ObjectiveAlthough tea and its bioactive constituents, particularly epigallocatechin gallate (EGCG), demonstrate promising anti-liver fibrotic potential, the global research landscape has yet to be systematically characterized through quantitative visualization, leaving research priorities and clinical translational barriers unclear. This bibliometric analysis aims to delineate the current status, emerging hotspots, and developmental trends in tea-related liver fibrosis research, providing strategic insights for future studies.MethodsA dual-database search with reciprocal verification was conducted in the Web of Science Core Collection (WoSCC) and Scopus using refined search strategies. Bibliometric analyses and visualizations were performed using R (v4.5.1), VOSviewer (v1.6.19), and CiteSpace (v6.4.R1).ResultsAnnual publication output in this field has increased steadily. China led in publications (n = 120), with Nutrients and Frontiers in Pharmacology as the leading journals. Tea bioactives exert anti-fibrotic effects through: (1) molecular mechanisms, including inhibition of hepatic stellate cell activation via TGF-β/Smad, Nrf2, NF-κB, AMPK, and MAPK pathways; (2) gut-liver axis modulation, such as intestinal microbiota remodeling, bile acid homeostasis restoration, and barrier integrity enhancement; (3) synergistic effects with other natural products; and (4) epidemiological evidence showing that regular tea/caffeine intake reduces fibrosis progression, cirrhosis, and hepatocellular carcinoma risk. However, EGCG clinical translation is limited by poor solubility, environmental instability, rapid clearance, low oral bioavailability, and dose-dependent hepatotoxicity. Nano-delivery systems and structural modifications have been developed to enhance its bioavailability.ConclusionThis study elucidates the therapeutic potential of tea and its bioactive constituents against liver fibrosis, encompassing their pharmacological mechanisms, emerging molecular targets, and bioavailability enhancement strategies. With advances in nanomedicine and pharmaceutical technologies, coupled with rigorously designed multicenter randomized controlled trials, tea-derived bioactives are anticipated to overcome current limitations and establish clinical value in liver fibrosis prevention and adjuvant therapy.

Hepatocellular carcinoma (HCC) represents a significant challenge in oncology, particularly in regions with high hepatitis B virus (HBV) prevalence. Traditional Chinese Medicine (TCM), with its multifaceted therapeutic approaches, offers promising avenues for HCC treatment. This study focused on Bielong Ruangan Decoction (BLRGD) and identified pentadecylic acid as a principal active compound through network pharmacological analyses. Our research demonstrated that pentadecylic acid significantly reduced the aggressiveness of HCC and HBV-related HCC cells by inhibiting cell viability, DNA synthesis, and cell migration, and by inducing apoptosis in both animal and cell models. Further analysis revealed Peroxisome Proliferator-Activated Receptor Delta (PPARD) as a crucial downstream target, with pentadecylic acid downregulating its expression. Additionally, pentadecylic acid was found to modulate the JAK2/STAT3 pathway, a key regulator in HCC progression. Collectively, our findings underscore the therapeutic potential of pentadecylic acid from BLRGD in HCC treatment, highlighting the integration of TCM into contemporary cancer management strategies.

This study aimed to systematically analyze the research status, hotspots, and trends of oncolytic virotherapy (OV) for hepatocellular carcinoma (HCC) from 2000 to mid-2025, scientifically predict future directions, facilitate clinical translation, and provide a reference for subsequent studies in this field. Based on the Web of Science Core Collection and Scopus databases, bibliometric methods were adopted combined with visualization analyses using R software (version 4.5.1), VOSviewer (version 1.6.19), and CiteSpace (version 6.4.R1). A total of 341 publications were retrieved from the WoSCC database and 624 from the Scopus database. Based on the combined analysis of both databases, the field exhibited a continuous upward trend in publication output. The top four countries in both databases were China, the USA, Germany, and Korea. China ranked first globally with 152 publications in WoSCC and 212 in Scopus, but its international co-authorship rates (13.2% and 17.5%, respectively) were markedly lower than those of the USA (34.4% and 34.9%) and Korea (40.0% and 33.3%). Molecular Therapy is the most influential core journal in this field. Research hotspots focus on four main areas: the mechanisms of oncolytic virus therapy for HCC, the evolution of genetically engineered armed vectors, combination therapies involving oncolytic viruses, and the challenges and breakthroughs in clinical translation. Future advances in this field will likely focus on three key directions: (1) optimizing transgene expression to balance antiviral and antitumor immunity; (2) developing personalized therapeutic strategies based on biomarkers such as immune cell subsets; (3) advancing clinical validation and regulatory approval of combination regimens through multicenter clinical studies. OV for HCC has entered a new integrated stage featuring mechanistic innovation, vector optimization, and precise combination therapy. The clear future directions can provide a well-defined roadmap for clinical translation, which is expected to yield more effective novel therapeutic strategies for HCC.

Quercetin is a natural plant flavonoid that has various biological properties. It is widely found in many fruits, vegetables, and Chinese herbs. Accumulating studies have demonstrated its significant inhibitory effects on liver cancer progression, mainly by inducing tumor cell apoptosis and inhibiting tumor cell proliferation, migration, and invasion. Furthermore, combination therapies incorporating quercetin have been shown to reduce multidrug resistance and potentiate anticancer efficacy. However, the clinical application of quercetin remains challenging due to its poor water solubility and low oral bioavailability. Current research efforts are primarily directed toward developing nano-delivery systems to overcome these pharmacological limitations. Before clinical implementation, systematic safety evaluations must be conducted to ensure therapeutic feasibility. This review comprehensively summarizes recent advances in quercetin-based liver cancer therapeutics, including mechanistic studies, clinical trial developments, nano-delivery system innovations, and safety assessments, and the related mechanisms of quercetin in the field of Traditional Chinese Medicine are summarized, aiming to provide the theoretical basis for the subsequent in-depth mechanism research and clinical development and application.

Hepatocellular carcinoma (HCC) is a malignant tumor of the liver. Treatment programs according to its physiological and pathological characteristics have reduced the number of new cases and deaths of HCC, but the morbidity and mortality are still high, posing a significant threat to human health. In recent years, the importance of mitophagy in the treatment of HCC has gradually been recognized. The activation of mitophagy inhibits the survival, proliferation and migration of HCC cells through a variety of pathways, promotes cell apoptosis, and can also reduce drug resistance, providing a new direction for the treatment of HCC. Studies have shown that Traditional Chinese medicine (TCM) monomers and their derivatives can improve the therapeutic efficacy of HCC and slow down disease progression by regulating mitophagy. This article summarizes the potential mechanism of mitophagy in the progression of HCC and comprehensively explores the potential of TCM monomers and their derivatives in the treatment of HCC, providing new perspectives and strategies for clinical treatment.

Chronic, unresolved inflammation correlates with persistent hepatic injury and fibrosis, ultimately progressing to hepatocellular carcinoma (HCC). Bisdemethoxycurcumin (BDMC) demonstrates therapeutic potential against HCC, yet its mechanism in preventing hepatic "inflammation-carcinoma transformation" remains incompletely understood. In the current research, clinical HCC specimens underwent analysis using hematoxylin-eosin (H&E) staining and immunohistochemistry (IHC) to evaluate the expression of fibrosis markers, M2 macrophage markers, and CXCL12. In vitro, transforming growth factor-β1 (TGF-β1)-induced LX-2 cells and a co-culture system of LX-2, THP-1, and HCC cells were established. Cell functions underwent assessment through 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), flow cytometry, and Transwell assays. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR), Western blotting and immunofluorescence evaluated the differential expression of molecules. The interaction between β-catenin/TCF4 and CXCL12 was examined using co-immunoprecipitation (Co-IP), dual luciferase, and chromatin immunoprecipitation (ChIP) assays. A DEN-induced rat model was developed to investigate BDMC's role in liver fibrosis-associated HCC (LFAHCC) development in vivo. Our results showed that clinical HCC tissues exhibited elevated fibrosis and enriched M2 macrophages. BDMC delayed liver fibrosis progression to HCC in vivo. BDMC inhibited the inflammatory microenvironment induced by activated hepatic stellate cells (HSCs). Furthermore, BDMC suppressed M2 macrophage-induced fibrosis and HCC cell proliferation and metastasis. Mechanistically, BDMC repressed TCF4/β-catenin complex formation, thereby reducing CXCL12 transcription in LX-2 cells. Moreover, CXCL12 overexpression reversed BDMC's inhibitory effect on macrophage M2 polarization and its mediation of fibrosis, as well as HCC proliferation and metastasis. BDMC significantly suppressed LFAHCC development through CXCL12 in rats. In conclusion, BDMC inhibited LFAHCC progression by reducing M2 macrophage polarization through suppressing β-catenin/TCF4-mediated CXCL12 transcription.

BACKGROUND:Huangjia Ruangan Granules (HRG) has shown promising therapeutic effects in treating hepatic fibrosis in China. This study aimed to assess its specific efficacy. METHODS:This 48-week phase II study was a multicenter, randomized, double-blind, placebo-controlled trial conducted at 14 centers in China (No. ChiCTR2400086796). patients with chronic hepatitis B (CHB) and an Ishak fibrosis score between 2 to 5 were eligible for inclusion. Patients were randomly assigned to three groups (1:1:1 ratio): ETV (0.5 mg/day) + HRG-10g (10g/day, once daily), ETV (0.5 mg/day) + HRG-20g (10 g, twice daily), and ETV (0.5 mg/day) + placebo. The primary outcome was the change in fibrosis stage according to the Ishak scale. Safety assessments were conducted throughout the trial. RESULTS:A total of 240 participants were randomly allocated to three treatment groups: ETV+HRG-10g (n=80), ETV+HRG-20g (n=79), or ETV+placebo (n=80). After 48 weeks, the ETV+HRG-20g group showed a significantly higher fibrosis regression rate (≥1 stage improvement in histopathology) was in the compared to both the ETV+HRG-10g group (67.09 % vs. 36.25 %; 95 % CI, 15.81-45.6) and the ETV+placebo group (67.09 % vs. 26.25 %; difference, 40.69 %; 95 % CI, 26.55-54.83). CONCLUSIONS:Combining a 20g dose of the TCM formula HRG with ETV significantly enhances liver fibrosis regression in CHB patients.

To explore the current status and future development of photodynamic therapy (PDT) for hepatocellular carcinoma (HCC). However, this field lacks a comprehensive bibliometric analysis. This study aims to investigate the research content and hotspots in PDT for liver cancer from 2012 to 2025, and to predict future research directions, providing references for subsequent studies. We chose the Web of Science Core Collection (WoSCC) database and retrieved articles published in the field between 2012 and 2025. Bibliometric and visualization analyses were performed using R (version 4.4.1), VOSviewer (version 1.6.19), and CiteSpace (version 6.4. R1). A total of 547 papers were included. We found that the number of publications in this field has steadily increased from 2012 to 2025. China leads with the highest number of publications, followed by the USA, Korea, Germany, and Japan. China has the lowest international co-authorship rate, while Germany and Japan show higher international collaboration rates. The International Journal of Nanomedicine is the most popular journal for publication, whereas Biomaterials ranks first in terms of citations. Our analysis of keywords and the most cited references revealed that current research focuses on the mechanism of PDT-induced apoptosis in HCC, the development of photosensitizers (PSs), nanotechnology-enhanced PDT, and synergistic treatment of HCC with PDT and other therapies. Nanotechnology and multimodal synergistic therapeutic strategies are driving the treatment of HCC. PDT, as a therapy for HCC, is expected to become a research hotspot. This paper analyzes PDT's current research for HCC, offering references for future research in related fields.

The present study aimed to investigate the effect and mechanism of Bupleuri Radix-Paeoniae Radix Alba medicated plasma on HepG2 hepatoma cells by regulating the microRNA-1297(miR-1297)/phosphatase and tensin homologue deleted on chromosome 10(PTEN) signaling axis. Real-time quantitative PCR(RT-qPCR) was carried out to determine the mRNA levels of miR-1297 and PTEN in different hepatoma cell lines. The dual luciferase reporter assay was employed to verify the targeted interaction between miR-1297 and PTEN. The cell counting kit-8(CCK-8) was used to detect cell proliferation, and the optimal concentration and intervention time of the medicated plasma were determined. The cell invasion and migration were examined by Transwell assay and wound healing assay. Cell cycle distribution was detected by PI staining, and the apoptosis of cells was detected by Annexin V-FITC/PI double staining. The mRNA levels of miR-1297, PTEN, protein kinase B(Akt), and phosphatidylinositol 3-kinase(PI3K) were determined by RT-qPCR. Western blot was employed to determine the protein levels of PTEN, Akt, p-Akt, caspase-3, caspase-9, B-cell lymphoma-2(Bcl-2), and Bcl-2-associated X protein(Bax). The results showed that HepG2 cells were the best cell line for subsequent experiments. The dual luciferase reporter assay confirmed that miR-1297 could bind to the 3'-untranslated region(3'UTR) in the mRNA of PTEN. The medicated plasma inhibited the proliferation of HepG2 cells, and the optimal intervention concentration and time were 20% and 72 h. Compared with the blank plasma, the Bupleuri Radix-Paeoniae Radix Alba medicated plasma, miR-1297 inhibitor, miR-1297 inhibitor + medicated plasma all inhibited the proliferation, invasion, and migration of HepG2 cells, increased the proportion of cells in the G_0/G_1 phase, decreased the proportion of cells in the S phase, and increased the apoptosis rate. The medicated plasma down-regulated the mRNA levels of miR-1297, PI3K, and Akt and up-regulated the mRNA level of PTEN. In addition, it up-regulated the protein levels of PTEN, Bax, caspase-3, and caspsae-9 and down-regulated the protein levels of p-Akt, p-PI3K, and Bcl-2. In conclusion, Bupleuri Radix-Paeoniae Radix Alba medicated plasma can inhibit the expression of miR-1297 in HepG2 hepatoma cells, promote the expression of PTEN, and negatively regulate PI3K/Akt signaling pathway, thereby inhibiting the proliferation and inducing the apoptosis of HepG2 cells.

OBJECTIVE:This study investigated how Radix Bupleuri-Radix Paeoniae Alba (BP) was active against hepatocellular carcinoma (HCC). METHODS:Traditional Chinese medicine systems pharmacology (TCMSP) database was employed to determine the active ingredients of BP and potential targets against HCC. Molecular docking analysis verified the binding activity of PTEN with BP ingredients. H22 cells were used to establish an HCC model in male balb/c mice. Immunofluorescence staining, immunohistochemistry, flow cytometry, western blotting, enzyme-linked immunosorbent assay, and real-time quantitative PCR were used to study changes in proliferation, apoptosis, PTEN levels, inflammation, and T-cell differentiation in male balb/c mice. RESULTS:The major active ingredients in BP were found to be quercetin, kaempferol, isorhamnetin, stigmasterol, and beta-sitosterol. Molecular docking demonstrated that these five active BP ingredients formed a stable complex with PTEN. BP exhibited an anti-tumor effect in our HCC mouse model. BP was found to increase the CD8+ and IFN-γ+/CD4+ T cell levels while decreasing the PD-1+/CD8+ T and Treg cell levels in HCC mice. BP up-regulated the IL-6, IFN-γ, and TNF-α levels but down-regulated the IL-10 levels in HCC mice. After PTEN knockdown, BP-induced effects were abrogated. CONCLUSION:BP influenced the immune microenvironment through activation of the PTEN/PD-L1 axis, protecting against HCC.

Background and Aims: The application of antifibrotic drugs to treat patients with chronic liver diseases who are receiving antiviral therapies for hepatocellular carcinoma (HCC) has not been established. Here, we aimed to assess the impact of the Traditional Chinese Medicine Fuzheng Huayu (FZHY) on the occurrence of HCC in patients with hepatitis B virus-related compensated cirrhosis receiving the antiviral drug entecavir (ETV). Methods: A multicenter retrospective cohort study was performed. Compensated liver cirrhosis patients were divided into the ETV+FZHY group or the ETV group according to treatment. The cumulative incidence of HCC was analyzed using Kaplan-Meier and log-rank tests. Propensity score matching was used for confounding factors. Stratified analysis and Cox regression were used to determine the effects of FZHY on the occurrence of HCC and liver function decompensation. Results: Out of 910 chronic hepatitis B patients, 458 were in the ETV+FZHY group and 452 were in the ETV group. After propensity score matching, the 5-year cumulative incidence of HCC was 9.8% in the ETV+FZHY group and 21.8% in the ETV group (p<0.01). The adjusted hazard ratio for HCC was 0.216 (0.108, 0.432) when FZHY treatment was >36 months. Age, diabetes, alanine aminotransferase, gamma-glutamyl transpeptidase, albumin, hepatitis B e-antigen, and fibrosis 4 score were associated with the occurrence of HCC. FZHY decreased the risk of HCC in patients aged >45 years with a hepatitis B virus DNA level of >= 2,000 IU/l. Conclusion: Adjunctive FZHY treatment reduced HCC occurrence in patients with hepatitis B virus cirrhosis who were treated with ETV, possibly due to the antifibrotic properties of FZHY.

目的:研究芍药苷对转化生长因子-β1(TGF-β1)诱导的肝星状细胞株LX-2活化及自噬的影响,初步探讨芍药苷抗肝纤维化的作用机制.方法:采用不同浓度芍药苷分别作用于LX-2及TGF-β1诱导的LX-2细胞,用MTT法检测芍药苷对细胞活力、细胞增殖的影响,选出最合适的芍药苷干预浓度;采用流式细胞学实验及MTT法检测芍药苷对细胞凋亡及增殖的影响;蛋白免疫印迹法检测芍药苷对细胞α-平滑肌肌动蛋白(α-SMA)、LC3-Ⅰ/Ⅱ、Beclin 1、Atg5、趋化因子CXC配体2(CXCL12)、趋化因子受体4(CXCR4)、β-catenin蛋白水平的变化;ELISA法检测芍药苷对细胞炎症因子TNF-α、CXCL12、IL-1β、IL-6的影响.结果:芍药苷能抑制TGF-β1诱导的LX-2细胞的活性及生存率(P<0.05).芍药苷能促进LX-2细胞的凋亡,抑制LX-2细胞的增殖;与对照组相比,TGF-β1诱导的LX-2细胞α-SMA、LC3-Ⅰ/Ⅱ、Beclin 1、Atg5、CXCL12、CXCR4、β-catenin蛋白水平及TNF-α、CXCL12、IL-1β、IL-6水平明显增加(P<0.05),而芍药苷预处理能逆转上述效应(P<0.05).TGF-β1能促进LX-2细胞炎症因子TNF-α、CXCL12、IL-1β、IL-6的表达(P<0.05),而芍药苷预处理能抑制上述炎症因子的表达水平(P<0.05).结论:芍药苷能抑制TGF-β1诱导的肝星状细胞活化及自噬水平.

文章考证鳖甲历代演变过程,为其临床应用及新药开发提供参考.通过检索网络数据平台及实地查阅文献等途径对古籍记载的鳖甲别名、基原、产地、品质、性能、采收炮制、功效主治、使用注意等方面进行系统梳理及分析.经考证可知,鳖甲别名多由鳖的别称或俗名加之背甲特点得来.基原上,中华鳖的背甲是唯一来源.鳖甲道地产区在邻长江水系的两湖地区.品质上,古代多以肋数评价鳖甲品质,现不建议将肋数作为评价标准.古籍记载其性味多为咸平.炮制上,净制鳖甲需注意不用"煮脱者",炮制辅料中醋占主导.基于考证结果,建议应用涉及鳖甲时选取中华鳖为基原,依功效更其性能为咸微寒,净制鳖甲不用"煮脱者".

目的:研究温法干预对HBV相关慢加急性肝衰竭(HBV-ACLF)阳黄证患者外周血树突状细胞(DC)功能的影响.方法:分别选取8例HBV-ACLF阳黄证患者作为阳黄组和8名健康对照者,收集两组人员外周抗凝血,体外诱导培养成成熟的DCs.将两组人员的DCs细胞分为5组:正常组、模型组、温法干预组、去温法干预组和空白组.并用大鼠温阳解毒化瘀方(温法)及温阳解毒化瘀方减附子、白术方(去温法)含药血清干预模型组(HBV-ACLF阳黄证患者)DCs.流式细胞仪分析DCs表面CD80、CD86、CD83、HLA-DR表达及平均荧光强度;ELISA法检测DCs分泌细胞因子IL-12、IL-6、IL-10水平;混合淋巴细胞反应(MLR)检测DCs对T淋巴细胞增殖的影响.结果:与正常组DCs比较,模型组DCs表面CD80、CD86、CD83、HLA-DR表达及平均荧光强度明显降低,DCs分泌细胞因子IL-12、IL-10显著减少,IL-6增多,促T淋巴细胞增殖功能下降(P<0.01);与模型组比较,温法干预组DCs表面CD80、CD86、CD83、HLA-DR表达及平均荧光强度显著升高,DCs分泌细胞因子IL-12、IL-10显著增多,IL-6减少,促T淋巴细胞增殖功能提高.结论:温法干预能明显提高HBV-ACLF阳黄证患者外周血DCs细胞功能,有利于清除HBV病毒、恢复患者紊乱的免疫功能.

慢性乙型肝炎(CHB)是一种全球性的传染性疾病,全世界估计有2.92亿人感染乙型肝炎病毒(HBV)[1],全球每年有超过88万人死于CHB导致的终末期肝病[2].目前西医治疗有多种手段,如:干扰素α(IFNα)、聚乙二醇干扰素α(PEG-IFNα)、核苷类似物(NAs)等[3],近十几年来,IFNα、NAs抗病毒治疗研究取得了令人瞩目的进展,但在经历快速发展之后,相关研究步伐明显减缓,当前正面临着抗病毒治疗发展的"瓶颈"[4-7].中医治疗CHB是目前研究的热点之一,补肾、健脾为主的中药复方在改善机体免疫状态,恢复和提高免疫细胞功能,重建免疫应答方面具有较好的作用[8-10].孙克伟教授结合CHB患者的临床特点以及在多年诊疗工作中积累的经验,提出"补肾解毒法"的学术思想,用以治疗肾虚湿毒型CHB,本文就此思想进行理论探讨.

目的:研究苯甲酰乌头原碱(Benzoylaconine,BAC)对HBV相关慢加急性肝衰竭(HBV related acute-on-chronic liver failure,HBV-ACLF)阳黄证和阴黄证患者外周血树突状细胞(dendritic cells,DCs)功能的影响.方法:体外诱导培养HBV-ACLF阳黄证与阴黄证患者DCs,CCK-8法检测BAC安全用药范围,流式检测BAC干预HBV-ACLF阳黄证与阴黄证患者DCs表面CD80、CD86、CD83和HLA-DR表达率变化情况,ELISA法检测DCs分泌IL-12水平.结果:与健康对照组比较,阳黄证、阴黄证空白组DCs表面CD80、CD86、CD83、HLA-DR表达降低(P<0.01),IL-12分泌减少(P<0.01);与阳黄证、阴黄证空白组比较,阳黄证、阴黄证BAC干预组DCs表面CD80、CD86、CD83、HLA-DR表达升高,IL-12分泌增多(P<0.01).结论:BAC可以促进HBV-ACLF阳黄证和阴黄证患者DCs功能恢复,间接促进T细胞活化.

我们经过40多年的研究,建立了"阳黄-阴阳黄-阴黄"模式治疗慢加急性肝衰竭(ACLF),对其发病机制有了新的认识,临床疗效明显提高.现结合我们的研究对其进行简要介绍. 1.发现慢加急性肝衰竭阴黄化趋势,提出"阴阳黄"病证名,建立"阳黄-阴阳黄-阴黄"辨证论治模式治疗ACLF 中医治疗ACLF参照黄疸辨证论治.黄疸辨证以阴阳为纲,阳黄以湿热与瘀热为主,属热属实;阴黄以寒湿与虚寒为主,属寒属虚.

Objective:To explore the key targets and mechanism of Bielong Ruangan decoction in the treatment of liver cancer based on network pharmacology and molecular docking.Methods:Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP) database, PubChem database and PharmMapper database were used to search and screen the chemical components and related targets of Bielong Ruangan decoction and the targets of liver cancer diseases. The network diagram of " Bielong Ruangan decoction-traditional Chinese medicine-active ingredient-predicted target-disease" was constructed; Protein-protein interaction (PPI) network were analyzed through String database; gene ontology (GO) enrichment analysis was performed through WebGestalt database; Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis was carried out through KEGG Orthology Based Annotation System (KOBAS) database; Molecular docking of the active components and core target proteins of Bielong Ruangan decoction was carried out by using PyMOL, Auto DockVina and other software.Results:Bielong Ruangan decoction had 67 active components, 154 liver cancer targets and 244 pathways. According to the analysis of network pharmacology, Bielong Ruangan decoction may play an anti-cancer role through key targets such as epidermal growth factor receptor (EGFR), mitogen activated protein kinase 1 (MAPK1), estrogen receptor 1 (ESR1), MAPK8, serine threonine protein kinase 1 (AKT1), MAPK14, cysteine protease 3 (CASP3), cyclin-dependent kinase 2 (CDK2), bone morphogenetic protein 2 (BMP2), aldose reductase (AKR1B1) and other key targets. KEGG enrichment analysis showed that the treatment of liver cancer by Bielong Ruangan decoction involved the regulation of vascular endothelial growth factor (VEGF) signaling pathway, tumor necrosis factor (TNF) signaling pathway, thyroid hormone signaling pathway, T cell receptor signaling pathway and other pathways. The results of molecular docking showed that the binding energy of all compounds to protein was less than -5.6 kcal/mol, indicating that each compound and each protein could bind well.Conclusions:Bielong Ruangan decoction participates in the treatment of liver cancer through " multi-component, multi-target and multi-channel" ways, and plays an anti-cancer role mainly by regulating the proliferation and invasion of tumor cells and tumor inflammatory microenvironment.

中医学认为气化是维持人体生命活动的基础,其实质内涵为"阳化气,阴化形",而"阳主阴从"是生化的有序稳态,气化贵在阳气流通.若阳气郁滞或阳气耗损,经络不通,脏腑形体受损,则百病丛生.故阳气气化是致病和治病的关键,临床上可以"通阳"为治则,以祛除邪气、调畅气机,从而通达肌腠、经络、关窍、脏腑之阳气,调平气血阴阳.

通过研究清代著名医家陈士铎的学术著作,总结发现其别具特色地从黄疸的分布、深浅来辨其病位.将黄疸病因归于五脏六腑,但认为病变关键在"湿".治疗上遵五脏生克之理:润肝泄心,辨治心疸,补土利金,辨治肺疸;补命门之火,解脾土之寒而治脾肾二疸;循通补旺胆,通利消疸之治则治疗胆疸、肝疸.处方用药上利湿青睐茯苓、茵陈,健脾独钟白术,消酒疸专用柞木.陈士铎辨治黄疸受仲景、"温补学派"诸家影响颇深,但其特色地从五行理论、脏腑功能的角度治疗黄疸的思路别有新意,对指导临床治疗具有极高的价值.