Current pharmaceutical design · 2026
Protective Mechanism of Licorice against Liver Injury Induced by Psoraleae Fructus and Epimedii Folium in Rats Based on Network Pharmacology and Metabolomics.
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Ma Taotao, Liu Hong, Hu Minmin, Lu Dingyan, Li Ruixi, Zheng Lin, Li Yongjun, Chen Shuaishuai, Liu Ting
Аннотация
BACKGROUND: The combination of Psoraleae Fructus (PF) with Epimedii Folium (EF) can cause drug-induced liver injury (DILI), which is a common type of hepatitis. Licorice (Lic) has been reported to mitigate the effects of hepatitis. However, the extent of Lic's protective effect against PF combined with EF -induced DILI and the underlying mechanisms remain unclear.
METHODS: A rat model of PF+EF-induced liver injury was established under lipopolysaccharide stimulation, and the levels of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and pro-inflammatory cytokines (tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β)) were determined by using a kit to evaluate the hepatoprotective effect of Lic. In addition, the potential mechanisms of Lic's hepatoprotective effects were systematically studied using a combined approach of network pharmacology and metabolomics analysis, and ERK, p-ERK, p38, and p-p38 proteins were detected by Western blotting.
RESULTS: Lic treatment significantly reduced serum levels of ALT, AST, TNF-α, IL-6, and IL-1β by approximately 46%, 40%, 22%, 11%, and 27%, respectively, and improved liver histopathology. Network pharmacology analysis identified 459 common targets shared between Lic and PF+EF-induced liver injury. Metabolomics revealed 12 differential metabolites, implicating pyrimidine and purine metabolism as the primary affected pathways. An integrated analysis of these metabolites and the 459 targets highlighted the mitogen- activated protein kinase (MAPK) pathway as the potential key mechanism through which Lic alleviates PF+EF-induced liver injury.
DISCUSSION: Our results indicate that Lic alleviates PF+EF-induced liver injury by suppressing inflammatory responses and correcting metabolic perturbations. The combined network pharmacology, metabolomics, and protein expression analyses consistently point to the MAPK pathway as a pivotal mechanism mediating these hepatoprotective effects. These findings provide mechanistic support for the potential use of Lic in the prevention and treatment of DILI.
CONCLUSION: Lic improves tissue injury and liver inflammation induced by PF+EF via regulating the MAPK pathway. This study provides a theoretical foundation for the therapeutic use of Lic in the treatment of hepatitis.
METHODS: A rat model of PF+EF-induced liver injury was established under lipopolysaccharide stimulation, and the levels of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and pro-inflammatory cytokines (tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β)) were determined by using a kit to evaluate the hepatoprotective effect of Lic. In addition, the potential mechanisms of Lic's hepatoprotective effects were systematically studied using a combined approach of network pharmacology and metabolomics analysis, and ERK, p-ERK, p38, and p-p38 proteins were detected by Western blotting.
RESULTS: Lic treatment significantly reduced serum levels of ALT, AST, TNF-α, IL-6, and IL-1β by approximately 46%, 40%, 22%, 11%, and 27%, respectively, and improved liver histopathology. Network pharmacology analysis identified 459 common targets shared between Lic and PF+EF-induced liver injury. Metabolomics revealed 12 differential metabolites, implicating pyrimidine and purine metabolism as the primary affected pathways. An integrated analysis of these metabolites and the 459 targets highlighted the mitogen- activated protein kinase (MAPK) pathway as the potential key mechanism through which Lic alleviates PF+EF-induced liver injury.
DISCUSSION: Our results indicate that Lic alleviates PF+EF-induced liver injury by suppressing inflammatory responses and correcting metabolic perturbations. The combined network pharmacology, metabolomics, and protein expression analyses consistently point to the MAPK pathway as a pivotal mechanism mediating these hepatoprotective effects. These findings provide mechanistic support for the potential use of Lic in the prevention and treatment of DILI.
CONCLUSION: Lic improves tissue injury and liver inflammation induced by PF+EF via regulating the MAPK pathway. This study provides a theoretical foundation for the therapeutic use of Lic in the treatment of hepatitis.