目的   基于结构方程模型（SEM）验证早产儿母亲育儿胜任感的多路径作用机制。方法  采用便利抽样法选取2024年6月—2025年6月在莆田学院附属医院分娩的早产儿母亲250例作为研究对象。采用一般资料调查表、中文版育儿胜任感量表（C-PSOC）、婴儿母亲育儿支持问卷（PSM）、角色适应问卷、简式亲职压力量表收集数据。通过单因素分析及多元线性回归分析母亲育儿胜任感的影响因素，使用AMOS软件构建结构方程模型，分析早产儿分娩后母亲育儿胜任感的作用路径。结果  250例早产儿母亲的C-PSOC得分为（61.93±6.02）分，多元线性回归分析结果显示，早产儿母亲育儿胜任感的影响因素包括产次、育儿支持、角色适应、亲职压力（均P＜0.05）。结构方程模型拟合良好（χ ² /df=1.026，GFI=0.987，AGFI=0.978，NFI=0.987，CFI=1.000，RMSEA=0.010），其中角色适应正向预测育儿胜任感（β=0.344），育儿支持（β=-0.477）与亲职压力（β=-0.283）负向预测（均P＜0.05），并且角色适应通过育儿支持、亲职压力间接提升育儿胜任感（效应值0.467）；产次经角色适应间接降低压力源影响（效应值0.529）。结论  早产儿母亲育儿胜任感受多路径机制调控，临床需针对角色适应、育儿支持及亲职压力设计级联干预策略。

       Objective  To verify the multi-pathway mechanism of parenting competence of premature infant mothers based on structural equation modeling（SEM）．Methods  A convenience sampling method was used to select 250 mothers of preterm infants who delivered in Affiliated Hospital of Putian University between June 2024 and June 2025 as the study subjects．Data was collected using a general information survey，the Chinese version of the Parenting Sence of Competence Scale（C-PSOC），the Parenting Support Questionnaire for Infant Mothers（PSM），the Role Adaptation Questionnaire，and the Simplified Parenting Stress Scale．By conducting  single factor analysis and multiple linear  regression analysis on the influencing factors of maternal parenting competence，a structural equation model was constructed using AMOS software to analyze the pathway of maternal parenting competence after premature birth．Results  The C-PSOC score of 250 mothers of premature infants was（61.93±6.02）．Multiple linear  regression analysis showed that the influencing factors of parenting competence among mothers of premature infants included parity，parenting support，role adaptation，and parental pressure（all P＜0.05）．The structural equation model fits well（2/df=1.026，GFI=0.987，AGFI=0.978，NFI=0.987，CFI=1.000，RMSEA=0.010），which  role adaptation  positively  predicted parenting competence（β=0.344），parenting support（β=-0.477）and parenting stress（β=-0.283）negatively predicted（all P＜0.05），and role adaptation indirectly enhanced parenting competence through parenting support and parenting stress（effect value 0.467）．The adaptation of roles during childbirth indirectly reduced the impact of stressors（effect value 0.529）．Conclusions  The multi-pathway mechanism of parental competence perception regulation in premature infant mothers requires the design of cascading intervention strategies targeting role adaptation，parenting support，and parental stress in clinical practice．

目的 运用数据挖掘、网络药理学和分子对接的方法,探讨中药复方治疗中枢性性早熟（CPP）的用药规律和作用机制,为其临床治疗提供更多依据。方法 在中国知网（CNKI）、万方数据（Wanfang）、维普中文期刊（VIP）等数据库中检索从建库至2022年10月发表的中药复方治疗CPP的文献,用Excel 2021 收集整理临床治疗CPP的常用中药复方,并通过Excel 2021、SPSS Modeler 18.0、SPSS Statistics 25.0等软件对其进行频次、关联规律等分析,研究CPP治疗的用药规律。在上述基础上采用网络药理学的研究方法,筛选出高频药对的活性成分、作用靶点以及疾病的相关靶点,构建蛋白互作网络,并通过基因本体和京都基因 基因组百科全书通路富集分析来阐明药物的作用机制。最后运用 Autodock Vina 软件进行分子对接对结果验证。结果 共筛选出224篇文献,包含方剂133首,中药188味。发现18味使用超过25次的高频药物;清热类、补虚类的药物应用较多;药物性味以寒及苦为主;归经之中以肝经占比最高;进一步关联分析得到高频药对14个;核心处方4个。网络药理学结果显示,共得到44个活性成分、200个药物靶点、1 287个疾病靶点、70个共有靶点、573条GO富集条目及136条KEGG通路,药物主要成分槲皮素、山奈酚、β-谷甾醇作用于雌激素受体、黄体酮受体等核心靶点,通过内分泌抵抗、雌激素等信号通路发挥治疗作用。分子对接结果显示药物主要活性成分与相应核心靶点具有较好的结合能力。结论 中药复方治疗CPP多为滋阴清热、补虚类药物,与药性寒,药味苦、甘,归肝、肾经的药物配伍使用。其中高频药对“知母-黄柏”通过多成分、多靶点调控内分泌抵抗、雌激素信号通路发挥治疗作用。

Objective To explore the prescription rules and mechanism of traditional Chinese medicine（TCM） in the treatment of central precocious puberty（CPP）by using data mining,network pharmacology and molecular docking,so as to provide more evidence for clinical treatment．Methods Using the literature on the treatment of CPP with TCM compounds,which was retrieved from the databases of CNKI,Wanfang,VIP and other databases from the establishment of the database to October 2022 as the data sources．Excel 2021 was used to collect and summarize the commonly used TCM prescriptions for CPP,and conducted frequency analysis and association rules analysis of CPP by Excel 2021,SPSS Modeler 18.0,SPSS Statistics 25.0 and other software,so as to study the composition rule of prescriptions for CPP．On the basis of these results,network pharmacology method was used to screen out the active ingredients and action targets of high-frequency drugs,and then screen out the disease related targets to construct PPI network．Mechanism of drugs was clarified through GO and KEGG pathway enrichment analysis．Finally,the molecular docking of autodock Vina（Vina）platform was used to verify the results．Results A total of 244 documents met the search criteria,including 133 prescriptions and 188 traditional Chinese medicines．It had been found that 18 high-frequency Chinese medicines were used more than 25 times．The drugs mainly focused on clearing heat and supplementing deficiency．The medicinal flavors were mainly cold and bitter,which belonged to the liver channel．Further correlation analysis yielded 14 high-frequency drug pairs and 4 core prescriptions．The results of network pharmacological analysis showed that 44 active components,200 drug targets,1 287 disease corresponding targets,70 common targets,573 GO enrichment entries and 136 KEGG pathways targets were obtained．It has been found that the main components of the drugs,such as quercetin,kaempferol and β-sitosterol,act on the core targets of ESR1,PGR and play a therapeutic role through endocrine resistance and estrogen signaling pathways．Finally,molecular docking results showed that the main active ingredients of the drug had good binding ability with the corresponding core targets．Conclusions In the treatment of CPP,traditional Chinese medicine is mainly used types of nourish Yin,clear heat and replenish deficiency,which is compatible with the drugs with cold properties,bitter and pliant taste,and the liver and spleen channels．Among them,high-frequency drug pair “ZhiMu-HuangBai” play a therapeutic role in the regulation of endocrine resistance and estrogen signaling pathways through multi-components and multi-targets．

目的 探讨柚皮素对人乳腺癌细胞株MCF-7和小鼠乳腺癌细胞系4T1的作用机制。方法 选择人乳腺癌细胞株MCF-7和小鼠乳腺癌细胞系4T1为实验对象,设置对照组和柚皮素组,其中柚皮素组分为20、40、80 和120 μmol/L 4个浓度,利用CCK-8、平板克隆形成实验检测柚皮素对乳腺癌细胞的增殖作用,应用流式细胞术检测柚皮素对乳腺癌细胞的凋亡作用。建立乳腺癌移植瘤模型,应用柚皮素作用于模型小鼠,探讨柚皮素在体内抗肿瘤作用。通过荧光定量PCR和蛋白免疫印迹实验检测自噬相关基因,分析其作用机制。结果 经柚皮素处理后,乳腺癌细胞的增殖明显受到抑制,正常乳腺癌细胞增殖情况变化不大,MCF-7乳腺癌细胞和小鼠乳腺癌4T1均出现明显的凋亡（P<0.001）。结论 柚皮素可以抑制乳腺癌细胞的增殖,且对正常乳腺细胞无明显毒副作用。柚皮素通过凋亡和自噬方式促进乳腺癌细胞的死亡,体内实验结果显示柚皮素具有抗肿瘤作用,并可促进其坏死。

目的 通过生物信息学方法,分析阿司匹林抗结直肠癌的作用机制。方法 在DrugBank 5.1.5中查找阿司匹林的直接作用蛋白靶点(direct protein targets,DPTs);构建阿司匹林DPTs的蛋白质-蛋白质相互作用(protein-protein interaction,PPI)网络并分析相关信号通路;从GEO数据库中获取结直肠癌表达谱芯片数据,筛选中心度最高的20个结直肠癌差异表达基因作为Hub基因;将DPTs相互关联基因与结直肠癌Hub基因求交集,确认阿司匹林抗结直肠癌的潜在作用靶点,分析其在TCGA数据库结肠腺癌样本中的表达情况,并进行GO功能富集分析和KEGG信号通路分析。最终通过RT-PCR和WB实验验证阿司匹林抗结直肠癌的潜在靶点。结果 在DrugBank 5.1.5中确定了11个阿司匹林DPTs,KEGG信号通路分析发现其中6个DPTs(EDNRA,IKBKB,NFKB2,NFKBIA,PTGS2,TP53)与癌症的发生发展有关。将DPTs相关联基因与筛选的20个结直肠癌Hub基因求交集,发现5个基因(CDK1,AURKA,CCNB1,MAD2L1,TPX2)可能是阿司匹林抗结直肠癌的潜在作用靶点,其在TCGA数据库结肠腺癌样本中均表达上调,基因功能主要富集于细胞周期调控。RT-PCR和WB实验结果显示阿司匹林可以降低人结肠癌细胞中CDK1,AURKA,CCNB1,MAD2L1,TPX2的mRNA水平和蛋白表达。结论 CDK1,AURKA,CCNB1,MAD2L1,TPX2可能是阿司匹林抗结直肠癌的潜在靶点,其可能通过影响细胞周期调控发挥抗肿瘤作用。

Objective To analyze the mechanism of aspirin against colorectal cancer(CRC)by bioinformatic analysis. Methods DrugBank 5.1.5 was used to identify direct protein targets (DPTs) of aspirin. The protein-protein interaction (PPI) network of DPTs was constructed and involved signaling pathways were analyzed. CRC-associated gene expression datasets were downloaded from GEO database, and the top twenty differentially expressed genes with the highest degree were screened out as Hub genes. Common genes between the genes associated with the DPTs and the Hub genes of CRC were the potential targets of aspirin against CRC. The potential targets in TCGA database colon adenocarcinoma (COAD) samples were examined. GO functional enrichment analysis and KEGG signaling pathway analysis of the potential targets were performed. The potential targets of aspirin against CRC cells were verified by reverse transcription-polymerase chain reaction (RT-PCR) and western blot (WB). Results Eleven DPTs of aspirin were identified in DrugBank 5.1.5. KEGG signaling pathway showed that 6 genes (EDNRA, IKBKB, NFKB2, NFKBIA, PTGS2, TP53) were associated with the occurrence and development of CRC. By intersecting 20 Hub genes of CRC with genes associated with the DPTs of aspirin, it was found that 5 genes (CDK1, AURKA, CCNB1, MAD2L1, TPX2) might be the potential targets of aspirin against CRC. They were all up-regulated in TCGA-COAD samples, and the gene functions were mainly enriched in cell cycle regulation. The results of RT-PCR and WB showed that aspirin could down-regulate the mRNA and protein expression levels of CDK1, AURKA, CCNB1, MAD2L1 and TPX2 in human colon cancer cells respectively. Conclusion CDK1, AURKA, CCNB1, MAD2L1 and TPX2 could be potential targets of aspirin against CRC by affecting the progress of cell cycle regulation.

目的 基于网络药理学方法预测银杏叶治疗心肌缺血的潜在靶点及信号通路。方法 利用 TCMSP 平台筛选生物利用度(OB)≥ 30% 和类药性(DL)≥ 0.18 的活性成分及作用靶点。利用GeneCards和OMIM数据库检索心肌缺血疾病相关靶点,并提取药物成分和心肌缺血疾病的共有靶点作为关键靶点。通过在线TRING平台构建PPI网络,并采用Cytoscape 软件构建可视化的“化合物-靶点-通路”网络,进一步进行GO 功能富集分析和KEGG通路富集分析。结果 筛选得到 27种潜在的药效成分,2 164个化合物靶点,531个心肌缺血相关靶基因。两者取交集后获得疾病-类药活性成分40个共同靶点,PPI 蛋白互作网络自由度较高的节点依次为:IL6、VEGFA、CASP3、MAPK8、MYC、NOS3。GO 功能富集分析得到42个 GO 条目,KEGG 通路富集分析得到42条信号通路。结论 银杏叶治疗心肌缺血主要GO 能力富集在半胱氨酸肽链内切酶活性,内肽酶活力,激活转录因子结合,DNA结合转录激活剂活性,RNA聚合酶II特异性等功能,调控TNF信号通路,糖尿病并发症的年龄愤怒信号, 细胞凋亡,PI3K-Akt信号通路等信号,进一步达到对心肌缺血疾病的治疗。

Objective To predict the potential targets and signal pathways of ginkgo leaf in the treatment of myocardial ischemia based on network pharmacology. Methods The active components and targets of bioavailability (OB) ≥ 30% and drug-like (DL) ≥ 0.18 were screened by TCMSP platform.The related targets of myocardial ischemic diseases were searched by GeneCards and OMIM database, the components and the common targets of myocardial ischemic diseases were extracted as the key targets. To build the PPI network through the online STRING platform, a visual “compound-target-pathway” network was constructed to further analyze the functional enrichment of GO and the enrichment of KEGG pathway. Results 27 potential active components, 2 164 compound targets and 531 myocardial ischemia related target genes were screened. After the intersection of the two, 40 common targets of disease-class active components were obtained. The nodes with higher degree of freedom of PPI protein interaction network were IL6、VEGFA、CASP3、MAPK8、MYC and NOS3.42 entries were obtained by GO functional enrichment analysis and 42 signal pathways were obtained by KEGG pathway enrichment analysis. Conclusion Ginkgo leaf may be a target of cysteine-type endopeptidase activity,endopeptidase activity,activating transcription factor binding,DNA-binding transcription activator activity, RNA polymerase II-specific function. TNF signaling pathway, AGE-RAGE signaling pathway in diabetic complications, apoptosis, PI3K-Akt signaling pathway were regualted to achieve the treatment of myocardial ischemia disease.

目的 利用GEPIA数据库,包括TCGA数据库和GTEX数据库,探讨二氢丹参酮I通过氧化应激治疗胃癌的潜在靶点。方法 在数据库中检索二氢丹参酮I在胃癌中潜在靶点的文献,利用GEPIA数据库工具分析二氢丹参酮I在胃癌中的潜在作用机制,分析潜在靶基因与表达关键抗氧化应激蛋白基因的相关性;二氢丹参酮I对胃癌潜在靶基因表达水平的分析;二氢丹参酮I对胃癌潜在靶基因的预后分析。结果 二氢丹参酮I对潜在靶基因的主要靶向基因(蛋白)为缺氧诱导因子-1(hif-1)和瓜氨酸组蛋白h3(cith3),其基因分别为HIF1 A和NOS2;GEPIA数据库显示HIF1 A与CAT(P=e-04,r=0.18)、GPX1(P=0.033,r=0.11)或NFE2L2呈正相关。(P=0,r=0.41),而NOS2与SOD1仅呈正相关(P=0.21,r=0.18),与其它三个基因均无相关性;HIF1 A和NOS2在胃癌组织中的表达水平高于正常胃旁组织;HIF1 A的高表达降低了胃癌患者的总生存率。结论 二氢丹参酮I可通过活性氧介导的氧化应激诱导AGS细胞凋亡,抑制HIF1 A和NOS2的表达,从而抑制AGS细胞的抗氧化应激,提高胃癌患者的总生存率。

Objective In this study, GEPIA database, including TCGA database and GTEx database, were used to explore the potential targets of dihydrotanshinone I on gastric cancer through oxidative stress. Methods Literatures on potential targets of dihydrotanshinone I in gastric cancer were searched in the database;GEPIA database tool was used to analyze the potential mechanism of dihydrotanshinone I on gastric cancer;taking analysis of the correlation between potential target genes and genes expressing key antioxidant stress proteins;We had analysis of expression level of dihydrotanshinone I on potential target genes in gastric cancer patients;and prognostic analysis of dihydrotanshinone I on potential target genes in gastric cancer patients. Results The main targeting genes(proteins) of dihydrotanshinone I on potential target genes were hypoxia inducible factor-1(hif-1) and citrulline histone H3(CITH3), whose genes were HIF1 A and NOS2, respectively;GEPIA database showed that there was a positive correlation between HIF1 A and CAT(P=2e-04, R=0.18), GPX1(P=0.033, R=0.11), or NFE2L2(P=0, R=0.41), while NOS2 only had a positive correlation with SOD1(P=0.21, R=0.18), and no correlation with other three genes. The expression levels of HIF1 A and NOS2 in gastric cancer tissues were higher than those in normal adjacent gastric tissues. The overall survival rate of patients with gastric cancer decreased with the high expression of HIF1 A. Conclusion Dihydrotanshinone I may induce apoptosis of AGS cells through reactive oxygen species mediated oxidative stress, and inhibit the expression of HIF1 A and NOS2, thus inhibit their antioxidative stress, which may improve the overall survival rate of gastric cancer patients.

目的 运用网络药理学方法预测生白术活性成分、作用靶点及生物学意义,探讨其防治便秘的作用机制,并结合导师临床应用取得的疗效进行进一步的验证。方法 借助TCMSP在线数据库查找白术的药效成份并选择其生物利用度(OB)>30%且类药性(DL)>0.18的化合物,并查询每种成分所对应的靶标。通过Gene Cards、OMIM共2个疾病相关靶点的数据库检索便秘相关靶点信息。将二者靶基因相映射获得交集靶点。借助 cytoscape 3.7.1 软件对查询结果进行可视化。所得到的基因通过相互作用数据库(STRING)进行相互作用蛋白查询并构建蛋白质相互作用(PPI)网络。使用R语言对关键靶点行GO和KEGG富集分析,以构建“成分-靶点-信号通路”的网络。结果 共得到白术人源靶蛋白7个,便秘相关的人源基因2 859个。发现其主要通过干预PGR、CHRM3、CHRM1、ACHE、CHRM2五个基因并参与胆碱能突触、钙信号通路、肌动蛋白细胞骨架的调控、神经活性配体-受体相互作用、cAMP信号通路、PI3K-AKT信号通路共6条信号通路以达到防治便秘的效果。结论 应用网络药理学方法分析预测得到重用生白术防治便秘的潜在药效成分、作用靶点及其信号通路,为临床应用提供了理论依据。

Objective To predict the active ingredients, targets and biological significance of Atractylodes macrocephala by network pharmacology, to explore the mechanism of its prevention and treatment of constipation, and to further verify its efficacy in combination with the clinical application of tutors. Methods The constituents of Atractylodes macrocephala were searched by TCMSP database and the compounds with bioavailability (OB) > 30% and drug-like property (DL) > 0.18 were screened, and the corresponding targets of each constituent were queried. Constipation-related target information was retrieved from two disease-related target databases of GeneCards and OMIM, mapping the two target genes to obtain intersecting targets, by visualization of query results with cytoscape 3.7.1. The resulting genes were queried by the interaction database (STRING) and the protein interaction (PPI) network was constructed. GO and KEGG enrichment analysis of key targets was carried out by R language in order to construct the network of “component-target-signal pathway”. Results Seven human target proteins and 2 859 constipation related human genes were obtained from Atractylodes macrocephala. It was found that the effect of prevention and treatment of constipation was mainly achieved by interfering with five genes of PGR, CHRM3, CHRM1, ACHE and CHRM2 and participating in six signaling pathways: cholinergic synapse, calcium signaling pathway, regulation of actin cytoskeleton, neuroactive ligand-receptor interaction, cAMP signaling pathway and PI3K-AKT signaling pathway. Conclusion The potential pharmacodynamic components, targets and signaling pathways of reuse Rhizoma atractylodis macrocephalae in the prevention and treatment of constipation can be predicted by network pharmacological method, which provides a theoretical basis for clinical application.

目的 探讨抗增殖蛋白2（PHB2）脓毒症心肌损伤线粒体功能的调控机制。方法 体外培养大鼠心肌细胞株（H9C2）,分为对照组、脂多糖（LPS）组、LPS+PHB2 siRNA（si-PHB2）组。检测氧化应激指标细胞内丙二醛（MDA）水平、荧光探针检测细胞内活性氧（ROS）水平;线粒体指标：三磷酸腺苷（ATP）水平、线粒体膜电位、线粒体电镜、线粒体半定量评分;免疫印迹法检测PHB2、PTEN诱导激酶1（PTNKI）、帕金蛋白（Parkin）、线粒体转录因子（TFAM）的表达。结果 LPS刺激后MDA水平和ROS水平升高、ATP水平低,LPS+si-PHB2组MDA（6.21±0.39 vs 3.59±0.33, P<0.05）、细胞内的ROS（15 131.37±88.72 vs 8 628.67±71.95, P<0.05）的水平较LPS组升高,ATP（3.46±0.34 vs 4.52±0.25, P<0.05）和线粒体膜电位水平（0.33±0.04 vs 0.55±0.09, P<0.05）进一步降低;电镜观察显示与正常组相比,LPS组、LPS+si-PHB2组出现不同程度线粒体损伤,线粒体损伤半定量评分显示LPS+si-PHB2组的损伤较LPS组更为明显（1.42±0.10 vs 0.81±0.04, P<0.05）; 免疫印迹法结果显示LPS处理后PHB2、PINK1、Parkin 表达上调,TFAM表达下调,LPS+si-PHB2组的线粒体自噬相关蛋白PINK1（1.33±0.06 vs 1.79±0.21, P<0.05）、Parkin（1.43±0.08 vs 1.86±0.09, P<0.05）和线粒体生物发生关键蛋白TFAM（0.29±0.01 vs 0.74±0.06, P<0.05）表达均较LPS组降低。结论 LPS可促进大鼠心肌细胞PHB2表达,si-PHB2干扰后线粒体自噬蛋白和生物发生蛋白表达抑制,心肌细胞氧化应激损害和线粒体功能障碍加重,提示PHB2表达上调可能恢复线粒体稳态改善脓毒症心肌损伤的线粒体功能。

Objective To explore the regulatory mechanism of septic myocardial injury by prohibitin 2（PHB2）. Methods Rat myocardial cell lines（H9C2）were cultured in vitro and divided into control group,LPS group,LPS + PHB2 siRNA（si-PHB2） group. The indicators for detecting oxidative stress include the levels of intracellular malondialdehyde（MDA）and reactive oxygen species（ROS）. The indicators for mitochondrial detection include adenosine triphosphate（ATP）levels,mitochondrial membrane potential,mitochondrial electron microscopy,and semi-quantitative mitochondrial scoring. Western blotting was used to detect the expression of PHB2,PTEN induced putative kinase（PINK1）,Parkin,mitochondrial transcription factor A（TFAM）. Results After LPS stimulation,MDA level and intracellular ROS level increased,ATP level decreased. Compared with LPS group,MDA（6. 21±0. 39 vs 3. 59±0. 33, P<0. 05）level and intracellular ROS level（15 131. 37±88. 72 vs 8 628. 67±71. 95, P<0. 05）in LPS + si-PHB2 group increased significantly,while ATP（3. 46±0. 34 vs 4. 52±0. 25, P<0. 05）and MMP（0. 33±0. 04 vs 0. 55±0. 09, P<0. 05）level further decreased. Compared with the normal group,the structure of mitochondria in LPS group and LPS + si-PHB2 group was damaged in different degree. The semi-quantitative score of mitochondrial damage showed that the damage in LPS + si-PHB2 group was more obvious than that in LPS group（1. 42±0. 10 vs 0. 81±0. 04, P<0. 05）. Western blotting showed that the expression of PHB2,PINK1 and Parkin were up-regulated and the expression of TFAM was down-regulated after LPS treatment,mitohagy-related proteins PINK1（1. 33±0. 06 vs 1. 79±0. 21, P<0. 05）,Parkin（1. 43±0. 08 vs 1. 86±0. 09, P<0. 05）and mitochondrial biogenetic protein TFAM（0. 29±0. 01 vs 0. 74±0. 06, P<0. 05）in LPS+si-PHB2 group were lower than those in LPS group. Conclusions LPS can promote the expression of PHB2 in rat cardiomyocytes. After interfering with PHB2 expression,we found that mitochondrial autophagy and biogenesis are inhibited,and mitochondrial dysfunction,oxidative stress exacerbated,suggesting that the up-regulation of PHB2 expression may restore mitochondrial homeostasis and improve mitochondrial function in septic myocardial injury.

       炎症性肠病（IBD）是一种以反复腹痛、腹泻、血便和体重降低为主要表现的慢性特发性性疾病，主要分为溃疡性结肠炎与克罗恩病两种类型。近年来，IBD的患病率随着城市化和工业化进展迅速升高，给中国和全球的公共健康带来沉重的负担。随着人类基因组技术的发展，越来越多的证据表明，遗传学因素在IBD发病过程中起着不可或缺的作用。在亚欧人群中，通过大规模全基因组关联研究现已明确了320个IBD易感基因位点。IBD易感基因在影响机体的细胞代谢、免疫功能调节、肠道上皮屏障和微生物清除等多个方面发挥着重要作用。本文就IBD相关易感基因及其多态性的研究进展进行综述，从基因层面揭示IBD发病的分子机制，并对探索IBD因人而异的个性化治疗方案提供帮助。

    Inflammatory bowel disease（IBD）is a chronic idiopathic disease characterized by recurrent abdominal pain，diarrhea，bloody stools，and weight loss．Ulcerative colitis and Crohn’s disease represent the two main types of IBD．In recent years，the prevalence of IBD has increased rapidly with the advancement of industrialization，imposing a heavy burden on public health in China and globally．Currently，with the development of genomics，a growing body of evidence suggests that genetic factors play an indispensable role in the pathogenesis of IBD．In the Eurasian population，320 IBD susceptibility gene loci have been identified through large-scale genome-wide association studies．IBD susceptibility genes play a crucial role in various aspects affecting cellular metabolism，immune function regulation，intestinal epithelial barrier，and microbial clearance．This article reviews the susceptibility genes and their polymorphisms associated with IBD，revealing the molecule mechanisms of IBD from gene perspectives and contributing to the development of personalized treatment strategies tailored to individual IBD patients．

       目的  采用网络药理学方法与分子对接技术分析白头翁汤治疗细菌性痢疾（BD）的潜在活性成分与作用机制。方法  借助中药系统药理学数据库与分析平台（TCMSP）及PubChem数据库检索筛选白头翁汤方的化学成分和作用靶点，通过Uniprot数据库校正基因名，同时通过比较毒物基因组学数据库（CTD）、药物靶标数据库（TTD）、GeneCards数据库和药物和药物靶标数据库（DRUGBANK）获得BD相关疾病靶点。经在线绘图平台微生信分析“活性成分-疾病”交集靶点，使用Cyoscape 3.7.2软件构建可视化的中药-活性成分-靶点网络、蛋白质互作网络，筛选潜在的关键活性成分与核心靶点；通过Metascape数据库对进行靶点的基因本体（GO）功能分析和京都百科全书基因和基因组通路数据库（KEGG）通路富集分析，同时使用Cyoscape 3.7.2软件构建基因-通路网络，筛选潜在的通路及其作用机制。同时采用分子对接技术对白头翁汤中关键活性成分和BD核心靶点进行分析。结果  白头翁汤共筛选出266个潜在活性成分，其中，槲皮素、β-谷甾醇、异鼠李素、异延胡索单酚碱、小檗红碱、豆甾醇等66个关键活性成分可通过肿瘤坏死因子（TNF）、白细胞介素-6（IL-6）、前列腺素内过氧化物合酶2（PTGS2）、丝氨酸/苏氨酸蛋白激酶1（AKT1）、血管内皮生长因子A（VEGFA）、V-rel网状内皮细胞病毒癌基因同源物A（RELA）、半胱氨酸天冬氨酸蛋白酶3（CASP3）、白细胞介素-8（CXCL8）、白细胞介素-1B（IL-1B）、丝裂原活化蛋白激酶1（MAPK1）、白细胞介素-10（IL-10）等33个潜在交集靶点作用于BD。GO基因功能分析共得到生物过程（BP）条目20个、细胞组成（CC）条目6个、分子功能（MF）条目9个（P＜0.01），主要涉及外部凋亡过程、细胞迁移正向调控、细胞因子受体结合、蛋白同源二聚活性、TNF受体超家族结合等生物进程。KEGG通路富集分析确定13条信号通路（P＜0.01），主要涉及癌症信号通路、白细胞介素-17（IL-17）信号通路等关键通路。分子对接结果显示槲皮素、β-谷甾醇、异鼠李素、异延胡索单酚碱等核心活性成分与TNF、IL-6、PTGS2核心靶点具有良好的结合效应（结合能＜-5 kJ/mol）。结论  白头翁汤主要通过槲皮素、β-谷甾醇等潜在的多种活性成分作用于TNF、IL-6、IL-1B、PTGS2、AKT1、VEGFA等潜在的关键靶点调控IL-17等信号通路，从而发挥治疗细菌性痢疾的作用，符合中药复方多成分、多靶标、多途径起效的显著特征。

      Objective To analyze the potential active ingredients and mechanism of Baitouweng Decoction in the treatment of bacillary dysentery（BD）by means of network pharmacology and molecular docking technology．Methods With the help of the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform（Traditional Chinese Medicine Systems Pharmacology Database，TCMSP）and PubChem database to search and screen the chemical composition and target of Baitouweng Decoction，the gene name was corrected through the Uniprot database，and the CTD database，TTD database，GeneCards database and DRUGBANK database obtain BD-related disease targets．The intersection target was obtained through the online  drawing platform，and Cytoscape 3.7.2 was used to construct a network of Pulsatilla active ingredient-component disease intersection target．The protein-protein interaction analysis of the intersection target was performed through the String database，and the Cytoscape 3.7.2 software was used for visualization．The Metascape database platform performed GO function analysis and KEGG pathway enrichment analysis on the target to predict its mechanism of action．The  key active ingredient compounds in Baitouweng Decoction were molecularly docked with the core protein in the intersection target．Results A total of 266 potential active ingredients in Baitouweng Decoction were screened，of which 66 key active ingredients such as quercetin，β-sitosterol，isorhamnetin，Isocorypalmine，berberine，stigmasterol，etc．It acts on BD through 33 potential intersection targets such as TNF，IL-6，PTGS2，AKT1，VEGFA，RELA，CASP3，CXCL8，IL-1B，MAPK1，IL-10．GO gene function analysis yielded a total of 20 biological process（BP）entries，6 cell composition（CC）entries，and 9 molecular function（MF）entries（P＜0.01），which mainly involve external apoptosis process and positive regulation of cell migration，Cytokine receptor binding，protein homodimerization activity，tumor necrosis factor receptor superfamily binding and other biological processes．KEGG pathway enrichment analysis identified 13 signal pathways（P＜0.01），mainly related to key pathways such as cancer signal pathway and IL-17 signal pathway．The results of molecular docking showed that the core active ingredients such as quercetin，β-sitosterol，isorhamnetin，Isocorypalmine and TNF，IL-6，PTGS2 core targets have good binding effects（binding energy ＜-5 KJ /mol）．Conclusions Baitouweng Decoction modulated signaling pathways involving IL-17 through its active constituents like quercetin and β-sitosterol，targeting key molecules such as TNF，IL-6，IL-1β，PTGS2，AKT1，and VEGFA，reflecting the multi-target therapeutic approach of traditional Chinese medicine．