Oxidative stress is an important cause of hepatic injury in fish and is frequently associated with inflammation, apoptosis, and impairment of liver function. This study investigated the protective effects of glycyrrhizic acid (GA) against Concanavalin A (Con A)-induced oxidative liver injury in orange-spotted grouper (Epinephelus coioides) through both in vivo and in vitro experiments. In the in vivo trial, E. coioides were fed diets supplemented with 50-400 mg/kg GA for 8 weeks before intraperitoneal injection of Con A (2.5 mg/mL). Liver samples were collected 24 h after injection for biochemical and molecular analyses. The results showed that dietary GA at 50-200 mg/kg significantly reduced the hepatic expression of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β), and alleviated inflammatory response and apoptosis (P < 0.05). In the in vitro experiment, GS cells were treated with GA at 0.025, 0.05, 0.1, and 0.2 mg/mL. Cell morphology was observed microscopically, cell viability was evaluated using the CCK-8 assay, and the expression of apoptosis-related genes (caspase-3 and caspase-8) and inflammatory genes (TNF-α, IL-1β, and IL-6) was determined by qRT-PCR. GA at 0.025-0.1 mg/mL significantly enhanced cell viability, reduced apoptosis, increased CAT and GSH activities, and reduced MDA levels (P < 0.05). Morphological observations further showed that GA effectively alleviated Con A-induced cellular damage. In conclusion, GA protects against Con A-induced oxidative liver injury by attenuating inflammatory response and apoptosis, providing a potential nutritional strategy for improving fish health.

BackgroundWhile the introduction of neoadjuvant therapy has innovated perioperative treatment strategies for locally advanced gastric cancer (LAGC), preventing postoperative recurrence and metastasis remains a key clinical challenge. Previous research has indicated that Shenqi Fuwei granules (SQFWG), a Traditional Chinese medicine (TCM) prescription, possesses anti-gastric cancer properties. However, evidence from perioperative intervention studies is lacking. Our trial aims to evaluate the efficacy and safety of SQFWG combined with perioperative therapy in reducing postoperative recurrence and metastasis in LAGC, to explore clinical characteristics of the benefiting population, and to provide an evidence base for developing treatment protocols.MethodsThis is a prospective, randomized, double-blind, placebo-controlled, multicenter clinical trial. We plan to recruit 286 perioperative LAGC patients from multiple hospitals in China. Participants will be randomly assigned (1:1) using a central interactive web response system with allocation concealment, stratified by the use of neoadjuvant chemotherapy ± immunotherapy, to either the control group (n=143, placebo containing 5% SQFWG) or the experimental group (n=143, SQFWG). Both groups will concurrently receive perioperative treatment (chemotherapy ± immunotherapy). Follow-up assessments will be conducted every 3 months for 3 years after treatment completion or upon reaching an endpoint event. The primary efficacy endpoint is event-free survival. Secondary outcomes include overall survival, cumulative 1-/2-/3-year recurrence and metastasis rates, surgical conversion rate, quality of life, and safety. At the same time, prespecified subgroup analyses will be performed according to the use of immunotherapy and the type of chemotherapy regimen, and the clinical applicability of SQFWG will be further explored.DiscussionTo our knowledge, this is one of the first multicenter randomized double-blind placebo-controlled trials evaluating the efficacy of SQFWG in perioperative LAGC. This trial is expected to provide high-level evidence for the role of TCM in perioperative comprehensive management of LAGC.Clinical trial registrationhttps://www.ClinicalTrials.gov, identifier NCT07098026, ITMCTR2025001212.

Heart failure is a common complication in patients with sepsis, and individuals who experience both sepsis and heart failure are at a heightened risk for adverse outcomes. This study aims to develop an effective nomogram model to predict the 7-day, 15-day, and 30-day survival probabilities of septic patients with heart failure in the intensive care unit (ICU). This study extracted the pertinent clinical data of septic patients with heart failure from the Critical Medical Information Mart for Intensive Care (MIMIC-IV) database. Patients were then randomly allocated into a training set and a test set at a ratio of 7:3. Cox proportional hazards regression analysis was used to determine independent risk factors influencing patient prognosis and to develop a nomogram model. The model's efficacy and clinical significance were assessed through metrics such as the concordance index (C-index), time-dependent receiver operating characteristic (ROC), calibration curve, and decision curve analysis (DCA). A total of 5,490 septic patients with heart failure were included in the study. A nomogram model was developed to predict short-term survival probabilities, using 13 variables: age, pneumonia, endotracheal intubation, mechanical ventilation, potassium (K), anion gap (AG), lactate (Lac), activated partial thromboplastin time (APTT), white blood cell count (WBC), red cell distribution width (RDW), hemoglobin-to-red cell distribution width ratio (HRR), Sequential Organ Failure Assessment (SOFA) score, and Charlson Comorbidity Index (CCI). The C-index was 0.730 (95% CI 0.719-0.742) for the training set and 0.761 (95% CI 0.745-0.776) for the test set, indicating strong model accuracy, indicating good model accuracy. Evaluations via the ROC curve, calibration curve, and decision curve analyses further confirmed the model's reliability and utility. This study effectively developed a straightforward and efficient nomogram model to predict the 7-day, 15-day, and 30-day survival probabilities of septic patients with heart failure in the ICU. The implementation of treatment strategies that address the risk factors identified in the model can enhance patient outcomes and increase survival rates.

Diets enriched with live microbes offer multiple health benefits. This study aimed to investigate the relationship between dietary intake of live microbes and accelerated biological age, as well as to examine the mediating role of insulin resistance. The study included 4,909 participants from the National Health and Nutrition Examination Survey (NHANES) conducted between 2007 and 2018. Dietary live microbes intake was assessed using a self-report questionnaire. Insulin resistance was measured using the HOMA-IR and plasma insulin levels. Biological age and accelerated aging were assessed using PhenoAge and PhenoAgeAccel. We performed weighted multiple linear regression, logistic regression, restricted cubic spline (RCS) analysis, mediation analyses, and interaction analyses to explore the relationships between dietary live microbe intake, insulin resistance, and accelerated aging. Higher intake of live dietary microbes, compared to lower intake, was associated with a slower rate of accelerated aging after full adjustment for confounders (β = 0.15; 95

Alcohol-associated Liver Disease (ALD) is one of the major chronic liver diseases worldwide and has high mortality and high incidence rate. microRNA-320 (miR-320), a highly conserved and widely expressed miRNA, has been reported to be involved in lipid metabolism; however, whether miR-320 affects the progression of ALD remains unclear. In this study, we demonstrated that hepatic miR-320 was significantly downregulated in chronic-plus-binge alcohol-fed mice. Interestingly, such downregulation might accelerate ALD progression as evidenced that hepatocyte-specific miR-320 deficient mice displayed higher susceptibility to acute-on-chronic alcohol feeding-induced steatosis and inflammation. Moreover, restoration of hepatic miR-320 ameliorated acute-on-chronic alcohol-induced hepatocyte damage and steatosis. Mechanistically, miR-320 inhibited alcohol-induced ferroptosis by targeting Transferrin Receptor 1 (TFRC) to suppress iron accumulation. Moreover, silencing of Tfrc in hepatocytes attenuated ethanol-induced iron accumulation, thus inhibiting ferroptosis and ultimately mitigating ALD. Taken together, these findings suggest that miR-320 plays an important role in limiting ALD progression via inhibiting ferroptosis, providing a therapeutic target for the treatment of ALD.

Patients with rheumatoid arthritis (RA) have an increased risk of ischemic heart failure (IHF), but the shared mechanisms are unclear. This study analyzed RNA sequencing data from five RA and IHF datasets to identify common biological mechanisms and significant biomarkers. One hundred and seventy-seven common differentially expressed genes (CDEGs) were identified, with enrichment analysis highlighting pathways related to sarcomere organization, ventricular myocardial tissue morphogenesis, chondrocyte differentiation, prolactin signaling, hematopoietic cell lineage, and protein methyltransferases. Five hub genes (CD2, CD3D, CCL5, IL7R, and SPATA18) were identified through protein-protein interaction (PPI) network analysis and machine learning. Co-expression and immune cell infiltration analyses underscored the importance of the inflammatory immune response, with hub genes showing significant correlations with plasma cells, activated CD4+ T memory cells, monocytes, and T regulatory cells. Single-cell RNA sequencing (scRNA-seq) confirmed hub gene expression primarily in T cells, activated T cells, monocytes, and NK cells. The findings underscore the critical roles of sarcomere organization, prolactin signaling, protein methyltransferase activity, and immune responses in the progression of IHF in RA patients. These insights not only identify valuable biomarkers and therapeutic targets but also offer promising directions for early diagnosis, personalized treatments, and preventive strategies for IHF in the context of RA. Moreover, the results highlight opportunities for repurposing existing drugs and developing new therapeutic interventions, which could reduce the risk of IHF in RA patients and improve their overall prognosis.

Guishao Yigong Decoction (GYD), a classical formula, has been used to treat colorectal cancer (CRC) in clinical practices. However, its mechanism is still unclear. Increasing evidence suggests that the gut microbiota may serve as a potential target for treating CRC. Therefore, this study aims to elucidate the amelioration and potential mechanism of GYD on CRC by comprehensively analyzing the metagenome of gut microbiota and fecal metabolome. The results indicated that GYD significantly reduced the number and size of adenomas in the mouse colon, decreased spleen index, alleviated mouse emaciation and rectal bleeding, and protected the colonic barrier. 16S rRNA gene sequencing analysis revealed that GYD could markedly improve the dysbiosis of gut microbiota in CRC mice, increasing the abundance of beneficial bacteria and decreasing the abundance of pathogenic bacteria. Furthermore, the disordered fecal metabolic profiling of CRC mice was notably reversed by GYD. Following GYD administration, metabolites such as thiamine pyrophosphate, 3-methylpentanoic acid, and propanoic acid significantly increased, whereas 2-hydroxy-2-methylpropanoic acid, levodopa, and stearic acid remarkably decreased. Correlation analysis further indicated a close relationship between differential gut microbiota and metabolites. In conclusion, the amelioration of GYD on CRC might involve the regulation of gut microbiota and its metabolism.

Guishao Yigong Decoction (GYD), a classic prescription that tonifies the spleen and qi, has been used in clinical practices for thousands of years to treat spleen deficiency. However, its in vitro and in vivo metabolic characteristics are still unclear. In this study, a rapid and reliable analytical method based on ultra-high-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF/MS) with automated data processing (MetaboLynx) was established to investigate the metabolites and metabolic pathways of GYD in vivo and in vitro. Based on the characteristics of protonated ions, eleven precursors (ginsenoside Re, ginsenoside Rg1, ginsenoside Rb1, atractylenolide I, atractylenolide III, paeoniflorin, glycyrrhizic acid, pachymic acid, liquiritin, nobiletin, and ferulic acid) and their corresponding metabolites were detected and tentatively identified. A total of 81 metabolites were identified, including 53 metabolites in vivo, 40 metabolites of liver microsomes, and 43 metabolites of intestinal flora in vitro. Distinct metabolic patterns were observed between intestinal flora and liver microsomes - the former primarily catalyzed phase I transformations (hydroxylation, methylation, dehydroxylation, demethylation, and reduction), while the latter also executed phase II metabolism, with glucuronidation being the predominant conjugation reaction. The metabolic profiling and pathways of active components in GYD were systematically analyzed, which was helpful in clarifying its potential mechanism and clinical application.

Background:Hypertension is a major risk factor for cardiovascular diseases,including AF,which is one of the most common cardiac arrhythmias globally.AF is strongly associated with an increased risk of stroke,heart failure(HF),and cardiovascular mortality.Although intensive blood pressure lowering has been shown to reduce adverse cardiovascular events,its effect on the risk of AF remains debated.Some studies suggest a beneficial effect,whereas others are inconclusive.Therefore,a comprehensive review and meta-analysis are needed to clarify these effects. Objective:This study aims to evaluate the impact of intensive blood pressure lowering on the incidence of atrial fibrillation(AF)in hyper-tensive patients. Methods:We performed a systematic review and meta-analysis by searching PubMed,EMBASE,Scopus,Web of Science,and the Cochrane Library up to September 2,2024,for randomized controlled trials comparing intensive blood pressure lowering with standard treatment in hypertensive patients.Studies were included if participants were 40 year or older with systolic blood pressure between 130 and 180 mm Hg(1 mm Hg≈0.133 kPa).Data extraction was conducted by 2 independent researchers,and statistical analysis was performed using Review Manager(RevMan)5.4.Risk ratios(RRs)and 95％confidence intervals(Cls)were calculated.A random-effects model was applied if heterogeneity was detected(I2＞50％). Results:A total of 6 randomized controlled trials involving 34,824 participants were included in the analysis.Intensive blood pressure lowering significantly reduced the risk of new-onset AF compared with standard treatment(RR=0.76,95％CI=0.62-0.93,p＜0.01,I2=0％).Reductions were also observed in stroke(RR=0.71,95％CI=0.58-0.87,p＜0.005,I2=7％),HF(RR=0.67,95％CI=0.45-0.99,p=0.05,I2=53％),and nonfatal coronary events(RR=0.80,95％CI=0.70-0.92,p＜0.005,I2=39％).However,intensive blood pressure lowering had no significant effect on cardiovascular mortality or all-cause mortality compared with standard treatment. Discussion:Intensive blood pressure lowering significantly reduces the risk of AF and other cardiovascular events,such as stroke,HF,and nonfatal coronary events,particularly among high-risk hypertensive patients.These findings support the potential benefits of inten-sive blood pressure management in reducing AF incidence and improving overall cardiovascular outcomes,but the evidence is limited.

ETHNOPHARMACOLOGICAL RELEVANCE:Ershen Wan (ESW), a classic traditional Chinese medicine (TCM) prescription composed of Psoralea corylifolia Linn. and Myristica fragrans Houtt., has been applied to treat gastrointestinal disorders in clinical practices for thousands of years. However, its potential molecular mechanism in alleviating ulcerative colitis (UC) remains to be elusive. AIM OF THE STUDY:The purpose of the study is to explore the underlying mechanism of ESW in treating UC. MATERIALS AND METHODS:The protective effect of ESW on dextran sodium sulfate (DSS)-induced UC mice was assessed by body weight, disease activity index (DAI), colon length, colon tissue pathology, and colonic inflammatory factors. Furthermore, network pharmacology was applied to dissect the possible targets and biological pathways regulated by ESW. The plasma and fecal metabolomics were comprehensively analyzed by UPLC-Q-TOF/MS. Subsequently, an efficient and feasible approach integrating network pharmacology, metabolomics, and molecular docking was used to explore the key targets obtained from the metabolite-reaction-enzyme-gene network. And the effect of ESW on the MAPK signaling mediated intestinal epithelial cell apoptosis was further investigated by in vitro and in vivo experiments. RESULTS:ESW could notably alleviate colon injury and inflammation of UC mice. Network pharmacology suggested that the bioactive components of ESW could mainly modulate signaling pathways associated with inflammation and metabolism. Consistently, plasma and fecal metabolomics further indicated that ESW could regulate the metabolic pathways of arachidonic acid, linoleic acid, sphingolipid, tryptophan, and glycerophospholipid. And the combined analysis of network pharmacology and metabolomics revealed that 14 pivotal targets were modulated by ESW, including PTGS1, PTGS2, CYP1A1, FADS1, CBR1, ALOX5, EPHX1, EPHX2, HPGD, PLA2G1B, PLA2G7, MGLL, ACHE, and SPHK1. Additionally, molecular docking suggested that bioactive components of ESW could bind well to these potential targets. And in vitro and in vivo experiments further verified that ESW could markedly ameliorate pathological symptoms of UC mice through inhibiting MAPK signaling mediated colonic epithelial cell apoptosis. CONCLUSION:Collectively, these findings indicated that ESW could effectively alleviate the pathological symptoms of UC mice, mainly involving in the modulation of lipid and amino acid metabolism pathways, and the suppression of MAPK signaling-mediated apoptosis. In this study, the potential mechanism of ESW for the treatment of UC was first clarified, which provided a solid scientific foundation for its clinical application. Notably, the proposed strategy facilitated a comprehensive prediction and validation of the efficacy and molecular mechanism of TCMs, and also provided a novel approach for revealing the intricate biological pathogenesis of diseases.

OBJECTIVE:Based on analyses of gut microbiota, fecal metabolomics and microbiota-gut-brain (MGB) axis, this study aimed to elucidate the potential mechanism of Dachengqi decoction (DCQ) in improving constipation. METHODS:High performance liquid chromatography was used to determine the contents of 10 active ingredients in DCQ. Next, the effects of DCQ on constipation rats was evaluated, and the contents of brain-gut peptides in rat plasma were detected. Additionally, high-throughput 16S ribosomal RNA gene sequencing combined with UPLC-Q-TOF-MS/MS-based metabolomics was used to explore the changes of gut microbiota and fecal metabolites. The concentrations of short-chain fatty acids (SCFAs) were quantified by HPLC, and key metabolic pathway enzymes and MGB axis-related biomarkers were evaluated by ELISA. RESULTS:DCQ significantly alleviated loperamide-induced constipation in rats, reversed abnormalities in intestinal transport function and brain-gut peptides, improved colon pathological damage. And further investigation indicated that DCQ could improve the disorder of gut microbiota in constipated rats. DCQ could obviously reverse the abnormal fecal metabolism in constipation rats and regulate the levels of 55 different metabolites, which were mainly related to four metabolic pathways such as arachidonic acid metabolism. Moreover, DCQ could significantly elevate levels of SCFAs and modulate key MGB axis components by reducing cortisol concentration and increasing serotonin production, thereby effectively ameliorating constipation symptoms. CONCLUSION:DCQ could significantly improve the pathological symptoms of constipated rats via the MGB axis. Furthermore, it could remarkably reverse the disorder of gut microbiota and fecal metabolic profiles in constipated rats, which might contribute to ameliorate the constipation.

AIMS:This study aims to develop and validate an optimal model for predicting worsening heart failure (WHF). Multiple machine learning (ML) algorithms were compared, and the results were interpreted using SHapley Additive exPlanations (SHAP). A clinical risk calculation tool was subsequently developed based on these findings. METHODS AND RESULTS:This nested case-control study included 200 patients with chronic heart failure (CHF) from the China-Japan Friendship Hospital (September 2019 to December 2022). Sixty-five variables were collected, including basic information, physical and chemical examinations, and quality of life assessments. WHF occurrence within a 3-month follow-up was the outcome event. Variables were screened using LASSO regression, univariate analysis, and comparison of key variables in multiple ML models. Eighty per cent of the data was used for training and 20% for testing. The best models were identified by integrating nine ML algorithms and interpreted using SHAP, and to develop a final risk calculation tool. Among participants, 68 (34.0%) were female, with a mean age (standard deviation, SD) of 68.57 (12.80) years. During the follow-up, 60 participants (30%) developed WHF. N-terminal pro-brain natriuretic peptide (NT-proBNP), creatinine (Cr), uric acid (UA), haemoglobin (Hb), and emotional area score on the Minnesota Heart Failure Quality of Life Questionnaire were critical predictors of WHF occurrence. The random forest (RF) model was the best model to predict WHF with an area under the curve (AUC) (95% confidence interval, CI) of 0.842 (0.675-1.000), accuracy of 0.775, sensitivity of 0.900, specificity of 0.833, negative predictive value of 0.800, and positive predictive value of 0.600 for the test set. SHAP analysis highlighted NT-proBNP, UA, and Cr as significant predictors. An online risk predictor based on the RF model was developed for personalized WHF risk assessment. CONCLUSIONS:This study identifies NT-proBNP, Cr, UA, Hb, and emotional area scores as crucial predictors of WHF in CHF patients. Among the nine ML algorithms assessed, the RF model showed the highest predictive accuracy. SHAP analysis further emphasized NT-proBNP, UA, and Cr as the most significant predictors. An online risk prediction tool based on the RF model was subsequently developed to enhance early and personalized WHF risk assessment in clinical settings.

Abstract Background Ischemic heart disease is one of the leading causes of mortality worldwide, and thus calls for development of more effective therapeutic strategies. This study aimed to identify potential therapeutic targets for coronary heart disease (CHD) and myocardial infarction (MI) by investigating the causal relationship between plasma proteins and these conditions. Methods A two-sample Mendelian randomization (MR) study was performed to evaluate more than 1600 plasma proteins for their causal associations with CHD and MI. The MR findings were further confirmed through Bayesian colocalization, Summary-data-based Mendelian Randomization (SMR), and Transcriptome-Wide Association Studies (TWAS) analyses. Further analyses, including enrichment analysis, single-cell analysis, MR analysis of cardiovascular risk factors, phenome-wide Mendelian Randomization (Phe-MR), and protein-protein interaction (PPI) network construction were conducted to verify the roles of selected causal proteins. Results Thirteen proteins were causally associated with CHD, seven of which were also causal for MI. Among them, FES and PCSK9 were causal proteins for both diseases as determined by several analytical methods. PCSK9 was a risk factor of CHD (OR = 1.25, 95% CI: 1.13–1.38, P = 7.47E-06) and MI (OR = 1.36, 95% CI: 1.21–1.54, P = 2.30E-07), whereas FES was protective against CHD (OR = 0.68, 95% CI: 0.59–0.79, P = 6.40E-07) and MI (OR = 0.65, 95% CI: 0.54–0.77, P = 5.38E-07). Further validation through enrichment and single-cell analysis confirmed the causal effects of these proteins. Moreover, MR analysis of cardiovascular risk factors, Phe-MR, and PPI network provided insights into the potential drug development based on the proteins. Conclusions This study investigated the causal pathways associated with CHD and MI, highlighting the protective and risk roles of FES and PCSK9, respectively. FES. Specifically, the results showed that these proteins are promising therapeutic targets for future drug development.

"虚—寒—毒—闭—衰"五期演变理论体系已明确诠释"寒"在肿瘤论治中的重要地位.本文以内寒为基、外寒为因、气机为引,从内外寒合阐述致瘤病理机制,提出寒聚不散、阳虚阴凝是肿瘤全程发展关键,即阳虚寒凝变毒而促进展、毒窜寒聚挟风而致复发转移,强调寒毒对肿瘤病机演化与预后转归的核心价值.治当温散,以调阳散寒,还应根据邪寒分源论治,内寒者当温补,脾肾共养改善免疫微环境;外寒者当辛温,散而通肺增强抗肿瘤活性.本文从"寒"论治肿瘤,冀以丰富中医肿瘤病机学说,为构建现代肿瘤中医理论与诊疗体系奠定基础.

Traditional Chinese medicine is an important part of complementary alternative medicine. Jiedu Qingjin formula (JDQJF) is an effective national invention patent for the treatment of non-small cell lung cancer (NSCLC). We investigated the molecular biological mechanisms based on network pharmacology, molecular docking, and molecular dynamics simulations. Compounds of JDQJF were screened through the TCMSP, ETCM, and literature. Targets were searched by DrugBank and predicted by SwissTargetPrediction. GEO database was applied for screening differentially expressed genes between cancerous tissues and healthy tissues of NSCLC. Subsequently, the protein-protein interaction between JDQJF and NSCLC were obtained by Cytoscape. Visual analyses were carried out to extract candidate genes, then subjected to Metascape for enrichment analyses. Finally, molecular docking was performed by AutoDock, and the best complexes were subjected to molecular dynamics simulation and binding energy calculations by MMPBSA. A total of 273 compounds, 390 targets, 3146 GO terms, and 174 KEGG pathways were obtained. Five potential compounds (quercetin, adenosine, apigenin, heptadecanoic acid, and luteolin) were notably modulated by key targets AKT1, MAPK3, and RAF1. Enrichment results included cell cycle process, growth transduction factor, immune response-activating transduction, and involved PI3K/AKT, MAPK, NF-κB and VEGF pathway. RAF1-quercetin showed the highest binding affinity (-9.1 kcal/mol), revealed stable interactions during the simulation, and the highest estimated relative binding energy of the RAF1-Heptadecanoic was -184.277 kcal/mol. This study suggested that EMT-related, inflammation-related, immune-related, and angiogenesis-related pathways may be associated with JDQJF, and involved in the advancement of NSCLC, which points out the research direction for subsequent utility mechanism validation.Communicated by Ramaswamy H. Sarma.

Introduction: Brain metastasis (BM) is a significant risk factor for survival and prognosis in non-small cell lung cancer (NSCLC). While surgical resection and radiotherapy are the primary treatment modalities, the overall prognosis in NSCLC patients with BM remains poor, and all therapies lead to adverse events. East Asian herbal medicine (EAHM) has broad prospects as an adjuvant treatment, but its efficacy and safety remain controversial. We propose to conduct a systematic review and meta-analysis to summarize the clinical efficacy and safety of EAHM for the treatment of NSCLC with BMs and to identify specific herbs that can improve the prognosis. Methods: The PubMed, EMBASE, CENTRAL, Web of Science, CBM, CNKI, Wanfang, VIP, Evidence Reports on Kampo Treatment, ICHUSHI, and Oriental Medicine Advanced Searching Integrated System databases will be searched from their inception to October 2022. Randomized controlled trials will be included. Two authors will evaluate the eligibility and quality of the included trials. The methodological quality will be assessed using the RoB 2 tool, and Stata 16 will be used for data synthesis. Publication bias will be assessed using funnel plots and Egger tests. The GRADE (Grading of Recommendations Assessment, Development, and Evaluation) system will evaluate the quality of the synthesized evidence. Further sensitivity analyses will be performed to determine the efficacies of specific herbs in EAHM. Discussion: Given there are currently no systematic reviews and meta-analyses of the efficacy of EAHM as a treatment for NSCLC with BMs, a compilation and analysis of the available high-quality clinical research evidence are essential. The results will help establish guidelines for the application of specific herbs as a complementary alternative therapy for BMs in NSCLC. The findings will be published in a peer-reviewed journal. PROSPERO registration number: CRD42022300527.

目的 观察左西孟旦对急性心肌梗死(AMI)合并心源性休克(CS)患者经皮冠状动脉介入治疗(PCI)术后的疗效及预后.方法 选取2019年5月至2021年5月于解放军总医院第七医学中心心脏重症监护病房68例AMI-CS PCI术后患者,按照治疗方案的不同分为观察组和对照组,每组各34例.对照组在常规治疗基础上以2.5～10.0 μg/(kg·min)速度泵入多巴酚丁胺,观察组在对照组基础上加用左西孟旦以0.1～0.2 μg/(kg·min)速度泵入,比较两组治疗前及治疗24 h、72 h后心功能指标[N末端脑钠肽前体(NT-proBNP)、左室射血分数(LVEF)]及血流动力学指标如心率(HR)、平均动脉压(MAP)、中心静脉压(CVP)、心脏指数(CI)、每搏输出量(SV)、左心室舒张末期容积(LVEDV)、组织灌注氧代谢变化如氧分压(PaO2)、氧合指数(OI)、中心静脉血氧饱和度(ScvO2)、乳酸(Lac)、乳酸清除率等,记录并比较两组患者住院期间不良反应发生率和28 d生存率.结果 治疗前两组患者一般临床资料比较无明显差异.与治疗前相比,治疗24 h、72 h后两组患者LVEF、SV、MAP、CI、PaO2、OI、ScvO2、乳酸清除率等均较治疗前升高,NT-proBNP、CVP、HR、LVEDV、Lac等均较治疗前下降(P＜0.05),且观察组LVEF、SV、MAP、CI、PaO2、OI、ScvO2、乳酸清除率均高于对照组(P＜0.05),NT-proBNP、CVP、HR、LVEDV、Lac均低于对照组(P＜0.05).治疗期间两组不良反应发生率比较无明显差异(P＞0.05).随访28 d,Kaplan-Meire生存曲线显示,两组生存率未见显著差异(P＞0.05).结论 左西孟旦可稳定AMI-CS PCI术后患者的血流动力学,改善左室功能和组织灌注,且安全性较好,但患者生存率未见明显提高.

OBJECTIVE:To reveal the anti-inflammatory mechanism of Guanxin V, which is prescribed for ventricular remodeling in clinical practice.METHODS:Guanxin V-, ventricular remodeling-, and inflammation-related targets were obtained through an integrated strategy of virtual screening and systematic pharmacology, and then the shared targets were visualised with a Venn diagram. Guanxin V network and the protein-protein interaction network were drawn, and enrichment analysis was conducted. Finally, the main results obtained from the integrated strategy were validated by molecular docking and in vivo experiments.RESULTS:A total of 251, 11,425, and 15,246 Guanxin V-, ventricular remodeling-, and inflammation-related targets were acquired, respectively. Then, 211 shared targets were considered to contribute to the mechanism of ventricular remodeling treated by Guanxin V. Guanxin network and the protein-protein interaction network were drawn, and enrichment analysis showed some cardiovascular-related biological processes and signaling pathways. Molecular docking revealed that the Guanxin V-derived compounds could align with key targets. Final in vivo experiments proved that Guanxin V reverses ventricular remodeling by inhibiting inflammation.CONCLUSION:Guanxin V relieves ventricular remodeling by regulating inflammation, which provides new ideas for the anti-ventricular remodeling mechanism of Guanxin V.