Mechanisms of Macrophage Glycolysis in Regulating Acute Lung Injury and TCM Intervention Strategies Based on Theory of "Spleen Failing to Disperse Essence"
10.13422/j.cnki.syfjx.20251325
- VernacularTitle:基于“脾不散精”理论探讨巨噬细胞糖酵解调控急性肺损伤的机制及中医药干预策略
- Author:
Qian XU
1
;
Maofu ZHANG
1
;
Xiali LIANG
1
;
Guoxiong HAO
1
;
Jingwei LI
1
;
Xiaojie JIN
2
;
Yongqi LIU
2
;
Xiangxia LUO
3
;
Zhiming ZHANG
1
Author Information
1. Clinical College of Chinese Medicine， Gansu University of Chinese Medicine， Lanzhou 730000，China
2. Gansu University Key Laboratory for Molecular Medicine & Chinese Medicine Prevention and Treatment of Major Diseases， Lanzhou 730000，China
3. Gansu Provincial Hospital of Traditional Chinese Medicine， Lanzhou 730050，China
- Publication Type:Journal Article
- Keywords:
acute lung injury;
spleen failing to disperse essence;
turbid pathogens;
macrophages;
glycolysis
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2026;32(18):218-226
- CountryChina
- Language:Chinese
-
Abstract:
Acute lung injury （ALI） is a critical respiratory emergency caused by various non-cardiogenic factors， including severe pulmonary and extrapulmonary infections， lung contusion， and sepsis. Its pathological features are centered on alveolar-capillary barrier dysfunction， uncontrolled inflammatory responses， and impaired alveolar fluid clearance， manifesting as refractory hypoxemia and respiratory distress， with a poor clinical prognosis. Modern studies have revealed that mitochondrial dysfunction and glucose metabolic reprogramming in macrophages， characterized by hyperactivated glycolysis， drive pro-inflammatory polarization and represent a key mechanism leading to excessive inflammatory responses and disease progression in ALI. Therefore， targeting macrophage glycolysis may be a potential therapeutic strategy for ALI. The Plain Questions： Special Discussion on Channels and Vessels in Huangdi's Internal Classic states that "The spleen disseminates essence upward to the lungs". When the spleen fails in transport and transformation， the distribution of refined nutrients becomes disordered， resulting in the endogenous generation of turbid pathogens that obstruct the pulmonary collaterals， causing failure of lung dispersion and descent and leading to dyspneic reversal. This forms the dynamic pathological pattern of ''deficiency in the root with excess in the manifestation''， thereby proposing the core pathogenesis of ALI as ''spleen deficiency with transport dysfunction and turbid pathogens obstructing the lungs''. This process is intrinsically associated with the inflammatory cascade triggered by disordered macrophage glucose metabolism. Taking the theory of ''spleen failing to disperse essence'' as the entry point， the present study systematically elucidates the progressive pathological mechanism of "energy metabolism disorder-cytokine storm'' in ALI from the perspectives of the ''spleen deficiency-turbid obstruction'' pathogenesis and macrophage glycolysis-pro-inflammatory polarization. In addition， we summarize Chinese medicine compound formulas and monomeric components that ''restore spleen transport and eliminate turbid pathogens''， and explore their potential mechanisms in the treatment of ALI by regulating macrophage metabolic phenotypes to improve the state of ''spleen failing to disperse essence''. This provides a molecular basis for elucidating the ''spleen-lung'' energy metabolism dialogue， deepens understanding of the multi-target regulatory mechanisms of herbal prescriptions， and promotes the deep integration of classical theory with modern medicine.
