Mechanisms of Action of Dendrobium officinale Against Non-alcoholic Fatty Liver Disease Base on Its Components in Blood
10.13422/j.cnki.syfjx.20250112
- VernacularTitle:基于入血成分探讨铁皮石斛防治非酒精性脂肪性肝病的作用机制
- Author:
Jilei ZHANG
1
;
Lei FENG
1
;
Yumei XU
1
;
Heyan YAO
1
;
Yanmei ZHANG
1
;
Shunzhen ZHANG
1
;
Jiao WANG
1
Author Information
1. Yunnan University of Chinese Medicine， Kunming 650500， China
- Publication Type:Journal Article
- Keywords:
drug component in blood;
network pharmacology;
Dendrobium officinale;
non-alcoholic fatty liver disease （NAFLD）;
mechanism of action
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2025;31(10):168-175
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the preventive effect and mechanism of Dendrobium officinale （DO） on non-alcoholic fatty liver disease （NAFLD） by network pharmacology and animal experiments. MethodsDO components in blood after administration were identified and analyzed using ultra-performance liquid chromatography-quadrupole-electrostatic field orbitrap high-resolution mass spectrometry （UPLC-QE-HF-MS/MS）. Network pharmacology and molecular docking methods were employed to obtain active ingredients and potential targets of DO for NAFLD control. High-fat feeds were used to replicate the NAFLD rat model. Biochemical kits were used for detecting the expression levels of blood lipids， hepatic lipids， and liver functions of rats. Hematoxylin-eosin （HE） staining and oil red O staining were employed to observe pathological changes in rat liver， and real-time fluorescence quantitative PCR （Real-time PCR） assay was performed to validate potential targets obtained from the network pharmacology analysis. ResultsA total of 13 DO components were identified in blood， including berberine， dihydrosanguinarine， and oxypeucedanin. A total of 14 potential targets were screened through network pharmacology， including Forkhead box protein O1 （FoxO1）， epidermal growth factor receptor （EGFR）， and insulin-like growth factor 1 （IGF-1R）， involving pathways such as the advanced glycation end product （AGE）/receptor for AGE （RAGE） signaling pathway， blood lipids and atherosclerosis， insulin resistance， and FoxO signaling. The results of animal experiments showed that the NAFLD rat model was successfully replicated. After the preventive treatment with DO for NAFLD rats， the indexes of blood lipids， hepatic lipids， and liver function were normalized； lipid deposition and lesions in the liver were significantly improved； the expression level of FoxO1 mRNA in the liver was significantly reduced （P<0.05）， and the mRNA expression levels of phosphatidylinositide 3-kinases （PI3K）， protein kinase B （Akt）， EGFR， and IGF-1R were significantly increased （P<0.05）. ConclusionDO has a preventive effect on NAFLD rats， and the mechanism of action may be related to the modulation of IGF1R and EGFR targets and activation of the PI3K/Akt/FoxO1 signaling pathway.
