrome Combination Models for Spleen Deficiency with Dampness Pattern in Ulcerative Colitis
10.13422/j.cnki.syfjx.20260263
- VernacularTitle:脾虚湿阻型溃疡性结肠炎病证结合模型的构建现状与评价思考
- Author:
Xuming HUANG
1
;
Leichang ZHANG
2
;
Na WU
2
;
Guangbin SHANG
1
;
Jie ZHANG
1
;
Jiaqi CHEN
1
;
Xiaojun YAN
1
Author Information
1. Jiangxi University of Chinese Medicine，Nanchang 330004，China
2. The Affiliated Hospital of Jiangxi University of Chinese Medicine，Nanchang 330006，China
- Publication Type:Journal Article
- Keywords:
ulcerative colitis;
spleen deficiency with dampness pattern;
disease-syndrome combination model;
energy metabolism;
immune homeostasis;
mucosal barrier;
intestinal microecology
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2026;32(13):233-243
- CountryChina
- Language:Chinese
-
Abstract:
The disease-syndrome combination model of spleen deficiency with dampness pattern in ulcerative colitis（SDDP-UC） is an important experimental carrier for traditional Chinese medicine （TCM） research on the prevention and treatment of ulcerative colitis （UC）， and the quality of model construction and evaluation directly influences the scientific rigor and translational value of related research conclusions. However， this field still lacks methodological synthesis and a standardized consensus. Based on a comprehensive review of existing literature， this paper summarized isomorphic cues between the spleen deficiency with dampness pattern and UC across four dimensions， including energy metabolism， immune homeostasis， mucosal barrier， and intestinal microecology. The cues were mainly involved in impaired mitochondrial energy supply and glucose metabolic reprogramming， a lowered pro-inflammatory threshold of innate immunity with insufficient adaptive immune regulation， disruption of epithelial barrier gating accompanied by compromised repair capacity， and attenuation of the luminal hypoxia barrier with accumulation of toxic metabolites. A mutually reinforcing process between local "form damage" and systemic "Qi depletion" was further interpreted from a holistic perspective. Regarding modeling strategies， existing studies predominantly use rats as the carrier， apply combined interventions such as improper diet， external damp exposure， and fatigue-related dysregulation to establish the spleen deficiency with dampness pattern background， and subsequently superimpose chemical stimulation to induce UC-like colonic damage， with a total modeling period generally spanning three to four weeks. In terms of the evaluation system， a multidimensional framework integrating syndrome assessment， histopathology， mechanistic indices， and pharmacodynamic counter-verification was outlined. On this basis， current methodological bottlenecks of models were systematically identified， including syndrome drift risk and compounded stress dilemma in temporal sequencing， syndrome confounding from etiological simulation， cross-sectional evaluation bias related to modeling duration， inadequate disease-syndrome linkage and control design within the evaluation system， and limited controls with overly single-track decision logic in formula-based syndrome verification. To address the above issues， a construction and evaluation strategy emphasizing streamlining of core etiological factors， multi-node dynamic monitoring， integration of core disease-syndrome indicator clusters， and establishment of a formula-based syndrome verification system was proposed， providing a reference for the standardized construction and scientific evaluation of the SDDP-UC model.
