Through molecular docking and experimental validation,24 SPF male KM mice were ran-domly divided into four groups:the control group(CON),model group(LPS),high-dose Yang Shuhua group(YSH-H),which was gavaged with drug solution containing 1 g/mL crude Yang Shuhua,and the low-dose Yang Shuhua group(YSH-L),which was gavaged with drug solution containing 0.5 g/mL crude Yang Shuhua for a 17-day experimental period.Mouse body weight was recorded during the experiment,and fecal scoring was done 1 h after intraperitoneal injection of LPS.At the end of the experiment,histopathological changes in the jejunum tissue were examined,and the expression of tight junction protein-related genes was detected.Compared to the CON group,mice in the LPS group showed significant decreases in villus height,villus height/crypt depth(V/C)ratio(P＜0.01),and significant increase in crypt depth(P＜0.01).The mRNA ex-pression levels of ZO-1 and claudin-1 were significantly decreased(P＜0.01).Compared to the LPS group,mice in the YSH-H group showed significant decrease in crypt depth(P＜0.05),significant increase in villus height(P＜0.05),and significant increase in V/C ratio(P＜0.01).The YSH-L group showed a significant increase in V/C ratio(P＜0.05),a trend of decreased crypt depth,and an increasing trend of villus height.The mRNA expression of ZO-1 in the YSH-H group showed a significant increase(P＜0.05)and claudin-1 showed an increasing trend.Luteolin,quercetin,kaempferol,eriodictyol,and the top 5 potential key targets TP53,IL-1β,TNF,AKT1,and IL-10 exhibited molecular docking scores less than-20.95 kJ/mol,indicating strong activity.GO and KEGG enrichment analysis suggested that Yang Shuhua compounds might act on enteritis through the TNF signaling pathway,IL-17 signaling pathway,and PI3K-Akt signaling pathway.The qPCR results showed an upward trend in the mRNA expression levels of TLR4 and AKT1,significant in-crease in Caspase-1 and ASC(P＜0.05),and significantly increased expression of NF-κB and NL-RP3(P＜0.01).The mRNA expression level of AKT1,TLR4,NLRP3,ASC,Caspase-1,and NF-κB decreased compared to the LPS group,with significant differences in Caspase-1 and NF-κB(P＜0.05).This study suggests that Yang Shuhua exerts anti-enteritis effects through multiple compo-nents and pathways,with blockade of the TLR4-AKT-NF-κB pathway possibly being a key thera-peutic mechanism for treating enteritis.

This study aims to investigate the medication rules of patented traditional Chinese medi-cine(TCM)compound formulas and molecular mechanisms of core drugs for treating sepsis using data mining and network pharmacology approaches.In the present study,we first searched the PubMed database,Web of Science database,and the China National Knowledge Infrastructure(CNKI)since the establishment of the library to April 30,2024 for the relevant literature on the treatment of sepsis by traditional Chinese medicine.The prescriptions were then statistically ana-lyzed for drug frequency and association analysis to obtain the core drugs.Then we screened the ef-fective active ingredients of the core drugs by TCMSP and other database platforms,obtained sep-sis-related genes in GeneCards and other databases,and statistically intersected targets,and predic-ted the mechanism of action of the core TCMs by subjecting the intersected targets to PPI analy-sis,GO function and KEGG pathway enrichment analysis.Finally,the relationship between key tar-gets and herbal components was examined in reverse by molecular docking method.The results showed that 64 compound formulas were obtained,with a total of 150 Chinese medicines,which were mostly sweet in taste,cold in nature,and belonged to the spleen,stomach and intestinal me-ridians.According to the association rules,the core drugs were identified as"mirabilite-peach ker-nel-rheum officinale".There were 79 intersecting targets between the core drugs and sepsis,with core targets such as IL-1β,EGFR and SRC.MAPK,TNF,IL-17 and other signaling pathways are involved to mediate inflammatory responses,apoptosis and other biological processes to exert ther-apeutic effects on sepsis.The molecular docking results indicated that the docking activity of the key targets with the main components of the drug,and sennoside E_qt has the lowest binding ener-gy and the best docking activity with SRC.In conclusion,this study showed that the prescription of Chinese medicine for sepsis is mostly based on tonifying the spleen and clearing heat.The mecha-nism of action of the core drug"mirabilite-peach kernel-rheum officinale"in the treatment of sep-sis is multilevel and multifaceted,which provides a certain theoretical basis for the treatment of sepsis by traditional Chinese medicine.

OBJECTIVE To compare the efficacy and safety of different daily doses of aspirin in the prevention of preeclampsia （PE）. METHODS The case-control studies and prospective randomized controlled trials on aspirin with daily dose ≥ 100 mg （trial group） vs. ＜100 mg （control group） in the prevention of PE were retrieved from PubMed， Medline， Embase， the Cochrane Library， CNKI， China Biomedical Literatue Database and Wanfang Data from base-building to January 2025. After literature screening， data extraction and quality evaluation， meta-analysis was performed by using RevMan 5.3 software. RESULTS A total of 11 literatures were included， involving 3 052 pregnant women. Meta-analysis showed the incidence of PE [RR＝0.63， 95%CI （0.53，0.76）， P＜0.000 01]， gestational hypertension [RR＝0.69， 95%CI （0.50，0.94），P＝0.02]， preterm birth [RR＝0.56， 95%CI （0.47，0.66）， P＜0.000 01]， and intrauterine growth retardation [RR＝0.73，95%CI （0.61，0.87），P＝0.000 5] in trial groups were significantly lower than control group. The incidence of postpartum hemorrhage between the two groups had no statistically significant difference [RR＝1.17， 95%CI （0.90，1.53），P＝0.25]. Subgroup analysis showed that the incidence of PE in Chinese pregnant women taking 150 mg of aspirin was significantly higher than taking 100 mg of aspirin [RR＝3.40， 95%CI （1.29， 8.93）， P＝0.01]； but there was no significant difference between the two groups in the incidences of postpartum hemorrhage， preterm birth （P＞0.05）. CONCLUSIONS Aspirin with daily dose ≥100 mg is more effective in preventing PE than daily dose ＜100 mg， with lower rates of gestational hypertension， preterm birth， and intrauterine growth retardation. It does not increase the risk of postpartum hemorrhage. For pregnant women in China， daily dose 100 mg of aspirin may be more effective in preventing PE than 150 mg.

Objective To investigate the clinical features of chronic hepatitis C(CHC)patients with hepatitis C virus genotype 3(HCV GT3)infection and the risk factors for disease progression.Methods A multicenter retrospective cohort study was conducted among 1 002 CHC patients from 11 clinical centers in Northwest China from December 2017 to November 2023,and according to their genotype,they were divided into GT1,GT2,GT3,and GT6 groups.Clinical features were compared between the patients with different genotypes.The one-way analysis of variance was used for comparison of normally distributed continuous data between groups,and the Scheffe test was used for further comparison between two groups.The Kruskal-Wallis H test was used for comparison of data with skewed distribution between groups;the chi-square test or Fisher test was used for comparison of categorical data between groups.The multivariate logistic regression analysis was used to explore the influencing factors for the progression of CHC to liver cirrhosis.Results In terms of the genotype,there were 427 patients with GT1 infection,242 with GT2 infection,299 with GT3 infection(210 patients with GT3a infection,87 with GT3b infection,and 2 with unclassified genotype),and 34 with GT6 infection.The patients with GT3 infection had a significantly younger age than those with GT1 infection(51.3±0.5 years vs 53.2±0.6 years,P<0.05)or GT2 infection(51.3±0.5 years vs 53.7±0.8 years,P<0.05),and for the patients with liver cirrhosis,the patients with GT3 infection had a significantly younger age than those with GT1 infection(52.1±0.5 years vs 59.4±0.9 years,P<0.001)or GT2 infection(52.1±0.5 years vs 58.1±1.1 years,P<0.001).Among the patients with GT3 infection,male patients accounted for 77.9%and the patients with liver cirrhosis accounted for 46.2%,which were significantly higher than those among the patients with GT1,GT2 or GT6 infection(all P<0.001).At baseline,the patients with GT3 infection had significantly higher levels of alanine aminotransferase(ALT)and aspartate aminotransferase(AST)than those with GT1 or GT2 infection,significantly higher aspartate aminotransferase-to-platelet ratio index(APRI)and fibrosis-4(FIB4)than those with GT1,GT2 or GT6 infection,a significantly lower platelet count(PLT)than those with GT2 or GT6 infection,a significantly higher level of alpha-fetoprotein than those with GT2 or GT6 infection,and a significantly lower level of albumin(Alb)than those with GT6 infection(all P<0.05).There were no significant differences between the patients with GT3a infection and those with GT3b infection in age,sex,the proportion of patients with liver cirrhosis,comorbidities,HCV RNA quantification,PLT,ALT,AST,alkaline phosphatase,Alb,APRI,and FIB-4(all P>0.05).The multivariate logistic regression analysis showed that PLT≤150×109/L(odds ratio[OR]=10.72,95%confidence interval[CI]:5.76-35.86,P<0.001)and Alb≤35 g/L(OR=3.74,95%CI:1.22-11.45,P=0.021)were risk factors for liver cirrhosis.Conclusion Most CHC patients with GT3 infection are male in Northwest China,and compared with the patients with other genotypes,such patients tend to have a younger age of onset and higher degrees of liver inflammation activity and fibrosis.Low PLT and a low level of Alb are risk factors for progression to liver cirrhosis in CHC patients with GT3 infection.

Based on network pharmacology,molecular docking,and experimental validation,this study explored the mechanism by which Hypericum japonicum Thunb-Prunella vulgaris treat liver injury.Mice were randomly divided into four groups:a control group(CON),a model group(CCl4),a high-dose drug group(TXD-H),and a low-dose drug group(TXD-L).A mouse liver in-jury model was established using CCl4 induction.The pathological morphology of liver tissue was observed,and the serum levels of aspartate aminotransferase(AST)and alanine aminotransferase(ALT)were measured.Active ingredients of traditional Chinese medicine and targets related to these medicines and diseases were obtained from databases such as TCMSP,PubChem,Swiss Tar-get Prediction,GeneCards,and DisGeNET.The intersection of these targets was used to identify potential drug targets.A network diagram illustrating the relationships between"drug-active com-ponent-intersection target"was constructed using Cytoscape.Potential targets were analyzed using the STRING database for protein-protein interaction(PPI)analysis and the DAVID database for Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway analysis.Molecular docking validation was performed using AutoDock Tools software.Subsequently,key target genes,including those related to the NLRP3 inflammasome and pyroptosis,were detected to validate the molecular docking results.Animal experimental results showed that compared to the CON group,serum AST and ALT activities in the CCl4 group mice were significantly increased(P＜0.01),while in the TXD-L group,serum AST and ALT activities were significantly decreased(P＜0.05)compared to the CCl4 group,and in the TXD-H group,AST and ALT activities were significantly decreased(P＜0.01).Through network pharmacology,135 potential targets were i-dentified,with key components found to be tetramethoxyluteolin,quercetin,kaempferol,luteolin and morin based on degree values,and key targets including TNF,SRC,AKT1,EGFR and ESR1.GO enrichment analysis yielded 304 entries,while KEGG enrichment analysis identified 91 biologi-cal pathways.Molecular docking results demonstrated strong binding between the main compo-nents of Hypericum japonicurn Thunb-Prunella vulgaris and key targets.qPCR results showed that compared to the CON group,the CCl4 group exhibited upregulated relative expression levels of SRC,EGFR,TNF-α,AKT1,and IL-18 mRNA,with significant increases in MyD88,NF-κB,IL-1β,NLRP3,Caspase-1,and ASC mRNA(P＜0.05),and significant upregulation of TLR4 and GS-DMD mRNA(P＜0.01).Compared to the CCl4 group,the TXD-H group displayed significant downregulation of EGFR,AKT1,TLR4,IL-1β,and GSDMD mRNA(P＜0.01),significant decrea-ses in TNF-α,MyD88,NF-κB,NLRP3,and ASC mRNA(P＜0.05),while SRC,IL-18,and Caspase-1 mRNA showed a downward trend.In conclusion,Hypericum japonicum Thunb-Prunel-la vulgaris exerts hepatoprotective effects through multiple components and pathways,among which inhibition of the NF-κB-NLRP3 pathway to reduce hepatocyte pyroptosis may be one of the important pathways for its protective effects.

Based on network pharmacology,molecular docking,and experimental validation,this study explored the mechanism by which Hypericum japonicum Thunb-Prunella vulgaris treat liver injury.Mice were randomly divided into four groups:a control group(CON),a model group(CCl4),a high-dose drug group(TXD-H),and a low-dose drug group(TXD-L).A mouse liver in-jury model was established using CCl4 induction.The pathological morphology of liver tissue was observed,and the serum levels of aspartate aminotransferase(AST)and alanine aminotransferase(ALT)were measured.Active ingredients of traditional Chinese medicine and targets related to these medicines and diseases were obtained from databases such as TCMSP,PubChem,Swiss Tar-get Prediction,GeneCards,and DisGeNET.The intersection of these targets was used to identify potential drug targets.A network diagram illustrating the relationships between"drug-active com-ponent-intersection target"was constructed using Cytoscape.Potential targets were analyzed using the STRING database for protein-protein interaction(PPI)analysis and the DAVID database for Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway analysis.Molecular docking validation was performed using AutoDock Tools software.Subsequently,key target genes,including those related to the NLRP3 inflammasome and pyroptosis,were detected to validate the molecular docking results.Animal experimental results showed that compared to the CON group,serum AST and ALT activities in the CCl4 group mice were significantly increased(P＜0.01),while in the TXD-L group,serum AST and ALT activities were significantly decreased(P＜0.05)compared to the CCl4 group,and in the TXD-H group,AST and ALT activities were significantly decreased(P＜0.01).Through network pharmacology,135 potential targets were i-dentified,with key components found to be tetramethoxyluteolin,quercetin,kaempferol,luteolin and morin based on degree values,and key targets including TNF,SRC,AKT1,EGFR and ESR1.GO enrichment analysis yielded 304 entries,while KEGG enrichment analysis identified 91 biologi-cal pathways.Molecular docking results demonstrated strong binding between the main compo-nents of Hypericum japonicurn Thunb-Prunella vulgaris and key targets.qPCR results showed that compared to the CON group,the CCl4 group exhibited upregulated relative expression levels of SRC,EGFR,TNF-α,AKT1,and IL-18 mRNA,with significant increases in MyD88,NF-κB,IL-1β,NLRP3,Caspase-1,and ASC mRNA(P＜0.05),and significant upregulation of TLR4 and GS-DMD mRNA(P＜0.01).Compared to the CCl4 group,the TXD-H group displayed significant downregulation of EGFR,AKT1,TLR4,IL-1β,and GSDMD mRNA(P＜0.01),significant decrea-ses in TNF-α,MyD88,NF-κB,NLRP3,and ASC mRNA(P＜0.05),while SRC,IL-18,and Caspase-1 mRNA showed a downward trend.In conclusion,Hypericum japonicum Thunb-Prunel-la vulgaris exerts hepatoprotective effects through multiple components and pathways,among which inhibition of the NF-κB-NLRP3 pathway to reduce hepatocyte pyroptosis may be one of the important pathways for its protective effects.

Based on network pharmacology,through molecular docking and experimental validation,the study explored the mechanism of the Hypericum japonicum-Rehmannia glutinosa-Salvia ple-beian compound(HRS)in the treatment of liver injury.Mice were randomly divided into a control group(CON group),a model group(CCL4 group),a high-dose drug group(HRS-H group),and a low-dose group(HRS-L group).A mouse liver injury model was established using CCL4 induction,liver tissue pathological morphology was observed,and the relative expression levels of liver in-flammatory cytokine genes was measured.Active ingredients of traditional Chinese medicine and targets related to Chinese medicine and diseases were obtained from databases such as Herb,TCM-SP,PubChem,Swiss Target Prediction,Gene Cards and DisGeNET.The intersection of targets was used to obtain potential drug targets.The potential targets were analyzed for protein-protein inter-action(PPI)using the string database and a network diagram of"drug-active component-intersec-tion target"was constructed using Cytoscape.DAVID database was used for GO and KEGG path-way analysis,and Auto Dock Tools software was used for molecular docking.Finally,the results of molecular docking by examining the expression of key target genes and downstream genes such as those related to the PI3K-AKT pathway and the autophagy pathway were experimentally valida-ted.Results:Animal experiment results showed that compared to the CON group,the CCL4 group of mice exhibited disrupted liver architecture,hepatocyte steatosis,vacuolization,and extensive in-flammatory cell infiltration.These characteristics were ameliorated by drug treatment groups with the HRS-H group demonstrating superior effects compared to the HRS-L group.RT-qPCR results from mouse livers showed significantly increased relative expression of TNF-α and INOS mRNA compared to the CON group in the CCL4 group(P＜0.01),and significantly increased IL-1β mR-NA relative expression(P＜0.05).Compared to the CCL4 group,the HRS-H group showed signifi-cantly decreased TNF-α,INOS,and IL-1β mRNA relative expressions(P＜0.01).155 potential tar-gets for HRS in alleviating liver damage were identified through network pharmacology,with top-ranked key target points including STAT3,SRC,PIK3R1,PIK3CA,AKT1,HSP90A11,EGFR,and ESR.Key active ingredients included Tetramethoxyluteolin,Hispidulin,Eupafolin,Kaempferol,and Eupaformonin.GO enrichment analysis yielded 940 entries,and KEGG enrichment analysis yielded 177 biological pathways.Molecular docking results showed a strong binding ability between the main components of HRS and key target points.RT-qPCR results showed increasing trends for EGFR,PI3KCA,HSP90A11,and NF-κB mRNA compared to the CON group in the CCL4 group,significantly increased AKT1 mRNA relative expression(P＜0.05),significant decreases in ULK1,ATG5,LC3B,and ATG7 mRNA relative expressions(P＜0.05),and extremely significant decreases in PTEN,ATG13,BECLIN-1,ATG16L1,ATG12,ATG4B,and ATG3 mRNA relative expressions(P＜0.01).Compared to the CCL4 group,the HRS-H group showed significantly de-creased PI3KCA,HSP90A11,and NF-κB mRNA relative expressions(P＜0.05),extremely signif-icantly decreased EGFR,AKT1,and mTOR mRNA relative expressions(P＜0.01),increased ULK1 relative expression trends,significantly increased PTEN,ATG16L1,ATG5,LC3B,and ATG7 mRNA relative expressions(P＜0.05),extremely significantly increased ATG13,BECLIN-1,ATG12,ATG4B,and ATG3 mRNA relative expressions(P＜0.01).Conclusion:The HRS ex-erts hepatoprotective effects through multi-component,multi-pathway approaches,with alleviating inflammation and promoting hepatocyte autophagy through PI3K-AKT pathway likely being im-portant mechanisms for its protective effects.

Based on network pharmacology,through molecular docking and experimental validation,the study explored the mechanism of the Hypericum japonicum-Rehmannia glutinosa-Salvia ple-beian compound(HRS)in the treatment of liver injury.Mice were randomly divided into a control group(CON group),a model group(CCL4 group),a high-dose drug group(HRS-H group),and a low-dose group(HRS-L group).A mouse liver injury model was established using CCL4 induction,liver tissue pathological morphology was observed,and the relative expression levels of liver in-flammatory cytokine genes was measured.Active ingredients of traditional Chinese medicine and targets related to Chinese medicine and diseases were obtained from databases such as Herb,TCM-SP,PubChem,Swiss Target Prediction,Gene Cards and DisGeNET.The intersection of targets was used to obtain potential drug targets.The potential targets were analyzed for protein-protein inter-action(PPI)using the string database and a network diagram of"drug-active component-intersec-tion target"was constructed using Cytoscape.DAVID database was used for GO and KEGG path-way analysis,and Auto Dock Tools software was used for molecular docking.Finally,the results of molecular docking by examining the expression of key target genes and downstream genes such as those related to the PI3K-AKT pathway and the autophagy pathway were experimentally valida-ted.Results:Animal experiment results showed that compared to the CON group,the CCL4 group of mice exhibited disrupted liver architecture,hepatocyte steatosis,vacuolization,and extensive in-flammatory cell infiltration.These characteristics were ameliorated by drug treatment groups with the HRS-H group demonstrating superior effects compared to the HRS-L group.RT-qPCR results from mouse livers showed significantly increased relative expression of TNF-α and INOS mRNA compared to the CON group in the CCL4 group(P＜0.01),and significantly increased IL-1β mR-NA relative expression(P＜0.05).Compared to the CCL4 group,the HRS-H group showed signifi-cantly decreased TNF-α,INOS,and IL-1β mRNA relative expressions(P＜0.01).155 potential tar-gets for HRS in alleviating liver damage were identified through network pharmacology,with top-ranked key target points including STAT3,SRC,PIK3R1,PIK3CA,AKT1,HSP90A11,EGFR,and ESR.Key active ingredients included Tetramethoxyluteolin,Hispidulin,Eupafolin,Kaempferol,and Eupaformonin.GO enrichment analysis yielded 940 entries,and KEGG enrichment analysis yielded 177 biological pathways.Molecular docking results showed a strong binding ability between the main components of HRS and key target points.RT-qPCR results showed increasing trends for EGFR,PI3KCA,HSP90A11,and NF-κB mRNA compared to the CON group in the CCL4 group,significantly increased AKT1 mRNA relative expression(P＜0.05),significant decreases in ULK1,ATG5,LC3B,and ATG7 mRNA relative expressions(P＜0.05),and extremely significant decreases in PTEN,ATG13,BECLIN-1,ATG16L1,ATG12,ATG4B,and ATG3 mRNA relative expressions(P＜0.01).Compared to the CCL4 group,the HRS-H group showed significantly de-creased PI3KCA,HSP90A11,and NF-κB mRNA relative expressions(P＜0.05),extremely signif-icantly decreased EGFR,AKT1,and mTOR mRNA relative expressions(P＜0.01),increased ULK1 relative expression trends,significantly increased PTEN,ATG16L1,ATG5,LC3B,and ATG7 mRNA relative expressions(P＜0.05),extremely significantly increased ATG13,BECLIN-1,ATG12,ATG4B,and ATG3 mRNA relative expressions(P＜0.01).Conclusion:The HRS ex-erts hepatoprotective effects through multi-component,multi-pathway approaches,with alleviating inflammation and promoting hepatocyte autophagy through PI3K-AKT pathway likely being im-portant mechanisms for its protective effects.

The objective of this study was to evaluate the protective effect and possible related mechanisms of Sophora subprostrate polysaccharide(SSP)on intestinal epithelial cell injury in-duced by Tert-Butyl hydroperoxide(TBHP).The optimal dose of TBHP and the safe concentra-tion range of SSP were determined using the MTT method.In this study,IPEC-J2 cells were divid-ed into five groups:the control group,the model group,the SSPL group,the SSPM group and the SSPH group,and the cell morphology,cell survival rate and LDH release rate were observed and measured.The content of intracellular reactive ROS was observed and determined by DCFH-DA staining.The content of MDA in the supernatant and the antioxidant index of cells were determined by the reagent kit.Transcriptome technology was employed to analyze the potential mechanisms by which SSP mitigates oxidative damage in IPEC-J2 cells.The results showed that treatment with 625 μmol/L TBHP for 2 h significantly reduced the activity of IPEC-J2 cells,markedly increased LDH release(P＜0.05),inhibited CAT superoxide SOD and glutathione GPX activities(P＜0.05),and significantly elevated MDA and ROS levels(P＜0.05).Compared to the model group,after SSP treatment,intracellular ROS levels were significantly reduced(P＜0.05),while CAT,SOD,and GPX activities were significantly increased(P＜0.05),and MDA content and LDH re-lease were significantly decreased(P＜0.05)in a dose-dependent manner.Transcriptome analysis revealed that TBHP treatment significantly altered the transcriptional profiles of IPEC-J2 cells,while SSP treatment could restore the transcriptional profiles of the damaged cells to a certain ex-tent.Gene ontology(GO)and Kyoto encyclopedia of genes and genomes(KEGG)indicated that the differentially expressed genes between the CC and TBHP groups were significantly enriched in oxidative phosphorylation,ribosome,and other pathways.Meanwhile,the differentially expressed genes between the SSP and TBHP groups were mainly enriched in oxidative phosphorylation,ap-optosis,glyoxylate and dicarboxylate metabolism,and other pathways.These results suggest that TBHP may disrupt normal oxidative respiration in IPEC-J2 cells by affecting oxidative phospho-rylation and interfering with metabolism pathways involving glycine,serine,and threonine,leading to oxidative damage in intestinal epithelial cells.Conversely,SSP treatment may potentially restore oxidative phosphorylation processes,alleviate lysosomal damage,reduce cell apoptosis,and miti-gate oxidative damage in intestinal epithelial cells through modulation of oxidative phosphoryla-tion,apoptosis,and lysosomal pathways.This discovery provides a theoretical basis for the clinical application of SSP in alleviating oxidative damage in the porcine intestinal tract.

Danggui Buxue decoction(DBD)is a classic prescription with immunomodulatory and hematopoietic effects.Previous studies have shown the DBD has potential to be used as an oral im-mune booster.However,its immunomodulatory effects and mechanism of action have not been thoroughly studied,especially the protective mechanism of immunomodulatory regulation in the state of immunosuppressive is still unclear.The aim of this study was to explore the protective mechanism of DBD in the immunosuppressive state using network pharmacology combined with animal experiments verification.The active components,core targets and signaling pathways of DBD in treating immunosuppression were obtained using network pharmacology tools.On this ba-sis,the active components of DBD were identified using HPLC-MS,and in vivo studies were con-ducted at the same time.The key active components of DBD obtained using network pharmacology included quercetin,kaempferol and formononetin.The core targets included TP53,RELA,TNF,AKT1,and IL-6.KEGG pathway enrichment analysis showed that phosphoinositide 3-kinase(PI3K)-protein kinase B(AKT)may play an important role in the treatment of immunosuppres-sive diseases using DBD.Molecular docking confirmed that each core target had good binding activ-ity with its corresponding compounds.Animal experiments showed that after DBD intervention,the mRNA gene and protein expression of RELA,TNF,and IL-6 in the serum was significantly down-regulated.The mRNA expression of PI3K and AKT in the ileum and PI3K protein expression were also downregulated.In conclusion,DBD exerts its role in treating immunosuppressive diseases by regulating the PI3K-AKT signaling pathway.