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.

To study the anticoagulant effect of Xiang-Qi-Tang (XQT),the mice model of endotoxemia was established to detect the expression of coagulation factors and their regulatory proteins in serum and aorta.The results showed that XQT could decrease the expression of TF and increase the expression of tPA in the aorta of mice with endotoxemia,and also decrease the expression of sEPCR in the serum.We further found that XQT caused the decrease of sEPCR through the regulation of PKC δ and ADAM17 to contribute the anticoagulation in mice.This study may provide a new strategy for treating endotoxin-induced disease and provide evidences for further researching the pharmacological action of XQT.