AIM:To study the mechanism of ac-tion of radix angelica sinensis and astragalus mong-holicus extract(RAS-AM)in inhibiting fibroblast transdifferentiation(CMT)and preventing radiation-induced myocardial fibrosis(RIMF)via the Jagged1/Notch1 pathway.METHODS:Sixty male Wistar rats were randomly divided into blank group,model group,benazepril hydrochloride group,low dose RAS-AM group,medium dose RAS-AM group,and high dose RAS-AM group,with 10 rats in each group.Except for the blank group,all other groups were induced with high-energy radiation at a dose of 38 Gy to establish RIMF models.The blank group and the model group received sterile distilled water by gavage,and the other groups received medica-tion for 4 weeks of intervention:benazepril hydro-chloride group(1.0 mg·kg-1·d-1),low dose RAS-AM group(150 mg·kg-1·d-1),medium dose RAS-AM group(300 mg·kg-1·d-1),and high dose RAS-AM group(600 mg·kg-1·d-1).The general condition of rats,the ultrastructure of myocardial tissue were observed using electron microscopy,changes in myocardial tissue fibers using Masson staining,and CMT related protein Vimentin and α-SMA expres-sion using immunohistochemical staining tech-niques.ELISA was used to detect serum inflammato-ry factors IL-6 and TNF-α in rats.The levels of cTnI and ST2,and the expression of Jagged1 and Notch1 were detected by Western blot.RESULTS:Com-pared with the blank group,the model group rats exhibited symptoms such as mental fatiguem an-orexiam and loose stools;The arrangement of some myofibrils in the myocardium is disordered,with dis-solution and breakage of myofibrilsm abnormal Z-line structure in some partsm disordered mitochon-drial arrangement,rupture of mitochondrial mem-branem,and rupture or disappearance of mitochon-drial ridge structure in some parts.A large amount of collagen fibers proliferate and deposit in the myo-cardium,and the fibrotic area significantly increases(P<0.01);The expression of myocardial tissue Vi-mentin α-SMA protein increased(P<0.05),while the expression of Jagged1 and Notch1 proteins de-creased(P<0.05);serum IL-6 and TNF-α,the expres-sion of inflammatory factors such as cTnI and ST2 in-creased(P<0.05).compared with the model group,the RAS-AM and benazepril hydrochloride groups showed varying degrees of improvement in general conditions;the pathological changes of myocardial ultrastructure have been improved,and myocardial fibrosis has been alleviated;The area of collagen fi-bers significantly decreased(P<0.01);Myocardial tis-sue Vimentin α-SMA protein expression decreased(P<0.05),while Jagged1 and Notch1 expression in-creased(P<0.05);Serum IL-6 and TNF-α,The expres-sion of inflammatory factors such as cTnI and ST2 decreased(P<0.05).CONCLUSION:RAS-AM may al-leviate RIMF by intervening in the Jagged1/Notch1 pathway to inhibit CMT.The specific mechanism still needs further investigation

AIM:To study the mechanism of ac-tion of radix angelica sinensis and astragalus mong-holicus extract(RAS-AM)in inhibiting fibroblast transdifferentiation(CMT)and preventing radiation-induced myocardial fibrosis(RIMF)via the Jagged1/Notch1 pathway.METHODS:Sixty male Wistar rats were randomly divided into blank group,model group,benazepril hydrochloride group,low dose RAS-AM group,medium dose RAS-AM group,and high dose RAS-AM group,with 10 rats in each group.Except for the blank group,all other groups were induced with high-energy radiation at a dose of 38 Gy to establish RIMF models.The blank group and the model group received sterile distilled water by gavage,and the other groups received medica-tion for 4 weeks of intervention:benazepril hydro-chloride group(1.0 mg·kg-1·d-1),low dose RAS-AM group(150 mg·kg-1·d-1),medium dose RAS-AM group(300 mg·kg-1·d-1),and high dose RAS-AM group(600 mg·kg-1·d-1).The general condition of rats,the ultrastructure of myocardial tissue were observed using electron microscopy,changes in myocardial tissue fibers using Masson staining,and CMT related protein Vimentin and α-SMA expres-sion using immunohistochemical staining tech-niques.ELISA was used to detect serum inflammato-ry factors IL-6 and TNF-α in rats.The levels of cTnI and ST2,and the expression of Jagged1 and Notch1 were detected by Western blot.RESULTS:Com-pared with the blank group,the model group rats exhibited symptoms such as mental fatiguem an-orexiam and loose stools;The arrangement of some myofibrils in the myocardium is disordered,with dis-solution and breakage of myofibrilsm abnormal Z-line structure in some partsm disordered mitochon-drial arrangement,rupture of mitochondrial mem-branem,and rupture or disappearance of mitochon-drial ridge structure in some parts.A large amount of collagen fibers proliferate and deposit in the myo-cardium,and the fibrotic area significantly increases(P<0.01);The expression of myocardial tissue Vi-mentin α-SMA protein increased(P<0.05),while the expression of Jagged1 and Notch1 proteins de-creased(P<0.05);serum IL-6 and TNF-α,the expres-sion of inflammatory factors such as cTnI and ST2 in-creased(P<0.05).compared with the model group,the RAS-AM and benazepril hydrochloride groups showed varying degrees of improvement in general conditions;the pathological changes of myocardial ultrastructure have been improved,and myocardial fibrosis has been alleviated;The area of collagen fi-bers significantly decreased(P<0.01);Myocardial tis-sue Vimentin α-SMA protein expression decreased(P<0.05),while Jagged1 and Notch1 expression in-creased(P<0.05);Serum IL-6 and TNF-α,The expres-sion of inflammatory factors such as cTnI and ST2 decreased(P<0.05).CONCLUSION:RAS-AM may al-leviate RIMF by intervening in the Jagged1/Notch1 pathway to inhibit CMT.The specific mechanism still needs further investigation

Objective To observe the effects of Angelica Sinensis Radix and Astragali Radix extract(ASR-AR)on HUVEC pyroptosis;To explore its mechanism of treating coronary microvascular disease.Methods HUVEC were divided into blank group,model group,MCC950 group,ASR-AR low-,medium-and high-dosage groups.After modeling and treatment with drug containing serum,cell viability was detected by CCK-8 method,and cell apoptosis was detected by flow cytometry,phalloidin staining was used to detect cytoskeletal morphology,immunofluorescence staining was used to detect the expressions of VEGF,eNOS,Ang-2,ROS,ET-1 and TXA2,ELISA was used to detect the contents of IL-1β and IL-18 in cell supernatant,Western blot was used to detect the expressions of NLRP3,ASC,Caspase-1 and GSDMD protein in cells.Results Compared with the blank group,the model group showed a decrease in HUVEC cell viability(P<0.01)and an increase in cell apoptosis rate(P<0.01),cellular microfilament structure was in disorder and knotting,the expressions of VEGF and eNOS decreased,and expressions of Ang-2,ROS,ET-1 and TXA2 increased,the contents of IL-1β and IL-18 in cell supernatant increased(P<0.01),and the expressions of NLRP3,ASC,Caspase-1 and GSDMD protein in cells increased(P<0.01).Compared with the model group,ASR-AR low-,medium-and high-dosage containing serum could increase cell viability(P<0.05),decrease cell apoptosis rate(P<0.05),improve cell microfilament structure,elevate VEGF and eNOS expressions,decrease Ang-2,ROS,ET-1,TXA2 expressions,reduce IL-1β and IL-18 contents in cell supernatant(P<0.05),and decrease NLRP3,ASC,Caspase-1 and GSDMD protein expressions(P<0.05).ASR-AR medium-dosage group was more obvious(P<0.05).Conclusion ASR-AR can inhibit pyroptosis of HUVEC induced by AngⅡ,attenuate endothelial cell dysfunction,thus treating coronary microvascular disease,and its mechanism may be related to the inhibition of the assembly of NLRP3 inflammasome.

Objective:To analyze the prognostic outcomes of 1 147 patients who underwent liver transplantation at Qingdao University Affiliated Hospital and to summarize measures to enhance the efficacy of liver transplantation.Methods:A retrospective analysis was conducted on the clinical and follow-up data of 1 147 liver transplant patients at Qingdao University Affiliated Hospital.Results:The overall postoperative 1-, 3-, and 5-year survival rates for the 1 147 liver transplant patients were 87.20%, 73.40%, and 65.60%, respectively. The survival rates for benign disease liver transplant recipients were 88.01%, 84.98%, and 81.39% at 1, 3, and 5 years post-transplant, respectively, compared to recipients transplanted for malignancies of 78.11%, 64.41%, and 60.06% (all P<0.001). Among the mid vs more recent period, patients' 1-year and 3-year postoperative survival rates were 84.20%, 70.80% vs 90.50%, 71.70%, respectively,significantly in favor of recently enrolled patients ( P=0.022). In the complex surgery group, patients' 1-, 3-, and 5-year survival rates were 82.70%, 65.50%, 56.70%, while in less complicated group, it was 89.00%, 76.50%, 69.20% ( P<0.001). The primary causes of death for benign disease recipients were multi-organ failure (4.1%), while in recipients with malignant disease primary cause of death was tumor recurrence (23.7%). Postoperative complications included primary graft dysfunction, delayed graft function recovery, portal vein thrombosis, hepatic artery thrombosis, biliary stricture, post-transplant lymphoproliferative disorder, and graft-versus-host disease, with occurrence rates of 1.05%, 6.89%, 1.92%, 0.44%, 2.00%, 0.61%, and 0.44%, respectively. Conclusions:With the continuous improvement in surgical techniques and perioperative care levels, the 3-year survival rate of recipients at our center has increased. Malignant diseases and complex liver transplantation remain crucial factors affecting recipient prognosis, highlighting the need to further enhance comprehensive treatment capabilities for patients with malignant diseases and complex surgeries.

Objective To analyse whether Resveratrol can inhibit the inflammatory response in septic cardiomyopathy by modulating the mammalian target of rapamycin-transcription factor EB(mTOR-TFEB)signaling pathway.Methods A total of 32 clean-grade male Sprague-Dawley(SD)rats were selected and divided into sham operation group(Sham group),sepsis model group[cecal ligation and puncture(CLP)group],Resveratrol group(Res group)and mTOR inhibitor group(Torin1 group),with 8 rats in each group.Sepsis was induced by CLP.The sham group only underwent laparotomy and did not perform CLP.In the Torin1 group,20 mg·kg-1·d-1 of mTOR inhibitor Torin l injection was injected intraperitoneally 10 days before molding,once a day for 10 days.The Sham group and the CLP group were given the same amount of normal saline through the same route before molding.The Res group was injected intraperitoneally with 60 mg/kg Resveratrol injection before molding.At 6 hours after model establishment,the heart function was evaluated by echocardiography;Serum cardiac troponin I(cTnI)levels were detected by enzyme linked immunosorbent assay(ELISA).The mRNA expressions of interleukin-6(IL-6)and tumor necrosis factor-α(TNF-α)were detected by real-time fluorescence quantitative polymerase chain reaction(RT-qPCR).The protein expressions of phosphorylation-mTOR(p-mTOR),TFEB(nuclear),TFEB(total)and light chain 3-Ⅱ(LC3-Ⅱ)of myocardial tissue were detected by Western blotting.The interaction between Resveratrol and mTOR was simulated using a network pharmacology approach.Results Compared with the sham group,the left ventricular ejection fraction(LVEF)and left ventricular short-axis shortening rate(FES)were significantly reduced in the CLP group[LVEF:0.37±0.02 vs.0.69±0.01,FES(%):17.8±3.1 vs.33.9±2.8,both P<0.01],serum cTnI levels were elevated(ng/L:1 935.96±47.78 vs.87.95±7.98,P<0.01),the mRNA expression levels of IL-6 and TNF-α were significantly up-regulated[IL-6 mRNA(2-ΔΔCt):26.10±2.08 vs.1.61±0.03,TNF-α mRNA(2-ΔΔCt):12.80±1.51 vs.1.26±0.22,both P<0.01),serum levels of inflammatory cytokines IL-6 and TNF-α mRNA were increased[IL-6 mRNA(2-ΔΔCt):26.10±2.08 vs.1.61±0.03,TNF-α mRNA(2-ΔΔCt):12.80±1.51 vs.1.26±0.22,both P<0.01),the expression level of p-mTOR protein in myocardial tissue was significantly increased(p-mTOR/β-actin:0.60±0.07 vs.0.30±0.05),while the protein levels of TFEB(total),TFEB(nuclear)and LC3-Ⅱwere significantly decreased[TFEB(total)/β-actin:0.52±0.08 vs.0.80±0.09,TFEB(nuclear)/H3:0.36±0.06 vs.0.09±0.07,LC3-Ⅱ/β-actin:0.25±0.08 vs.0.48±0.08,all P<0.01];Compared with the CLP group,the Res group and the Torin1 group had significantly higher LVEF and FES[LVEF:0.66±0.02,0.67±0.03 vs.0.37±0.02;FES(%):32.5±3.5,33.7±3.3 vs.17.8±3.1,both P<0.01],serum cTnI level was decreased(ng/L:1 216.88±36.66,1 225.78±35.64 vs.1 935.96±47.78,both P<0.01),mRNA levels of serum inflammatory cytokines IL-6 and TNF-α were decreased[IL-6 mRNA(2-ΔΔCt):3.91±0.46,4.14±0.39 vs.26.1±2.08,TNF-α mRNA(2-ΔΔCt):4.67±1.16,5.16±1.25 vs.12.8±1.51,both P<0.01],the p-mTOR protein expression in myocardial tissue was significantly decreased(p-mTOR/β-actin:0.22±0.05,0.24±0.06 vs.0.60±0.07,all P<0.01),the protein levels of TFEB(total),TFEB(nuclear),LC3-Ⅱwere significantly increased[TFEB(total)/β-actin:0.86±0.06,0.84±0.07 vs.0.52±0.08;TFEB(nuclear)/H3:0.96±0.08,0.86±0.07 vs.0.36±0.06;LC3-Ⅱ/β-actin:0.57±0.07,0.55±0.06 vs.0.25±0.08,all P<0.01].Network pharmacology was used to verify that resveratrol binds well to mTOR.Conclusion Resveratrol enhanced cardiac autophagy via the mTOR-TFEB pathway,thereby attenuating myocardial inflammation and subsequent cardiac injury in septic rats.

AIM:To explore the potential targets and mechanisms of Angelica sinensis and Astraga-lus membranaceus ultrafiltration(RAS-AM)in the treatment of radiation induced myocardial fibrosis(RIMF)through network pharmacology combined experimental validation.METHODS:Using the TC-MSP database TCM@TAIWAN The Taiwan Tradition-al Chinese Medicine Database and TCMID Tradition-al Chinese Medicine Database screen the compo-nents and targets of RAS-AM,and use the Swiss Target Prediction database for target prediction.Obtain RIMF disease targets from Gene Cards and OMIM databases,obtain intersection targets of dis-eases and drugs through Wayne's online tool,ob-tain protein interaction relationships(PPIs)through STRING database,and use Cytoscape 3.9.1 soft-ware to construct a visualized network topology di-agram of"drug component target disease".Con-duct GO and KEGG enrichment analysis on core tar-gets through the David database,and use the mi-crobiome platform for mapping.Experimental veri-fication:Sixty Wistar rats were randomly divided in-to a blank group,a model group,a positive drug group,a RAS-AM low-dose group,a RAS-AM medi-um dose group,and a RAS-AM high-dose group.A RIMF model was established using a 38Gy dose of radiation induction,and was administered orally for 4 weeks.The general condition of the rats was also observed.After blood and heart collection in rats,HE staining was used to observe the morpho-logical changes of myocardial tissue,and ELISA and Western blot methods were used to detect key tar-gets for network pharmacology prediction.RE-SULTS:Network pharmacology analysis revealed 34 active components and 705 targets of Angelica si-nensis and Astragalus membranaceus ultrafiltra-tion,with a total of 154 targets,with IL-6,VEGFA,MMP2,MMP9,and ACE as the top five core tar-gets;GO enrichment analysis screened a total of 153 entries,and KEGG enrichment had 25 path-ways.Experimental part:HE staining results showed that the degeneration and necrosis of myo-cardial cells improved in each medication group,the infiltration of inflammatory cells in the myocar-dial interstitium decreased,and the proliferation of fibrous connective tissue in the myocardial intersti-tium decreased.ELISA and Western blot results showed that compared with the normal group,the expression of IL-6,VEGFA,and MMP-9 in the mod-el group increased.Compared with the model groupthe expression of IL-6,VEGFA,and MMP-9 in each medication group decreased to varying de-grees,in a dose-dependent manner.CONCLUSION:RAS-AM may inhibit RIMF by downregulating core targets such as IL-6,VEGFA protein,MMP-9 pro-tein,and regulating inflammatory pathways,colla-gen degradation,and other processes.

Objective To analyse whether Resveratrol can inhibit the inflammatory response in septic cardiomyopathy by modulating the mammalian target of rapamycin-transcription factor EB(mTOR-TFEB)signaling pathway.Methods A total of 32 clean-grade male Sprague-Dawley(SD)rats were selected and divided into sham operation group(Sham group),sepsis model group[cecal ligation and puncture(CLP)group],Resveratrol group(Res group)and mTOR inhibitor group(Torin1 group),with 8 rats in each group.Sepsis was induced by CLP.The sham group only underwent laparotomy and did not perform CLP.In the Torin1 group,20 mg·kg-1·d-1 of mTOR inhibitor Torin l injection was injected intraperitoneally 10 days before molding,once a day for 10 days.The Sham group and the CLP group were given the same amount of normal saline through the same route before molding.The Res group was injected intraperitoneally with 60 mg/kg Resveratrol injection before molding.At 6 hours after model establishment,the heart function was evaluated by echocardiography;Serum cardiac troponin I(cTnI)levels were detected by enzyme linked immunosorbent assay(ELISA).The mRNA expressions of interleukin-6(IL-6)and tumor necrosis factor-α(TNF-α)were detected by real-time fluorescence quantitative polymerase chain reaction(RT-qPCR).The protein expressions of phosphorylation-mTOR(p-mTOR),TFEB(nuclear),TFEB(total)and light chain 3-Ⅱ(LC3-Ⅱ)of myocardial tissue were detected by Western blotting.The interaction between Resveratrol and mTOR was simulated using a network pharmacology approach.Results Compared with the sham group,the left ventricular ejection fraction(LVEF)and left ventricular short-axis shortening rate(FES)were significantly reduced in the CLP group[LVEF:0.37±0.02 vs.0.69±0.01,FES(%):17.8±3.1 vs.33.9±2.8,both P<0.01],serum cTnI levels were elevated(ng/L:1 935.96±47.78 vs.87.95±7.98,P<0.01),the mRNA expression levels of IL-6 and TNF-α were significantly up-regulated[IL-6 mRNA(2-ΔΔCt):26.10±2.08 vs.1.61±0.03,TNF-α mRNA(2-ΔΔCt):12.80±1.51 vs.1.26±0.22,both P<0.01),serum levels of inflammatory cytokines IL-6 and TNF-α mRNA were increased[IL-6 mRNA(2-ΔΔCt):26.10±2.08 vs.1.61±0.03,TNF-α mRNA(2-ΔΔCt):12.80±1.51 vs.1.26±0.22,both P<0.01),the expression level of p-mTOR protein in myocardial tissue was significantly increased(p-mTOR/β-actin:0.60±0.07 vs.0.30±0.05),while the protein levels of TFEB(total),TFEB(nuclear)and LC3-Ⅱwere significantly decreased[TFEB(total)/β-actin:0.52±0.08 vs.0.80±0.09,TFEB(nuclear)/H3:0.36±0.06 vs.0.09±0.07,LC3-Ⅱ/β-actin:0.25±0.08 vs.0.48±0.08,all P<0.01];Compared with the CLP group,the Res group and the Torin1 group had significantly higher LVEF and FES[LVEF:0.66±0.02,0.67±0.03 vs.0.37±0.02;FES(%):32.5±3.5,33.7±3.3 vs.17.8±3.1,both P<0.01],serum cTnI level was decreased(ng/L:1 216.88±36.66,1 225.78±35.64 vs.1 935.96±47.78,both P<0.01),mRNA levels of serum inflammatory cytokines IL-6 and TNF-α were decreased[IL-6 mRNA(2-ΔΔCt):3.91±0.46,4.14±0.39 vs.26.1±2.08,TNF-α mRNA(2-ΔΔCt):4.67±1.16,5.16±1.25 vs.12.8±1.51,both P<0.01],the p-mTOR protein expression in myocardial tissue was significantly decreased(p-mTOR/β-actin:0.22±0.05,0.24±0.06 vs.0.60±0.07,all P<0.01),the protein levels of TFEB(total),TFEB(nuclear),LC3-Ⅱwere significantly increased[TFEB(total)/β-actin:0.86±0.06,0.84±0.07 vs.0.52±0.08;TFEB(nuclear)/H3:0.96±0.08,0.86±0.07 vs.0.36±0.06;LC3-Ⅱ/β-actin:0.57±0.07,0.55±0.06 vs.0.25±0.08,all P<0.01].Network pharmacology was used to verify that resveratrol binds well to mTOR.Conclusion Resveratrol enhanced cardiac autophagy via the mTOR-TFEB pathway,thereby attenuating myocardial inflammation and subsequent cardiac injury in septic rats.

Objective:To investigate the surgical efficacy of split liver transplantation.Methods:Patients who underwent liver transplantation at the Affiliated Hospital of Qingdao University between January 2015 and December 2022 were retrospectively analyzed. They were divided into split liver transplantation group ( n=60) and whole liver transplantation group ( n=765)according to graft types.In the split liver transplantation group, there were 23 males and 37 females, aged (52.5±10.2) years, and the body mass index was (22.4±3.3) kg/m 2. In the whole liver transplantation group, there were 630 males and 135 females, aged (51.2±9.6) years, and body mass index was (24.5±3.7) kg/m 2.The basic data of the two groups were matched 1∶1 using the propensity score matching method. The independent sample t test and χ2 test were used to compare the intraoperative and postoperative recovery of the two groups of donors and recipients. The overall survival rate and the graft survival rate of the two groups were analyzed by Kaplan-Meier method and the cumulative survival rate was compared by the Log-rank test. Results:Fifty-one well-matched pairs of data with similar baseline characteristics were obtained. The ratio of graft mass to recipient body weight in the matched split liver transplantation group was (1.78±0.55)%. Operation time( M(IQR))(10.8(1.5)hours vs. 8.0(1.9)hours, U=6.608, P<0.01) and cold ischaemia time(5.4(1.3)hours vs. 4.6(2.2)hours, U=2.825, P=0.005) were significantly longer in the split liver transplantation group than those in the whole liver transplantation group. Intra-operative anhepatic phase(53.0(15.0)minutes vs. 57.0(24.0)minutes, U=1.048, P=0.295),bleeding volume(1 000(1 400)ml vs. 1 200(1 200)ml, U=0.966, P=0.334) and intraoperative instillation of red blood cells(9.0(6.5)U vs. 11.0(11.0)U, U=1.732, P=0.083) were not significantly different between the two groups. However,the split liver transplantation group showed significantly longer postoperative intensive care unit stay(5.0(3.0)days vs. 4.0(4.0)days, U=2.677, P=0.007) and postoperative hospital stay(30.0(15.0)days vs. 26.0(15.0)days, U=2.237, P=0.025) and significantly higher incidence of postoperative complications(56.8%(29/51) vs. 36.6%(19/51), χ2=3.935, P=0.047) than the whole liver transplantation group. Furthermore,levels of alanine transaminase and aspartate aminotransferase were significantly higher on postoperative days 1,4 and 7 in the split liver transplantation group(all P<0.05) than in the whole liver transplantation group;however,there were no significant differences in these levels on postoperative days 14 and 28. The time to restoration of normal liver function in both groups(12.5(13.7)days vs. 9.0(12.5)days, U=1.607, P=0.108) was not statistically significant. Furthermore,the median follow-up time after surgery was 25.6 months in both groups. In postoperative years 1,2,3 and 5, the graft survival rates were 88.1%,80.8%,77.8% and 66.7% in the whole liver transplantation group and 80.3%,70.3%,67.3% and 60.5% in the split liver transplantation group( P=0.171),respectively. The patient survival rates in post-operative years 1,2,3 and 5 were 88.1%,80.8%,77.8% and 66.7% in the whole liver transplantation group and 80.3%,75.9%,70.3% and 63.3% in the split liver transplantation group,respectively( P=0.252). However,the differences of graft survival rates and patient survival rates between the two groups were not significant. Conclusion:Although it affects the early recovery of patients after liver transplantation,split liver transplantation has no effect on long-term survival rates and demonstrates surgical efficacy similar to that of whole liver transplantation.

AIM: To study the mechanism of Ginseng Yixin granules (QSYXG) in treating ejection fraction preserved heart failure (HFpEF) based on network pharmacology. METHODS: Effective chemical composition information of QSYXG particles was collected through TCMSP database; DisGeNET, GeneCards, OMIM database for obtaining HFpEF related targets; Metascape GO and KEGG enrichment analysis of the intersection targets of HFpEF; STRING Construction and analysis of the database PPI network; Cytoscape3.7.2 Software construction network diagram; Docking of the major active components to the core target with the AutoDock Vina software molecules, the results were visualized and analyzed with pymol. RESULTS: A total of 66 components and corresponding targets were obtained, HFpEF corresponds to 1 931 targets, The intersection of 127 targets, the main active ingredients are quercetin, kaempferol, β-sitosterol, etc.; TNF, AKT1, IL-6, P53 and JUN as the core targets, Good docking of the key components with the core targets; Mainly involving the positive regulation of gene expression, signal transduction, negative regulation of apoptotic process, positive regulation of cell proliferation and senescence, hypoxia response, negative regulation of gene expression, inflammatory response and so on, PI3K-Akt, AGE-RAG, MAPK, TNF, IL-17, and HIF-1 are the main associated signaling pathways. CONCLUSION: QSYXG may treat HFpEF by activating targets of TNF, AKT1, IL-6, P53, JUN, and regulating apoptotic process, cell proliferation, hypoxia response, and inflammatory response.

Objective:To investigate whether stress hyperglycemia (SH) is an independent risk factor for the occurrence and mortality of sepsis-associated encephalopathy (SAE).Methods:From August 2016 to October 2021, sepsis patients admitted to the ICU of Guangdong Provincial People's Hospital were selected as the study subjects. According to whether they developed to SH (RBG>11.1 mmol/L) within 7 days of enrollment, the pat ients were divided into the SH group and the non-SH group for analysis. Logistic regression was used to analyze whether SH was an independent risk factor for SAE occurrence, and ROC curve was used to analyze the predictive value of SH to SAE. Kaplan-Meier curve was used to compare the 90-day survival of SAE patients with or without SH. Cox regression analysis was used to analyze the risk factors of 28-day and 90-day death in SAE patients.Results:A total of 183 sepsis patients were included, including 62 patients in the SH group and 121 in the non-SH group. Logistic regression analysis demonstrated that SH was an independent risk factor for SAE ( OR=4.452, 95% CI: 2.021-9.808, P <0.001). ROC curve demonstrated that SH could accurately predict SAE (AUC=0.831; Sensitivity=78.4%; Specificity=76.8%; and Yoden index=0.553). Kaplan-Meier curve demonstrated that the 90-day survival of SAE patients with SH significantly declined (log-rank test: P<0.01). Cox regression analysis suggested that SH was a risk factor for death at day 28 and day 90 in SAE patients (28 d, HR=2.272, 95% CI: 1.212-4.260, P=0.010; 90 d, HR=2.456, 95% CI: 1.400-4.306, P<0.01). Conclusions:SH is an independent risk factor for SAE and can predict SAE occurrence. SH significantly reduces 90-day survival and increase mortality at 28 and 90 days in SAE patients.