To screen potential drugs for the treatment of acute Liver Injury(ALI)through network pharmacology and mitochondrial dynamics,and to investigate their actions and mechanisms.Based on the commonly utilized Liver Pure Tablets and Liver-Protecting Capsules in the market,a com-ponent library of liver disease drugs was screened and established.Pharmacological anchoring anal-ysis was carried out.Potential liver disease therapeutic drugs were screened out through molecular docking,and feedback verification was performed using animal experiments.Acute liver injury mouse models were established through excessive induction with acetaminophen(APAP),and the histopathological changes of liver tissues were examined.The protective effect of the drug on ALI was evaluated by detecting alanine aminotransferase(ALT),aspartate aminotransferase(AST),superoxide dismutase(SOD),catalase(CAT),glutathione(GSH),and malondialdehyde(MDA)using enzyme-linked immunosorbent assay(ELISA).qRT-PCR was employed to detect peroxi-some proliferator-activated receptor gamma coactivator 1-alpha(PPARG1A),mitofusin 1(MFN1),mitofusin 2(MFN2),dynamin-related protein 1(DRP1),optic atrophy 1 protein(OP A1),Steroid receptor coactivator(SRC),and advanced glycosylation end-product specific re-ceptor(AGER)to explore the protective mechanism of the drug on ALI.The result showed that Network pharmacology identified a total of 662 intersection targets of three types of prescription drugs and ALI.Eventually,72 core targets were screened out.Pathway enrichment analysis indi-cates that the potential mechanism might be associated with the lipid and atherosclerosis signaling pathways.The results of the relevant molecular docking indicate that the most likely optimal drug might be emodin(EMO).EMO ameliorated the pathological damage in mice with acute liver inju-ry,significantly decreased the contents of transferase factors ALT and AST,simultaneously in-creased the contents of antioxidant enzymes CAT,GSH and SOD,and reduced the content of oxi-dative metabolic end product MDA.It also upregulated the mRNA expression levels of MFN1、MFN2,OPA1,DRP1,SRC and PPARGC1A proteins in liver tissue,and inhibited the mRNA ex-pression level of AGER protein.The drug EMO,jointly screened out by network pharmacology through anchoring and molecular docking,might promote mitochondrial fusion metabolism,allevi-ate liver oxidative stress,and improve liver injury in ALI mice via the Lipid and atherosclerosis pathway.

To screen potential drugs for the treatment of acute Liver Injury(ALI)through network pharmacology and mitochondrial dynamics,and to investigate their actions and mechanisms.Based on the commonly utilized Liver Pure Tablets and Liver-Protecting Capsules in the market,a com-ponent library of liver disease drugs was screened and established.Pharmacological anchoring anal-ysis was carried out.Potential liver disease therapeutic drugs were screened out through molecular docking,and feedback verification was performed using animal experiments.Acute liver injury mouse models were established through excessive induction with acetaminophen(APAP),and the histopathological changes of liver tissues were examined.The protective effect of the drug on ALI was evaluated by detecting alanine aminotransferase(ALT),aspartate aminotransferase(AST),superoxide dismutase(SOD),catalase(CAT),glutathione(GSH),and malondialdehyde(MDA)using enzyme-linked immunosorbent assay(ELISA).qRT-PCR was employed to detect peroxi-some proliferator-activated receptor gamma coactivator 1-alpha(PPARG1A),mitofusin 1(MFN1),mitofusin 2(MFN2),dynamin-related protein 1(DRP1),optic atrophy 1 protein(OP A1),Steroid receptor coactivator(SRC),and advanced glycosylation end-product specific re-ceptor(AGER)to explore the protective mechanism of the drug on ALI.The result showed that Network pharmacology identified a total of 662 intersection targets of three types of prescription drugs and ALI.Eventually,72 core targets were screened out.Pathway enrichment analysis indi-cates that the potential mechanism might be associated with the lipid and atherosclerosis signaling pathways.The results of the relevant molecular docking indicate that the most likely optimal drug might be emodin(EMO).EMO ameliorated the pathological damage in mice with acute liver inju-ry,significantly decreased the contents of transferase factors ALT and AST,simultaneously in-creased the contents of antioxidant enzymes CAT,GSH and SOD,and reduced the content of oxi-dative metabolic end product MDA.It also upregulated the mRNA expression levels of MFN1、MFN2,OPA1,DRP1,SRC and PPARGC1A proteins in liver tissue,and inhibited the mRNA ex-pression level of AGER protein.The drug EMO,jointly screened out by network pharmacology through anchoring and molecular docking,might promote mitochondrial fusion metabolism,allevi-ate liver oxidative stress,and improve liver injury in ALI mice via the Lipid and atherosclerosis pathway.

Macrophages,key cells in the heart's innate immune system,are highly heterogeneous and plastic,playing dual roles in cardiac physiology and pathology.In recent years,macrophage-derived exosomes have drawnsignificant attention for their regulatory mechanisms and potential therapeutic applications in heart disease,as they serve as crucial mediators of intercellular communication.This paper aims to comprehensively summarize the origin,distribution,and function of cardiac-resident macrophages.It also explores the roles of M1and M2 macrophages in cardiac inflammatory responses and tissue repair,and delves into the regulatory mechanisms and therapeutic application prospects of macrophage exosomes in heart disease.In the acute phase of cardiac injury,M1 macrophages secrete pro-inflammatory cytokines to induce inflammation and clear cellular debris.Nevertheless,their overactivation can result in myocardial cell damage and fibrosis.During the recovery phase,M2 macrophages take the lead,releasing anti-inflammatory cytokines and growth factors to inhibit inflammation and facilitate tissue repair.Macrophage exosomes,which contain proteins,lipids,and nucleic acids,can regulate inflammation,tissue repair,and angiogenesis.In various types of heart disease,including myocardial infarction,ischemia-reperfusion injury,atherosclerosis,myocarditis,and dilated cardiomyopathy,macrophage exosomes exhibit different functions.While M1-derived exosomes often exacerbate cardiac damage through pro-inflammatory actions,M2-derived exosomes protect cardiac tissue via anti-inflammatory and pro-repair effects.These findings offer new insights and targets for developing macrophage-exosome-based heart disease therapies,which is expected to promote the innovative development of diagnosis and treatment for heart diseases,improve patients'prognosis,and alleviate the burden of public health.