Objective To evaluate the effects of honeysuckle extract and its active component, luteolin, on the autistic-like behaviors and neuroinflammatory responses in NDE1-deficient autism spectrum disorder (ASD) zebrafish models. Also, to assess whether differences exist in their behavioral improvement effects and impacts on brain inflammatory factor expression levels. Methods Behavioral phenotyping (hyperactivity, stereotypic back-and-forth swimming, and 1VS6 social preference/grouping tests) and molecular analyses (quantification of NF-κB, IL6, TNFα, and IL1β) were performed on NDE1-deficient zebrafish treated with honeysuckle extract or luteolin. Results Honeysuckle extract improved two core symptoms of ASD, small circling repetitive stereotyped behavior and 1VS6 social preference behavior. While luteolin enhanced one core symptom, shoaling behavior, and one comorbid symptom, hyperactive locomotor activity. Molecularly, honeysuckle extract normalized IL6 levels, and luteolin reduced IL1β overexpression; their effects on brain inflammation in the NDE1-deficient autism model differed. Conclusion Both honeysuckle extract and luteolin demonstrated behavioral rescue and anti-neuroinflammatory effects in NDE1-deficient ASD zebrafish models. The ameliorating effects of luteolin on ASD-related behaviors and neuroinflammation are supported by literature, while the beneficial effects of honeysuckle on ASD-related behaviors represent a novel finding of this study, highlighting medicinal plants and plant-derived compounds as potential ASD therapeutics. Given honeysuckle's traditional Chinese medicinal and food uses, established safety, and superior improvement of core ASD symptoms compared to luteolin, it may offer a safer autism treatment option than luteolin-based small-molecule medication.

ABSTRACT The properties theory of traditional Chinese medicine (TCM), characterized by cold, hot, warm, and cool four properties, is fundamental to its development, distinguishing it from natural, botanical, and chemical medicines. However, despite its significance, there is no unified theoretical definition, bioscientific characterization, or standardized evaluation of TCM's medicinal properties, as scholars use diverse methods and hold varying opinions. Historically, TCM practitioners relied on intuitive physical perspectives due to limited scientific knowledge and tools. This study aims to investigate the fundamental nature and core standards of TCM's medicinal properties from an underlying logical thinking and physics perspective, with a focus on the four properties of TCM and the ‘macro‐micro’ doctrine extension and integration outlook. The research examines the current state, progress, and trends in TCM properties, exploring their relationship with the ‘thermodynamic outlook of TCM properties' and the use of microcalorimetry. This paper adopts a systematic approach, drawing on theories, research methodologies, and practical results from various TCM practitioners. Microcalorimetry is employed as a method to explore the four properties of TCM and their broader implications. The research highlights the connection between the four properties of TCM and thermodynamics, demonstrating the effectiveness of microcalorimetry in understanding these properties. It presents a structured outlook on “quality differentiation of drug properties–drug properties are characterized by curative effect–curative effect monitoring clinical (‘Q’–P–‘C’)” and introduces the new concept of “stylization of TCM.” By integrating both shared characteristics and individual differences of theories, research methods, and practical achievements from multiple TCM scholars, this provides a feasible approach to standardizing TCM's medicinal properties, thereby further deepening the understanding and application of TCM through a structured, physics‐based framework.

The supplementary data contain Supplementary Tables S1 to S9. Supplementary Table S1. Human Liver Donor Details and Tissue Histology Supplementary Table S2. Incubation Conditions for CYP Activity Assays Supplementary Table S3. Analytical Parameters for Activity Assays of CYPs. Supplementary Table S4. Sequences and MRM Transitions of Proteotypic Peptides for Quantifying CYP Enzymes Supplementary Table S5. Oligonucleotide PCR Primers for Human CYP Enzymes and GAPDH Supplementary Table S6. Summary of Enzyme Kinetic Parameters for Seven CYP Activities in Pooled Human Liver Microsomes. Supplementary Table S7. Summary of Seven CYP Enzymes Activities in Tumor Tissues and Pericarcinomatous Tissues of Patients with HCC Supplementary Table S8. Summary of Seven CYPs Protein Expression Levels in Tumor Tissues and Pericarcinomatous Tissues of Patients with HCC Supplementary Table S9. Summary of Seven CYPs mRNA Expression Levels in Tumor Tissues and Pericarcinomatous Tissues of Patients with HCC

Idiosyncratic drug-induced liver injury (IDILI) is common in hepatology practices and, in some cases, lethal. Increasing evidence show that tricyclic antidepressants (TCAs) can induce IDILI in clinical applications but the underlying mechanisms are still poorly understood. We assessed the specificity of several TCAs for NLRP3 inflammasome via MCC950 (a selective NLRP3 inhibitor) pretreatment and Nlrp3 knockout (Nlrp3−/−) BMDMs. Meanwhile, the role of NLRP3 inflammasome in the TCA nortriptyline-induced hepatotoxicity was demonstrated in Nlrp3−/− mice. We reported here that nortriptyline, a common TCA, induced idiosyncratic hepatotoxicity in a NLRP3 inflammasome-dependent manner in mildly inflammatory states. In parallel in vitro studies, nortriptyline triggered the inflammasome activation, which was completely blocked by Nlrp3 deficiency or MCC950 pretreatment. Furthermore, nortriptyline treatment led to mitochondrial damage and subsequent mitochondrial reactive oxygen species (mtROS) production resulting in aberrant activation of the NLRP3 inflammasome; a selective mitochondrial ROS inhibitor pretreatment dramatically abrogated nortriptyline-triggered the NLRP3 inflammasome activation. Notably, exposure to other TCAs also induced aberrant activation of the NLRP3 inflammasome by triggering upstream signaling events. Collectively, our findings revealed that the NLRP3 inflammasome may act as a crucial target for TCA agents and suggested that the core structures of TCAs may contribute to the aberrant activation of NLRP3 inflammasome induced by them, an important factor involved in the pathogenesis of TCA-induced liver injury.

NLRP3 (NOD-, LRR-, and pyrin domain-containing protein 3) is a cytosolic pattern recognition receptor (PRR) that recognizes multiple pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). Once activated, NLRP3 initiates the inflammasome assembly together with the adaptor ASC and the effector caspase-1, leading to caspase-1 activation and subsequent cleavage of IL-1β and IL-18. Aberrant NLRP3 inflammasome activation is linked with the pathogenesis of multiple inflammatory diseases, such as cryopyrin-associated periodic syndromes, type 2 diabetes, non-alcoholic steatohepatitis, gout, and neurodegenerative diseases. Thus, NLRP3 is an important therapeutic target, and researchers are putting a lot of effort into developing its inhibitors. The review summarizes the latest advances in the mechanism of NLRP3 inflammasome activation and its pharmacological inhibitors.

Glycyrrhiza uralensis polysaccharides (GUP) has biological activities such as immune regulation, anti-tumor, and liver protection, and has good development prospects in the fields of medicines and health products, but its specific mechanism of action is not yet clear. In our study, we confirmed that GUP can effectively inhibit the activation of the NLRP3 inflammasome. Mechanistically, GUP blocked the activation of the inflammasome by significantly inhibiting the oligomerization and speckle aggregation of the apoptosis-related protein ASC. In addition, GUP effectively ameliorated LPS-induced acute lung injury in mice. Our findings indicate that the Traditional Chinese Medicine (TCM) GUP has broad-spectrum anti-inflammatory effects and is a potential drug candidate for the treatment of inflammasome-related diseases.

Objective: By analyzing the Chinese literatures related to the teaching reform of traditional Chinese medicine chemistry included in the database of China National Knowledge Infrastructure（CNKI）, this paper summarizes the main research development trends, characteristics and hotspots, so as to provide reference for the follow-up teaching research of traditional Chinese medicine chemistry. Methods: This study adopts the research ideas and methods of bibliometrics,takes the knowledge map as the research carrier, and uses Excel, VOSviewer, CiteSpace and other analysis software as the research tools, and conducts network co-occurrence analysis on the keywords and author cooperation in the selected data, respectively. Make graphs and analyze data about output trends, publishing institutions and their regions, disciplines and funding distribution, types of published journals and the number of article pages, as well as the number of references,paper downloads, and citation frequency. Results: From 2002 to 2022, the China National Knowledge Infrastructure（CNKI） database included 76 literatures related to the teaching reform of traditional Chinese medicine chemistry, and the annual publication volume generally showed an upward trend. The proportion of funding is relatively high, but it is mainly concentrated in provincial and municipal funds; the number of downloads of papers is high, indicating that the number of people concerned is more, but the number of citations is low; the research areas and scholars are widely distributed. Conclusion The: reform of Chinese medicine chemistry teaching in China is in a period of vigorous development. It is necessary to further explore, innovate teaching methods and teaching models, and strengthen communication among scholars to further improve the quality of Chinese medicine chemistry teaching reform.

An acute lung injury (ALI) is a serious lung disease with a high mortality rate, warranting the development of novel therapies. Previously, we reported that 1,2,3,4,6-O-pentagalloylglucose (PGG) could afford protection against ALI, however, the PGG-mediated protective effects remain elusive. Herein, PGG (60 and 30 mg/kg) markedly inhibited the lung wet/drug weight ratio and attenuated histological changes in the lungs (p < 0.05). A pretreatment with PGG (60 and 30 mg/kg) reduced the number of total leukocytes and the production of pro-inflammatory cytokines IL-6 and IL-1β in bronchoalveolar lavage fluid (p < 0.05). In addition, PGG (60 and 30 mg/kg) also attenuated oxidative stress by reducing the formation of formation and the depletion of superoxide dismutase to treat an ALI (p < 0.05). To further explore the PGG-induced mechanism against an ALI, we screened the PGG pathway using immunohistochemical analysis, immunofluorescence assays, and Western blotting (WB). WB revealed that the expression levels of adenosine monophosphate-activated protein kinase phosphorylation (p-AMPK), phosphoinositide 3-kinase (PI3K), protein kinase B phosphorylation (P-Akt), and nuclear factor erythroid 2-related factor (Nrf2) were significantly higher in the PGG group (60 and 30 mg/kg) than in the lipopolysaccharide group (p < 0.05); these findings were confirmed by the immunohistochemical and immunofluorescence results. Accordingly, PGG could be effective against an ALI by inhibiting inflammation and oxidative stress via AMPK/PI3K/Akt/Nrf2 signaling, allowing for the potential development of this as a natural drug against an ALI.

Ethnopharmacological relevance: Keguan-1, a new traditional Chinese medicine (TCM) prescription contained seven Chinese herbs, is developed to treat coronavirus disease 19 (COVID-19). The first internationally registered COVID-19 randomised clinical trial on integrated therapy demonstrated that Keguan-1 significantly reduced the incidence of ARDS and inhibited the severe progression of COVID-19. Aim of the study: To investigate the protective mechanism of Keguan-1 on ARDS, a lipopolysaccharide (LPS)induced acute lung injury (ALI) model was used to simulate the pathological state of ARDS in patients with COVID-19, focusing on its effect and mechanism on ALI. Materials and methods: Mice were challenged with LPS (2 mg/kg) by intratracheal instillation (i.t.) and were orally administered Keguan-1 (low dose, 1.25 g/kg; medium dose, 2.5 g/kg; high dose, 5 g/kg) after 2 h. Bronchoalveolar lavage fluid (BALF) and lung tissue were collected 6 h and 24 h after i.t. administration of LPS. The levels of inflammatory factors tumour necrosis factor alpha (TNF-alpha), interleukin (IL)-6, IL-1 beta, keratinocyte-derived chemokine (KC or mCXCL1), macrophage inflammatory protein 2 (MIP2 or mCXCL2), angiotensin II (Ang II), and endothelial cell junction-associated proteins were analysed using ELISA or western blotting. Results: Keguan-1 improved the survival rate, respiratory condition, and pathological lung injury; decreased the production of proinflammatory factors (TNF-alpha, IL-6, IL-beta, KC, and MIP2) in BALF and the number of neutrophils in the lung tissues; and ameliorated inflammatory injury in the lung tissues of the mice with LPS-induced ALI. Keguan-1 also reduced the expression of Ang II and the adhesion molecule ICAM-1; increased tight junction proteins (JAM-1 and claudin-5) and VE-cadherin expression; and alleviated pulmonary vascular endothelial injury in LPS-induced ALI. Conclusion: These results demonstrate that Keguan-1 can improve LPS-induced ALI by reducing inflammation and pulmonary vascular endothelial injury, providing scientific support for the clinical treatment of patients with COVID-19. Moreover, it also provides a theoretical basis and technical support for the scientific use of TCMs in emerging infectious diseases.

Background: Increasing evidence shows that tricyclic antidepressant s ( TCA s) could induce relative rare but severe idiosyncratic drug-induced liver injury (IDILI) in clinical applications, while the underlying mechanisms are still poorly understood. We sought to determine the molecular mechanism of TCAs-induced hepatotoxicity, and facilitated the potential approach to increase of the biosafety of TCAs.Methods: We examined the effect of TCAs on downstream effector cytokines. MCC950 pretreatment and conditional knockouts of Nlrp3 were applicated to verify the specificity of TCAs for NLRP3 inflammasome and inductively coupled plasma mass spectrometry (ICP-MS), immunoblot, immunoprecipitation, Enzyme-linked immunosorbent assay (ELISA) and histology staining were used to investigate the related mechanisms.Findings: Nortriptyline, used as a common TCA agent, induced the altering of aminotransferase level, hepatic inflammation and hepatocyte death in a NLRP3-dependent manner. In parallel in vitro studies, Nortriptyline directly induced inflammasome activation as evidenced by the caspase-1 activation, IL-1β generation and gasdermin D (GSDMD)-mediated pyroptosis, while these changes were blocked by the selective NLRP3 inhibitor MCC950 treatment or Nlrp3 deficiency. Mechanistically, Nortriptyline treatment led to increased accumulation of mitochondrial reactive oxygen species (mtROS) resulting in the aberrant activation of NLRP3 inflammasome, and ROS scavenger pretreatment completely abrogated Nortriptyline-induced caspase-1 maturation and IL-1β release. Moreover, exposure to other TCAs that have been reported to induced liver injury, including Imipramine, Amitriptyline and Protriptyline, also led to NLRP3 inflammasome aberrant activation, as well as subsequent inflammatory cytokines release.Interpretation: NLRP3 inflammasome may acts as a crucial target for TCA agents and suggest that aberrant activation of NLRP3 inflammasome may contribute to pathogenesis of TCAs-induced liver injury.Funding: This work was granted by National Natural Science Foundation of China (81630100, 81874368), National Science & Technology Major Project “Key New Drug Creation and Manufacturing Program” (2018ZX09101002- 001-002), Beijing Nova Program (Z181100006218001), Chinese Postdoctoral Science Foundation (grant number: 2020M673676), Youth Foundation of Chinese PLA General Hospital (QNF19065).Declaration of Interest: The authors declare no conflict of interest.Ethical Approval: This study was approved by the Animal Ethics Committee of the FifthMedical Center, Chinese People's Liberation Army General Hospital (Beijing, China).

Oligoasthenozoospermia (OA) is one of the most common types of male infertility affecting sperm count and sperm motility. Unfortunately, it is difficult for existing drugs to fundamentally improve the sperm quality of OA patients, because the pathological mechanism of OA has not been fully elucidated yet. Morinda officinalis-Lycium barbarum coupled-herbs (MOLBCH), as traditional Chinese Medicines, has been widely used for treating OA over thousands of years, but its molecular mechanism is still unclear. For this purpose, we adopted a comprehensive approach integrated network pharmacology and molecular docking to reveal the bioactive components and potential targets of MOLBCH against OA. The results showed that MOLBCH alleviated apoptosis, promoted male reproductive function, and reduced oxidant stress in the treatment of OA. Ohioensin-A, quercetin, beta-sitosterol and sitosterol were the key bioactive components. Androgen receptor (AR), Estrogen receptor (ESR1), Mitogen-activated protein kinase 3 (MAPK3), RAC-alpha serine/threonine-protein kinase (AKT1), Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) were the core potential targets. PI3K/Akt signaling pathway, prostate cancer, AGE-RAGE signaling pathway in diabetic complications were the most representative pathways. Moreover, molecular docking was performed to validate the strong binding interactions between the obtained core components and targets. These observations provide deeper insight into the pathogenesis of OA and can be used to design new drugs and develop new therapeutic instructions to treat OA.

Hepatic fibrosis represents an important event in the progression of chronic liver injury to cirrhosis, and is characterized by excessive extracellular matrix proteins aggregation. Early fibrosis can be reversed by inhibiting hepatocyte injury, inflammation, or hepatic stellate cells activation, so the development of antifibrotic drugs is important to reduce the incidence of hepatic cirrhosis or even hepatic carcinoma. Here we demonstrate that Schisandrol B (SolB), one of the major active constituents of traditional hepato-protective Chinese medicine, Schisandra sphenanthera, significantly protects against hepatocyte injury, while Wedelolactone (WeD) suppresses the TGF-β1/Smads signaling pathway in hepatic stellate cells (HSCs) and inflammation, the combination of the two reverses hepatic fibrosis in mice and the inhibitory effect of the combination on hepatic fibrosis is superior to that of SolB or WeD treatment alone. Combined pharmacotherapy represents a promising strategy for the prevention and treatment of liver fibrosis.

[This corrects the article DOI: 10.3389/fphar.2021.655531.].

PURPOSE:One of the most common types of male infertility is recognized as oligoasthenozoospermia (OA), characterized by low sperm count and quality in males. As a traditional Chinese medicine (TCM), Cuscutae Semen-Mori Fructus coupled-herbs (CSMFCH) has been known to act a curative effect on OA for thousands of years. Nevertheless, the substantial basis and molecular mechanism of CSMFCH in treating OA remain elusive.METHODS:Herein, an integrated approach, including network pharmacology, molecular docking, and experiment validation, was utilized to reveal the new candidate active component and mechanism of CSMFCH in treating OA.RESULTS:The results show that kaempferol is the most significant bioactive component of CSMFCH on OA. The mechanism and targets of CSMFCH against OA are relevant to hormone regulation, oxidant stress, and reproductive promotion. In order to validate network pharmacology results, molecular docking and experiment validation were conducted. In detail, molecular docking was employed to verify the strong binding interactions between kaempferol and the core targets. UHPLC-Q-Orbitrap-MS was used to identify kaempferol in the CSMFCH extract. In vitro and in vivo experiments further proved CSMFCH and kaempferol could enhance the mouse Leydig (TM3) and mouse Sertoli (TM4) cell viability, improve the male reproductive organ weights, sperm quality, and decrease testis tissue damage in the OA mouse model induced by CP.CONCLUSION:Our results not only identify the new candidate active component of CSMFCH in treating OA but also provide new insights into the mechanisms of CSMFCH against OA.

In ischemic stroke sequela phase, Rehmanniae Radix Praeparata-Corni Fructus drug pair has the effect in protecting damaged neurons, but its mechanism has not been clear. In this study, network pharmacology was used to predict the mechanism of Rehmanniae Radix Praeparata-Corni Fructus in the treatment of ischemic stroke sequela. Through database search and literature retrie-val, 40 active ingredients of Rehmanniae Radix Praeparata and Corni Fructus were obtained, and their targets were obtained through STITCH and TCMSP databases. The targets of ischemic stroke sequela were obtained through OMIM,GAD,TTD and DrugBank databases. By screening the intersections of active ingredients targets and stroke treatment targets, 21 potential targets were obtained. The DAVID database was used for GO enrichment analysis and KEGG pathway analysis of potential targets. GO enrichment analysis showed that Rehmanniae Radix Praeparata-Corni Fructus were mainly involved in regulation of blood pressure, negative regulation of extrinsic apoptotic signaling and positive regulation of angiogenesis. KEGG pathway analysis showed that Rehmanniae Radix Praeparata-Corni Fructus could inhibit inflammatory response and apoptosis signaling pathway by regulating HIF-VEGFA signaling pathway in neural stem cell proliferation, TNF signaling pathway and NF-kappaB signaling pathway. Molecular docking technique was used to verify that Rehmanniae Radix Praeparata-Corni Fructus component has a good binding activity with potential targets. The results showed that in ischemic stroke sequela phase, Rehmanniae Radix Praeparata-Corni Fructus drug pair could play an important role in recovering neural function, promoting the proliferation of neural stem cells, angiogenesis, preventing neural cells apoptosis and regulating inflammatory factors.

目的:研究中药熟地黄不同提取分离部位对体外培养的海马神经干细胞(NSCs)增殖活性的影响.方法:采用系统溶剂法以及柱色谱分离将熟地黄分成不同部位,采用CCK-8法测定熟地黄各部位对体外培养的海马NSCs增殖活性的影响,并筛选出最佳作用浓度.结果:熟地黄正丁醇部位(0.8、0.4μg/mL,P＜0.01)、乙酸乙酯部位(0.8μg/mL,P＜0.01)和剩余水部位(0.8、0.4、0.2μg/mL,P＜0.01)对NSCs增殖活性有明显促进作用,且乙酸乙酯部位的二氯甲烷-甲醇20:1洗脱样品(0.2μ g/mL,P＜0.01)及正丁醇部位的10％乙醇洗脱样品(0.4 μgmL,P＜0.01)对NSCs增殖的促进效果最佳.结论:熟地黄乙酸乙酯部位、正丁醇部位和剩余水部位可能含有促NSCs增殖的潜在活性成分.

目的:应用网络药理学方法,从双黄连方剂中预测具有抗肿瘤活性的组分中药,并通过离体细胞实验与动物实验对其抗CT26结肠癌活性进行初步验证.方法:基于中药系统药理学数据库(Traditional Chinese Medicine Systems Pharmacology Database,TCMSP),《中药活性成分分析手册》,药品生物信息学和化学信息学数据库(DrugBank),信号通路数据库(Reactome)及人类蛋白质参考数据库(Human protein reference database,HPRD),构建蛋白-蛋白相互作用网络(proteinprotein interactions network,PPI)和化合物靶标网络,挖掘化合物的药理作用,发现与PPI网络节点距离较短的化合物,确定组成中药的配伍.以CT26结肠癌细胞为实验材料,结合离体和在体实验初步验证组分中药的抗肿瘤作用.结果:从双黄连组分中预测并发现“黄芩苷、连翘酯苷A和绿原酸”3个化合物配伍具有潜在抗肿瘤活性.验证结果表明,细胞实验中,与空白组比较,双黄连组分中药能显著抑制CT26细胞的增殖和迁移(P＜0.01);动物实验中,与荷瘤模型组比较,双黄连组分中药治疗组小鼠皮下肿瘤体积增长缓慢、肿瘤重量显著降低(P＜0.01).结论:结合数据库挖掘和化合物靶点网络构建、分析等方法从双黄连方剂中发现具有抗肿瘤活性的组分中药“黄芩苷、连翘酯苷A和绿原酸”.经验证,该组分中药具有较好的抗CT26结肠癌活性.

The invention relates to a screening method of a gene composition set influenced by expression of a d-limonene mixture, further relates to the gene composition set defined as a gene difference index,and provides a calculation method for evaluating whether a cancer patient is sensitive to the d-limonene mixture or not based on the gene composition set. The method comprises the following steps: 1)respectively detecting the expression value of each gene in the gene composition set in a cancer and para-carcinoma tissue; 2) calculating a gene expression difference ratio of the same gene in the cancer and para-carcinoma tissue, and performing natural logarithm processing to obtain a patient difference gene index; 3) calculating the product of the gene difference index and the patient difference gene index; and 4) after the product is processed through a sign function, calculating the sign summation, corresponding to one cancer patient, of all gene difference products, and judging whether the patient is sensitive to the anti-cancer effect of the d-limonene mixture or not according to the summation value obtained through calculation. The method can screen out the patient sensitive to theanti-cancer effect of the d-limonene mixture.

目的:研究牛膝不同提取分离部位对体外培养的神经干细胞增殖的作用.方法:采用系统溶剂法以及柱色谱法将牛膝分成不同部位,以CCK-8法检测牛膝各部位对体外培养的神经干细胞增殖的效果,并筛选出较好的作用部位和浓度.结果:牛膝正丁醇部位(25μg/mL,P<0.01)和其多糖部位(12.5μg/mL,P<0.01)对神经干细胞增殖活性有明显促进作用.结论:牛膝正丁醇部位和多糖部位可能是其促神经干细胞增殖的主要活性部位.

目的 研究淫羊藿与甘草不同比例配伍时淫羊藿主要化学成分的影响.方法 将淫羊藿与甘草分别按照不同比例配伍,水煎,制备供试样品,采用HPLC法测定淫羊藿苷的含量,Kromasil C18 (250 mm×4.6mm,5μm)型色谱柱,以水为流动相A,乙腈为流动相B,在流速为1.0 mL· min-1下进行洗脱;检测波长:270 nm;柱温:25℃.结果 淫羊藿与甘草配伍后,各配伍组淫羊藿中淫羊藿苷等多种成分的含量均有不同程度的增加,在淫羊藿与甘草的配伍比例为5∶1时含量增加最明显,有些成分含量则无明显改变.结论 淫羊藿与甘草配伍后药材中淫羊藿苷等成分溶出量较单味淫羊藿提高,可为二药配伍应用提供参考.