心肌纤维化是心力衰竭等心血管疾病演化过程中的关键性病理改变，该病的进展机制依赖巨噬细胞与成纤维细胞的相互调控。现有现代医学研究证实巨噬细胞可凭借M1、M2表型极化行为介导炎症反应与组织修复过程，成纤维细胞能够分化形成肌成纤维细胞并推动细胞外基质异常沉积，两类细胞可依托TGF-β/Smad、CSF-1/CSF-1R等信号通路构建相互调控的作用网络并介导心肌纤维化恶化。中医痰瘀互结病机理论指出痰浊与瘀血可相互滋生、交织阻滞，是各类慢性迁延性疾病的关键发病基础。本文以中医痰瘀互结理论为研究切入点，剖析该病机理论与巨噬细胞、成纤维细胞交互作用的内在关联，整合现代医学关于两种细胞交互作用的现有研究成果，深入分析细胞互作在心肌纤维化发病过程中的协同机制与病理关联，旨在为心肌纤维化的中西医协同防治提供理论依据，为相关动物实验及临床应用研究筑牢研究基础。

Myocardial fibrosis is a key pathological change in the progression of cardiovascular diseases such as heart failure. The progression mechanism of this disease relies on the reciprocal regulation between macrophages and fibroblasts. Current modern medical research has confirmed that macrophages can mediate inflammatory responses and tissue repair processes through M1 and M2 phenotypic polarization behaviors, and fibroblasts can differentiate into myofibroblasts and promote abnormal extracellular matrix deposition. The two types of cells can construct a reciprocal regulatory network through signaling pathways such as TGF-β/Smad and CSF-1/CSF-1R, thereby mediating the deterioration of myocardial fibrosis. The theory of phlegm and blood stasis intermingling in traditional Chinese medicine suggests that phlegm turbidity and blood stasis can mutually generate and interweave to cause obstruction, serving as a key pathological basis for various chronic and persistent diseases. This article takes the traditional Chinese medicine theory of phlegmblood stasis intermingling as a research entry point, analyzes the intrinsic relationship between this pathological theory and the interaction of macrophages and fibroblasts, integrates existing modern medical research findings on the interaction between the two cell types, and deeply analyzes the synergistic mechanisms and pathological correlations of cellcell interactions in the pathogenesis of myocardial fibrosis. The aim is to provide a theoretical basis for the integrated traditional Chinese and Western medicine prevention and treatment of myocardial fibrosis, and also to lay a solid research foundation for related animal experiments and clinical application studies.

心肌纤维化是心力衰竭等心血管疾病演化过程中的关键性病理改变，该病的进展机制依赖巨噬细胞与成纤维细胞的相互调控。现有现代医学研究证实巨噬细胞可凭借M1、M2表型极化行为介导炎症反应与组织修复过程，成纤维细胞能够分化形成肌成纤维细胞并推动细胞外基质异常沉积，两类细胞可依托TGF-β/Smad、CSF-1/CSF-1R等信号通路构建相互调控的作用网络并介导心肌纤维化恶化。中医痰瘀互结病机理论指出痰浊与瘀血可相互滋生、交织阻滞，是各类慢性迁延性疾病的关键发病基础。本文以中医痰瘀互结理论为研究切入点，剖析该病机理论与巨噬细胞、成纤维细胞交互作用的内在关联，整合现代医学关于两种细胞交互作用的现有研究成果，深入分析细胞互作在心肌纤维化发病过程中的协同机制与病理关联，旨在为心肌纤维化的中西医协同防治提供理论依据，为相关动物实验及临床应用研究筑牢研究基础。

Myocardial fibrosis is a key pathological change in the progression of cardiovascular diseases such as heart failure. The progression mechanism of this disease relies on the reciprocal regulation between macrophages and fibroblasts. Current modern medical research has confirmed that macrophages can mediate inflammatory responses and tissue repair processes through M1 and M2 phenotypic polarization behaviors, and fibroblasts can differentiate into myofibroblasts and promote abnormal extracellular matrix deposition. The two types of cells can construct a reciprocal regulatory network through signaling pathways such as TGF-β/Smad and CSF-1/CSF-1R, thereby mediating the deterioration of myocardial fibrosis. The theory of phlegm and blood stasis intermingling in traditional Chinese medicine suggests that phlegm turbidity and blood stasis can mutually generate and interweave to cause obstruction, serving as a key pathological basis for various chronic and persistent diseases. This article takes the traditional Chinese medicine theory of phlegmblood stasis intermingling as a research entry point, analyzes the intrinsic relationship between this pathological theory and the interaction of macrophages and fibroblasts, integrates existing modern medical research findings on the interaction between the two cell types, and deeply analyzes the synergistic mechanisms and pathological correlations of cellcell interactions in the pathogenesis of myocardial fibrosis. The aim is to provide a theoretical basis for the integrated traditional Chinese and Western medicine prevention and treatment of myocardial fibrosis, and also to lay a solid research foundation for related animal experiments and clinical application studies.

冠心病是临床高发的心血管疾病，其病理核心为动脉粥样硬化，而炎症反应异常激活是推动病变进展的关键驱动力。PI3K/Akt通路通过调控炎症反应等，在CHD进程中发挥双向调节作用。现代研究表明，该通路保护性激活不足可加剧血管内皮损伤与斑块不稳定性，而炎症反应的持续又可进一步抑制PI3K/Akt通路活性，形成恶性循环。当动脉粥样斑块破裂，AMI发生后炎症级联反应放大，该通路异常激活，诱发MIRI。“荣泣卫除”出自《黄帝内经》，指营气耗损（荣泣）、卫气失守（卫除），荣卫失和则气血运行不畅、脉络瘀阻。本团队结合该理论与现代研究，认为CHD中PI3K/Akt通路介导的异常炎症反应的病理机制，与“荣泣卫除”理论内涵存在对应关系。研究发现，通过调控PI3K/Akt通路活性，抑制炎症因子激活与炎症蛋白表达，可抑制CHD发生发展进程。故本文基于“荣泣卫除”理论，系统梳理了PI3K/Akt通路介导的炎症反应在CHD中的作用及与中医病机的内在关联，总结中医药防治的研究进展，为中西医结合防治CHD提供参考依据。

Coronary heart disease is a clinically prevalent cardiovascular disease, with atherosclerosis as its core pathology. Abnormal activation of the inflammatory response is a key driving force for disease progression. The PI3K/Akt pathway exerts bidirectional regulatory effects on the progression of CHD by modulating inflammatory responses, among other functions. Modern studies indicate that insufficient protective activation of this pathway can exacerbate vascular endothelial injury and plaque instability, while persistent inflammation further suppresses PI3K/Akt pathway activity, forming a vicious cycle. Following atherosclerotic plaque rupture and the onset of AMI, the inflammatory cascade is amplified, leading to aberrant activation of this pathway and triggering MIRI. The theory of "depletion of nutritive level and exhaustion of defensive level" originates from the?Yellow Emperor's Inner Classic, referring to the depletion of nutritive level (Rong Qi) and the exhaustion of defensive level (Wei Qi), resulting in disharmony between nutritive and defensive levels, which impedes the smooth flow of Qi and blood and causes stasis in the collaterals. By integrating this theory with modern research, our team proposes a correspondence between the pathological mechanism of abnormal PI3K/Akt pathway-mediated inflammatory response in CHD and the theoretical connotation of "depletion of nutritive level and exhaustion of defensive level". Studies have found that modulating PI3K/Akt pathway activity to inhibit the activation of inflammatory factors and expression of inflammatory proteins can suppress the occurrence and progression of CHD. Therefore, based on the theory of "depletion of nutritive level and exhaustion of defensive level", this paper systematically reviews the role of the PI3K/Akt pathway-mediated inflammatory response in CHD and its intrinsic relationship with traditional Chinese medicine pathogenesis, summarizes research progress in TCM prevention and treatment, and provides a reference for the integrated traditional Chinese and Western medicine management of CHD.

扩张型心肌病（DCM）以左心室或双心室扩大并伴心肌收缩功能下降为主要特征，左心室逆重构（LVRR）可反映治疗后心室结构和功能恢复，并与患者预后改善相关。近年来，中医药联合常规西医治疗DCM的研究逐渐增多，部分研究显示其可改善左心室射血分数、左心室内径或容积、BNP或NT-proBNP、6min步行距离及生活质量等LVRR相关指标。现有证据提示，中医药可能通过改善心肌细胞损伤与能量代谢、减轻心肌纤维化与细胞外基质重塑、调节神经内分泌激活与心室负荷等环节参与DCM患者左心室结构重塑改善和收缩功能恢复，从而促进LVRR。然而，现有研究对LVRR的判定标准尚未统一，相关临床证据仍需进一步规范和验证。鉴于此，本文旨在围绕DCM-LVRR的概念、评价指标、中医药临床证据及可能机制进行叙述性综述，以期为DCM的中西医结合治疗及后续临床研究设计提供参考。

Dilated cardiomyopathy (DCM) is mainly characterized by left ventricular or biventricular dilatation accompanied by impaired myocardial systolic function. Left ventricular reverse remodeling (LVRR) reflects the recovery of ventricular structure and function after treatment and is associated with improved prognosis. In recent years, studies on traditional Chinese medicine (TCM) combined with conventional Western medical therapy for DCM have gradually increased. Some studies have shown that such combined treatment may improve LVRR-related indicators, including left ventricular ejection fraction, left ventricular diameter or volume, BNP or NT-proBNP, 6-minute walking distance, and quality of life. Current evidence suggests that TCM may contribute to left ventricular structural remodeling and systolic functional recovery in patients with DCM by alleviating myocardial cell injury, improving energy metabolism, attenuating myocardial fibrosis and extracellular matrix remodeling, and modulating neuroendocrine activation and ventricular load, thereby promoting LVRR. However, the criteria for defining LVRR remain inconsistent across existing studies, and the relevant clinical evidence requires further standardization and validation. Therefore, this narrative review aims to summarize the concept, evaluation indicators, clinical evidence of TCM, and potential mechanisms related to DCM-LVRR, with the aim of providing a reference for integrated Chinese and Western medical treatment of DCM and the design of future clinical studies.

扩张型心肌病（DCM）以左心室或双心室扩大并伴心肌收缩功能下降为主要特征，左心室逆重构（LVRR）可反映治疗后心室结构和功能恢复，并与患者预后改善相关。近年来，中医药联合常规西医治疗DCM的研究逐渐增多，部分研究显示其可改善左心室射血分数、左心室内径或容积、BNP或NT-proBNP、6min步行距离及生活质量等LVRR相关指标。现有证据提示，中医药可能通过改善心肌细胞损伤与能量代谢、减轻心肌纤维化与细胞外基质重塑、调节神经内分泌激活与心室负荷等环节参与DCM患者左心室结构重塑改善和收缩功能恢复，从而促进LVRR。然而，现有研究对LVRR的判定标准尚未统一，相关临床证据仍需进一步规范和验证。鉴于此，本文旨在围绕DCM-LVRR的概念、评价指标、中医药临床证据及可能机制进行叙述性综述，以期为DCM的中西医结合治疗及后续临床研究设计提供参考。

Dilated cardiomyopathy (DCM) is mainly characterized by left ventricular or biventricular dilatation accompanied by impaired myocardial systolic function. Left ventricular reverse remodeling (LVRR) reflects the recovery of ventricular structure and function after treatment and is associated with improved prognosis. In recent years, studies on traditional Chinese medicine (TCM) combined with conventional Western medical therapy for DCM have gradually increased. Some studies have shown that such combined treatment may improve LVRR-related indicators, including left ventricular ejection fraction, left ventricular diameter or volume, BNP or NT-proBNP, 6-minute walking distance, and quality of life. Current evidence suggests that TCM may contribute to left ventricular structural remodeling and systolic functional recovery in patients with DCM by alleviating myocardial cell injury, improving energy metabolism, attenuating myocardial fibrosis and extracellular matrix remodeling, and modulating neuroendocrine activation and ventricular load, thereby promoting LVRR. However, the criteria for defining LVRR remain inconsistent across existing studies, and the relevant clinical evidence requires further standardization and validation. Therefore, this narrative review aims to summarize the concept, evaluation indicators, clinical evidence of TCM, and potential mechanisms related to DCM-LVRR, with the aim of providing a reference for integrated Chinese and Western medical treatment of DCM and the design of future clinical studies.

       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．

       纤毛是细胞表面的重要细胞器，广泛参与细胞运动、感知外界信号和维持器官功能等生理过程。纤毛的形成，即纤毛发生（ciliogenesis）是一个高度复杂且受精密调控的过程，涉及大量与纤毛结构和功能相关基因的表达与调控。近年来，随着基因组学和发育生物学的发展，越来越多的研究揭示了多种关键转录因子在纤毛发生中的调控作用，包括RFX家族、FOXJ1、MCIDAS、GEMC1、MYB、E2F等。这些转录因子共同构成了一个多层次、多通路交织的调控网络，调控纤毛组装、基体复制、纤毛定位和功能维持等多个方面。本文系统综述了纤毛相关基因转录调控的研究进展，特别是关键转录因子的功能、相互作用及其在纤毛病中的作用，为深入理解纤毛的发育机制和疾病治疗提供参考。

       Cilia are crucial cell-surface organelles involved in cell movement，signal sensing，and organ function maintenance．Their formation，or ciliogenesis，is a complex and  precisely controlled  process that  requires the expression and regulation of numerous cilia-related genes．Recent advances in genomics and developmental biology have uncovered the  regulatory roles of key transcription factors like the RFX family，FOXJ1，MCIDAS，GEMC1，MYB，and E2F in ciliogenesis．These factors form a multi-level，interconnected regulatory network that oversees cilium assembly，basal body replication，ciliary positioning，and function preservation．This review systematically examines current research on transcriptional regulation of ciliary genes，with a focus on the roles，interactions，and contributions of these key transcription factors to ciliopathies，offering insights into ciliary development and disease treatment．

目的 探讨长链非编码核糖核酸肺腺癌转移相关转录本 1（LncMALAT1）通过竞争性结合微小RNA-506-3p（miR-506-3p）调控Zeste同源物增强子2（EZH2）影响膀胱癌增殖的机制。方法 收集2023年1月—2024年10月的92例外科手术切除的膀胱癌组织及对应的癌旁组织标本, 利用Western blot和定量实时逆转录聚合酶链式反应（qRT-PCR）方法检测LncMALAT1和EZH2的表达情况。根据患者预后分为不良组（n=34）和良好组（n=58）, 收集患者的性别、年龄、肿瘤直径、血管侵袭情况、TNM分期、远处转移情况等临床指标, 结合临床病理指标分析LncMALAT1和EZH2与膀胱癌患者预后的关系。通过体外实验,包括qRT-PCR、Western blot、平板克隆和EdU实验,验证LncMALAT1对EZH2表达和膀胱癌细胞增殖的影响。利用生物信息学技术预测LncMALAT1与miR-506-3p的相互作用,并通过qRT-PCR验证在膀胱癌细胞中上调LncMALAT1表达后miR-506-3p的表达变化。结果 单因素结果显示, 血管侵袭情况、TNM分期、远处转移情况、LncMALAT1及EZH2表达水平均与膀胱癌患者预后不良有关, 差异有统计学意义（均P<0.05）。分析结果发现LncMALAT1与EZH2在膀胱癌组织中的表达呈正相关。体外实验结果显示, 上调LncMALAT1表达后, EZH2的表达显著上调, 且膀胱癌细胞的增殖能力显著提高（均P<0.05）。qRT-PCR验证表明,上调LncMALAT1表达后,miR-506-3p的表达显著下调（P<0.05）, 提示LncMALAT1通过竞争性结合miR-506-3p调控EZH2,进而影响膀胱癌细胞的增殖进展。结论 LncMALAT1通过竞争性结合miR-506-3p调控EZH2促进膀胱癌增殖功能,进而加快膀胱癌细胞的增殖进展, 可为膀胱癌的治疗提供新的潜在靶点。

Objective To explore the mechanism of long non-coding ribonucleic acid metastasis - associated lung adenocarcinoma transcript 1（LncMALAT1）regulating enhancer of Zeste homolog 2（EZH2）through competitive combination with microRNA-506-3p（miR-506-3p）to affect the proliferation of bladder cancer．Methods A total of 92 pairs of bladder cancer tissues and corresponding adjacent normal tissues were collected from surgical resections between January 2023 and October 2024．The expression levels of LncMALAT1 and EZH2 were detected using Western blot and qRT-PCR．The patients were divided into poor group（n=34）and good group（n=58）according to their prognosis．Clinical data, such as gender, age, tumor diameter, vascular invasion, TNM stage, and distant metastasis were collected, and the relationship between LncMALAT1 and EZH2 and the prognosis of bladder cancer patients was analyzed with clinical pathological indicators．Through in vitro experiments, including qRT-PCR Western blot, plate cloning and EdU experiment were conducted to verify the effect of LncMALAT1 on EZH2 expression and bladder cancer cell proliferation．Bioinformatics technology was used to predict the interaction between LncMALAT1 and miR-506-3p, and qRT-PCR was used to verify the change of miR-506-3p expression after up regulating LncMALAT1 expression in bladder cancer cells．Results The univariate results showed that vascular invasion, TNM stage, distant metastasis, LncMALAT1 and EZH2 expression levels were related to the poor prognosis of bladder cancer patients, and the difference was statistically significant（all P<0.05）．The results showed that the expression of LncMALAT1 and EZH2 in bladder cancer was positively correlated．In vitro experiment results showed that after up regulating LncMALAT1 expression, EZH2 expression was significantly up-regulated, and the proliferation ability of bladder cancer cells was significantly improved（all P<0.05）．QRT-PCR validation showed that the expression of miR-506-3p was significantly down regulated after the expression of LncMALAT1 was up-regulated（P<0.05）, suggesting that LncMALAT1 could regulate EZH2 through competitive combination with miR-506-3p, thereby affecting the proliferation and progression of bladder cancer cells．Conclusions LncMALAT1 can promote the proliferation of bladder cancer cells by competitively combining with miR-506-3p to regulate EZH2, and then accelerate the proliferation of bladder cancer cells, which can provide a new potential target for the treatment of bladder cancer．

目的 探讨非编码长链 RNA ANRIL（lncRNA-ANRIL）通过调控miR‐181b 介导磷酸酶及张力蛋白同源物基因（PTEN）对冠状动脉粥样硬化性心脏病（冠心病）心肌损伤影响的机制。方法 纳入2023年10月—2024年6月广州市第一人民医院30例确诊为冠心病的患者为观察组, 另选择同期本院体检中心30名健康者为对照组,检测两组研究者血压指标、血脂指标以及血清 lncRNA-ANRIL、miR-181b、PTEN水平, 并比较检测结果。结果 两组的性别、年龄、BMI、吸烟、高血压一般资料对比差异无统计学意义（P>0.05）; 观察组收缩压、舒张压水平以及总胆固醇、甘油三酯、低密度脂蛋白胆固醇水平均高于对照组,而高密度脂蛋白胆固醇则低于对照组（P<0.05）; 观察组血清 lncRNA ANRIL Exon 1-2、lncRNA ANRIL Exon 17-18相对表达水平以及PTEN水平低于对照组（t=12.623、7.741、8.231, P=0.001）, 而miR-181b水平则高于对照组（t=37.250, P=0.001）。结论 相较于正常人群, 冠心病患者血清lncRNA-ANRIL和PTEN水平明显降低,而miR-181b水平升高,提示lncRNA-ANRIL可通过调控miR-181b来调节PTEN的表达, 从而影响冠心病心肌损伤的过程。

Objective To explore the mechanism of competitive binding of non coding long stranded RNA ANRIL（lncRNA-ANRIL）to miR-181b to mediate phosphatase and tensin homolog gene（PTEN）on myocardial injury in coronary heart disease．Methods Thirty patients diagnosed with coronary heart disease in our hospital from October 2023 to June 2024 were included as the observation group,and another 30 individuals from physical examination center during the same period were selected as the control group．Blood pressure indicators,blood lipid indicators, and serum levels of lncRNA-ANRIL, miR-181b, and PTEN were measured in the two groups of patients, and the test results were compared．Results There was no significant difference between the two groups in terms of gender, age, BMI, smoking and hypertension（P>0.05）．The levels of systolic blood pressure（SBP）, diastolic blood pressure（DBP）, total cholesterol（TC）, triglycerides（TG）, and low-density lipoprotein cholesterol（LDL-C） in the observation group were higher than those in the control group,while high-density lipoprotein cholesterol（HDL-C） was lower than that in the control group（P<0.05）．The relative expression levels of lncRNA-ANRIL Exon 1-2, Exon 17-18, and PTEN levels in the observation group were lower than those in the control group（t=12.623, 7.741, 8.231, P=0.001）, while the level of miR-181b was higher than that in the control group（t=37.250, P=0.001）．Conclusions Compared with healthy individuals, serum levels of lncRNA-ANRIL and PTEN are significantly reduced in patients with coronary heart disease, while miR-181b levels are elevated, indicating that lncRNA ANRIL can regulate PTEN expression by miR-181b, thereby affecting the process of myocardial injury in coronary heart disease．

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．