Application of Ferroptosis Regulation in Chronic Atrophic Gastritis Based on Spleen Deficiency and Turbid Toxin
10.13422/j.cnki.syfjx.20242437
- VernacularTitle:基于“脾虚浊毒”探讨铁死亡调控在慢性萎缩性胃炎中的应用
- Author:
Yuxi GUO
1
;
Xuemei JIA
1
;
Jie WANG
1
;
Yanru CAI
1
;
Pengli DU
1
;
Yao DU
1
;
Diangui LI
1
;
Qian YANG
1
Author Information
1. Hebei Hospital of Chinese Medicine， Shijiazhuang 050013， China
- Publication Type:Journal Article
- Keywords:
chronic atrophic gastritis;
ferroptosis;
spleen deficiency and turbid toxin
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2025;31(13):279-285
- CountryChina
- Language:Chinese
-
Abstract:
Chronic atrophic gastritis （CAG）， a common digestive system disease， has an unclear pathogenesis. Currently， it is mostly believed to be related to Helicobacter pylori （Hp） infection， immune factors， dietary factors， bile reflux， long-term use of antibiotics and anti-inflammatory drugs， and other factors. Ferroptosis is a regulated cell death mechanism that is iron-dependent and characterized by disruption of iron metabolism and accumulation of lipid peroxides. More and more studies have found that ferroptosis is closely related to the onset of CAG. Professor LI Diangui， a master of traditional Chinese medicine， first proposed the turbid toxin theory， which holds that spleen deficiency and turbid toxin is the main pathogenic mechanism of CAG. Abnormal iron metabolism regulation is a prerequisite for the accumulation of turbid toxin in CAG， and ferroptosis is in accordance with the pathogenic mechanism （spleen deficiency and turbid toxin） of CAG. This article explores the pathological mechanism of spleen deficiency and turbid toxin in CAG from the perspectives of iron metabolism， oxidative stress， and lipid peroxidation， providing theoretical support of traditional Chinese medicine for the modern research on CAG. It enriches the modern scientific connotation of the turbid toxicity theory and provides new ideas and breakthrough points for the clinical treatment of CAG.
