ABSTRACT
Aim To systematically evaluate the heat-clearing mechanism of Arnebiae Radix on two mouse models of blood heat syndrome. Methods The drug-forming molecules were screened by comprehensive network pharmacology methods, and the correlation between drug efficacy and related factors and targets was evaluated on the mouse model of short effect blood heat syndrome constructed by 2, 4-dinitrophenol (DNP) and the mouse model of severe blood heat syndrome (heat stroke) constructed by high temperature combined with lipopolysaccharide (LPS). Results A total of 277 shikonin related targets were collected, mainly involving biological processes such as inflammatory reaction, oxidation reaction and coagulation reaction. Shikonin, a representative compound, significantly improved the main syndromes of mice with blood heat syndrome, reduced the levels of inflammatory factors IL-1β, IL-6 and TNF-α in the two models, and reduced the contents of oxidative damage indexes LPO and MDA, and the two showed correlation. The main mechanism was to inhibit the expression of NF-ΚB p65 and up-regulate the expression of Nrf2. Conclusions Shikonin plays a pharmacological role in the prevention and treatment of blood heat syndrome by inhibiting inflammation and improving antioxidant capacity, which provides a pharmacological basis for shikonin in the prevention and treatment of blood heat syndrome.