Effect of Tamarix ramosissima Ledeb on alcoholic liver injury based on network pharmacology and molecular docking technology
Objective To determine the mechanism of the natural plant Tamarix ramosissima Ledeb on alcoholic liver injury(ALI)in mice by network pharmacology and molecular docking technology.Methods The active ingredients were screened,with the oral availability(≥30％)and druglikeness(≥0.18)pre-ordained.ALI related targets were screened by databases like GeneCards and DrugBank.Via VennDiagram,an intersection target(Tamarix ramosissima Ledeb and ALI)was obtained.Based on the disease-active ingredients-intersection target network,the main active ingredients and key pathogenic targets were ultimately selected for molecular docking.Animal experiments were conducted with chronic alcohol feeding and acute gastric lavage to establish the C57BL/6J mouse ALI model.By detecting malondialdehyde(MDA),aspartate transaminase(AST),alanine transaminase(ALT),liver index,HE staining,NF-κB p65,the Tamarix ramosissima Ledeb action mechanism on ALI was validated.Results Through network pharmacology screening,12 active ingredients were obtained,with 151 targets intersecting with ALI.It was speculated that the main active components,included quercetin,kaempferol,and isorhamnetin.Via the key targets(RELA/NF-κB p65,JUN,MAPK1,and AKT1)signal pathways were regulated,like lipid and atheroscierosis,diabetes complications AGE-RAGE,fluid shear stress and atheroscierosis were controled to play the anti-ALI role.The molecular docking showed that the binding energy of the main active components and pathway key target proteins were-28.8696 kJ·mol-1.The experimental research on mice showed the liver index,MDA,ALT,AST and NF-κB p65 levels all decreased in the Tamarix ramosissima Ledeb groups,and the liver tissue degeneration reduced.Conclusion Tamarix ramosissima Ledeb has a certain protective effect on ALI through multiple ingredients,targets,and pathways.
NETL
NSTL
万方数据
