Ulcerative colitis (UC) is one of the most important chronic inflammatory bowel diseases (IBD), and the aetiology of UC involves the interplay of genetic susceptibility, immune dysregulation, gut microbes and environmental factors. The cAMP response element modulator (CREM), a major effector of cAMP signalling, is a key transcription factor belonging to the cAMP response element binding protein (CREB) family. It integrates multiple upstream signaling pathways with distinct functions, such as cAMP/PKA, Ca2+/CaMKIV and AKT/mTOR. According to the urgent research, aberrant CREM expression occurs in colonic mucosal tissues and immune cells of UC patients which suggests its significant role in UC pathogenesis through multiple mechanisms. This review systemically summarizes the basic biological features of CREM, which comprises structural characteristics, isoform diversity, and regulatory networks in cellular signaling. In addition, we systematically analyse the main mechanisms by which CREM facilitates UC including the functions of immune cells, T cells, B cells and NK cells. Then we discuss the balance between pro-inflammatory and anti-inflammatory cytokines and the impact on intestinal barrier and gut microbiota. Ultimately, we will address the emerging resources, clinical potential of CREM as a healing target and pathway for future research. The purpose of this review is to provide novel insights into the pathogenesis of UC, which may contribute to optimizing clinical treatment and developing new therapeutic drugs.

Mitochondria, as regulators of cellular energy production and metabolism, play a crucial role in tumor growth and survival. Tumors are reprogrammed to accommodate rapid proliferation through the Warburg effect. This reprogramming leads to the accumulation of metabolites such as lactate and ketone bodies, thereby lowering the pH of the tumor microenvironment, inhibiting the activity of effector T cells and NK cells, while promoting the infiltration of regulatory T cells and MDSCs, forming an immunosuppressive microenvironment. ROS produced by mitochondria can affect immune cell function by modulating their signaling pathways. Mitochondria also release DAMPs, which activate the antigen-presenting capacity of dendritic cells and initiate anti-tumor immune responses. Currently, various methods have been employed, such as DLCs modifications and mitochondrial targeted delivery, which enable drugs to penetrate the lipid bilayer and enter the mitochondria, thereby helping to reduce immunosuppression in the tumor microenvironment. In this review, we will discuss the impact of mitochondria on tumor immunity, strategies to target tumor cell mitochondria, and progress on the discovery of mitochondria-targeted drugs to enhance tumor immunity, providing potential directions for developing new cancer therapeutic strategies.

BACKGROUND:Gastric motility disorder is an increasingly common problem among people with diabetes. Neurotransmitters have been recognized as critical regulators in the process of gastric motility. Previous study has shown that herb pair huanglian-banxia (HL-BX) can improve gastric motility, but the underlying mechanism is still unclear. The aim of this study was to further investigate the role of HL-BX in modulating brain-gut neurotransmission to promote gastric motility in diabetic rats, and to explore its possible mechanism.METHODS:The diabetic rats were divided into five groups. Gastric emptying rate, intestinal propulsion rate, body weight, and average food intake were determined. Substance P (SP), 5- hydroxytryptamine (5-HT), and glucagon-like peptide -1 (GLP-1) in the serum were measured by enzyme-linked immunosorbent assay. Dopamine (DA) and norepinephrine (NE) in the brain were analyzed by high-pressure liquid chromatography with a fluorescence detector. Protein expression of the tissues in the stomach and brain was determined by Western blot.KEY RESULTS:HL-BX reduced average food intake significantly, increased body weight, and improved gastric emptying rate and intestinal propulsion rate. HL-BX administration caused a significant increase in SP, GLP-1, and 5-HT, but a significant decrease in DA and NE. Interestingly, HL-BX regulated simultaneously the different expressions of MAPK and its downstream p70S6K/S6 signaling pathway in the stomach and brain. Moreover, berberine exhibited a similar effect to HL-BX.CONCLUSIONS:These results indicated that HL-BX promoted gastric motility by regulating brain-gut neurotransmitters through the MAPK signaling pathway. HL-BX and MAPK provide a potential therapeutic option for the treatment of gastroparesis.

BackgroundUlcerative colitis (UC) is an inflammatory bowel disease characterized by persistent colonic inflammation. Here, we performed a systematic analysis to gain better insights into UC pathogenesis.MethodsWe analyzed two UC-related datasets extracted from the gene expression omnibus database using several bioinformatics tools. The primary cell types and key subgroups of primary cells associated with UC and differentially expressed genes (DEGs) between UC and control samples were identified. The molecular regulation of the key genes was also predicted. The gene ontology and Kyoto encyclopedia of genes and genomes enrichment analyses of marker genes of key cell subgroups and model genes were performed. The expression of key enriched genes was validated in 10 clinical samples using real-time quantitative polymerase chain reaction (RT-qPCR).ResultsMonocytes were identified as the major cell type. Ten differentially expressed marker genes were obtained by intersecting the 3121 DEGs, 38 marker genes in major cell types, and 104 marker genes in key cell subgroups. Four essential genes, associated with immune response, were obtained using support vector machine recursive feature elimination and least absolute shrinkage and selection operator analyses. The four essential genes were highly expressed in Cluster 0 during differentiation. Validation of the four key genes in colonic mucosal biopsy specimens from 10 normal and 10 UC patients revealed that CREM was highly expressed in both the lesion-free sites and lesion sites colonic mucosa of UC patients compared with normal adults.ConclusionsWe identified CREM involved in UC pathogenesis, which is expected to provide a new therapeutic target for UC.

BACKGROUND:Chronic Kidney Disease (CKD) leads to structural and functional abnormalities of the kidneys and seriously jeopardizes human health. Shenyan Oral Liquid (SOLI), a Chinese medicinal preparation, has been reported to protect podocytes in patients with chronic kidney disease (CKD). OBJECTIVE:The objective of this study is to investigate the mechanism of action of the Chinese medicinal preparation Senyan Oral Liquid (SOLI) in the treatment of CKD by protecting podocytes through network pharmacology technology and experimental validation. METHODS:Compounds of SOLI and targets of CKD disease were collected and screened. The SOLI network of bioactive compounds targeting CKD and the protein-protein interaction (PPI) network were constructed using Cytoscape software and the STRING online database. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed using the R software Cluster Profiler package. Molecular docking was performed using Autodock software to verify the binding ability of bioactive compounds and target genes. Subsequently, the potential mechanism of SOLI on CKD predicted by network pharmacological analysis was experimentally studied and verified in an adriamycin-induced nephropathy rat model. RESULTS:A total of 81 targets of SOLI components acting on CKD were identified. The results of the PPI analysis clarified that five key target genes (TNF, AKT1, IL6, VEGFA, and TP53) play a critical role in the treatment of CKD by SOLI. The GO analysis and KEGG enrichment analysis indicated that SOLI acts through multiple pathways, including the PI3K/AKT signaling pathway against CKD. Molecular docking showed that the main compounds of SOLI and five key genes had strong binding affinity. In a rat model of adriamycin-induced nephropathy, SOLI significantly ameliorated disease symptoms and improved renal histopathology. Mechanistic studies showed that SOLI upregulated the expression level of Nephrin, inhibited the PI3K/AKT pathway in renal tissues, and ultimately suppressed the activation of autophagy-related proteins in CKD. CONCLUSION:SOLI exerted a renoprotective effect by regulating the Nephrin-PI3K/AKT autophagy signaling pathway, and these findings provide new ideas for the development of SOLI-based therapeutic approaches for CKD.

BACKGROUND:Dachshund homolog 1 (DACH1) is widely acknowledged for its involvement in regulating diverse cell fates, but its precise regulatory mechanism in ferroptosis remains elusive. In this study, we investigated whether DACH1 modulates ferroptosis through affecting P53/solute carrier family 25 member 37 (SLC25A37) signaling in hepatic fibrogenesis. METHODS:CRISPR-Cas9 system was used to knockout DACH1 in HSC to determine the effect of DACH1 on ferroptosis. Immunoprecipitation, pulldown, and mouse model of hepatic fibrogenesis were used to analyze the potential molecular mechanism of ferroptosis regulation by DACH1. RESULTS:We found that ferroptosis inducers increased the protein expression of DACH1 by suppressing the ubiquitin-proteasome signaling. DACH1 knockout can resist ferroptosis, whereas DACH1 knockin can enhance it. Interestingly, the upregulation of DACH1 resulted in the mitochondrial translocation of p53 by inducing phosphorylation at serine 392. The mutation of serine 392 can prevent the combination of DACH1 and p53, the mitochondrial translocation of p53, and DACH1-mediated ferroptosis. Moreover, SLC25A37 was identified as a candidate target for mitochondrial p53. The binding of p53 to SLC25A37 can enhance the iron uptake capacity of SLC25A37, which may cause an overload of iron in the mitochondria and hyperactive mitochondrial electron transport chain. Knockdown of SLC25A37 can impair p53-mediated mitochondrial iron overload and ferroptosis. Furthermore, treatment with erastin can induce HSC ferroptosis and relieve fibrotic lesion damage in the mouse model of hepatic fibrogenesis. HSC-specific knockdown of DACH1, p53, and SLC25A37 can abolish the induction of HSC ferroptosis and reversal of hepatic fibrogenesis by erastin treatment. CONCLUSIONS:Our findings suggest that the DACH1/P53/SLC25A37 signaling pathway is a promising target for fibrotic disorders and reveals new regulatory mechanisms of ferroptosis.

Abstract Background Huangkui Lianchang Decoction (HLD) is a traditional Chinese herbal formula for treating ulcerative colitis (UC). However, its mechanism of action remains poorly understood. The Study aims to validate the therapeutic effect of HLD on UC and its mechanism by integrating network pharmacology, bioinformatics, and experimental validation. Methods UC targets were collected by databases and GSE19101. The active ingredients in HLD were detected by ultra-performance liquid chromatography-tandem mass spectrometry. PubChem collected targets of active ingredients. Protein–protein interaction (PPI) networks were established with UC-related targets. Gene Ontology and Kyoto Encyclopedia (KEGG) of Genes and Genomes enrichment were analyzed for the mechanism of HLD treatment of UC and validated by the signaling pathways of HLD. Effects of HLD on UC were verified using dextran sulfate sodium (DDS)-induced UC mice experiments. Results A total of 1883 UC-related targets were obtained from the GSE10191 dataset, 1589 from the database, and 1313 matching HLD-related targets, for a total of 94 key targets. Combined with PPI, GO, and KEGG network analyses, the signaling pathways were enriched to obtain IL-17, Toll-like receptor, NF-κB, and tumor necrosis factor signaling pathways. In animal experiments, HLD improved the inflammatory response of UC and reduced UC-induced pro-inflammatory factors such as Tumor Necrosis Factor Alpha (TNF-α), interleukin 1β (IL-1β), and interleukin 6 (IL-6). HLD suppressed proteins TLR4, MyD88, and NF-κB expression. Conclusions This study systematically dissected the molecular mechanism of HLD for the treatment of UC using a network pharmacology approach. Further animal verification experiments revealed that HLD inhibited inflammatory responses and improved intestinal barrier function through the TLR4/MyD88/NF-κB pathway.

目的:了解我院制剂近3年的使用情况,展望其发展方向.方法:通过医院HIS系统,结合制剂室3年制剂使用量报表以及库房制剂流通量报表,得到我院2020-2022年制剂品种、出库数量及销售额等数据,对这些数据进行整理、统计,分析出医院制剂的使用特点和发展态势.结果:2020-2022年,我院院内制剂销售金额呈逐年上升趋势.中药制剂中扶正胶囊、祛风Ⅱ号胶囊稳居用药频度(DDDs)前2位,扶正胶囊、宽筋散、咳可合剂、健脾合剂、羌菊感冒颗粒、妇科洗液的销售金额逐年上升;西药制剂多为皮肤科用药,且各品种销售金额均逐年升高.结论:近3年来,我院制剂整体发展态势较好,应在对现有制剂保质保量的基础上,抓住机遇,做好吴医特色制剂发展工作.

Tumor angiogenesis, which may be affected by microenvironmental inflammation and promotes tumor development and metastasis, is one of the key reasons contributing to increased mortality. The goal of this study is to investigate how lignin analogs, specifically honokiol (HNK), block angiogenesis induced by the inflammatory milieu of lung cancer. The human lung cancer cell lines A549 and H460 were treated with HNK. Interleukin-1 was employed to mimic an inflammatory tumor microenvironment. Findings demonstrated that HNK drastically decreased the cell viability of A549 and H460 cells. In A549 and H460 cells, HNK also reduced the production of vascular endothelial growth factor (VEGF), the most important marker of tumor angiogenesis. Signal pathway studies revealed that HNK blocked the NF-KB signaling pathway. This effect, in turn, prevented the expression of VEGF by inhibiting the NF-KB signaling pathway. Human umbilical vein endothelial cells (HUVECs) from A549-conditioned medium cultures were subjected to HNK treatment, which decreased tubulogenesis, horizontal and vertical migration, and cell proliferation in HUVECs. Overall, HNK inhibited the NF-KB pathway. This effect resulted in the downregulation of VEGF, thus reducing the viability and angiogenesis of human lung cancer cell lines. In A549 cell xenografts, HNK decreased VEGF expression, tumor angiogenesis, and tumor development. Our research shows that HNK is a potential antiangiogenic molecule for the treatment of lung cancer.

Xiben Pills (XBP) are a Chinese medicine prescription with long history of use against lung cancer. Modern pharmacological experiments proved that XBP and its main compounds have anti-tumor effects. However, the mechanism by which XBP inhibits the progression of non-small cell lung cancer remains unclear.This study aimed to explore the potential targets and mechanism of XBP in the treatment of non-small cell lung cancer by network pharmacology and biological experiments.Network pharmacology was used to screen the prospective targets, pathways, and central genes of XBP in the treatment of non-small cell lung cancer. Based on the results of network pharmacology, the active ingredients of XBP were docked with the core target molecules of NSCLC. The viability of A549 and H460 cells was detected by CCK-8 method. Flow cytometry and Hoechst staining were used to detect cell apoptosis and Caspase 3 expressions in each group. Western blot verified the key protein expression underlying XBP’s therapeutic effect on NSCLC. A549 xenograft tumor model was used to evaluate the inhibitory effect of XBP on lung cancer. Apoptotic proteins Bax and Bcl-2 were detected in the tumor by immunohistochemistry.Ninety active ingredients and 191 potential drug targets were screened from XBP. A total of 280 pathways were enriched. Through these analyses, AKT1 was identified as a potential target for XBP to inhibit NSCLC. Molecular docking results showed that XBP ingredients had high affinity with AKT1. XBP significantly inhibited cell proliferation in A549 and H460 in a concentration-dependent manner. XBP induced the apoptosis of A549 cells and increased Caspase 3 expression. XBP significantly increased Bax and Caspase 3 expressions and inhibited Bcl-2 protein level. The mechanism of action was XBP’s inhibition of AKT phosphorylation. Xenograft results showed that XBP could inhibit lung cancer tumor growth and induce tumor cell apoptosis.Our research proved the anti-NSCLC effect of XBP through network pharmacology analysis and experiments. Results give a theoretical basis for XBP’s clinical anti-tumor effect and lay the foundation for further research on XBP.

目的 探讨和厚朴酚(honokiol,HNK)对肿瘤炎性微环境诱导的肺癌细胞H460血管生成的影响及其可能的机制.方法 采用CCK-8检测HNK对H460细胞和人脐静脉内皮细胞(HUVECs)增殖的影响;RT-PCR、Western blot、免疫荧光检测血管内皮生长因子(VEGF)的表达;Western blot检测信号通路蛋白p-IκBα、p-IKKα和NF-κB p65蛋白表达.采用划痕试验、Transwell迁移试验和成管试验检测HNK抑制HUVEC细胞的迁移和血管生成能力.结果 HNK作用H460细胞24、48、72 h后,浓度和时间依赖地抑制H460细胞增殖.HNK能够浓度依赖的抑制HUVEC细胞的存活.HNK还降低了H460细胞中血管内皮生长因子(VEGF)的蛋白质和mRNA表达水平.随后,HNK浓度依赖性地抑制了NF-κB信号通路中IκBα、NF-κB和p-IKKα.划痕试验、Tran-swell小室迁移试验和成管试验显示HNK处理的H460条件培养基具有抑制HUVEC细胞的迁移和血管生成能力.结论 HNK可以通过抑制NF-κB途径导致VEGF的下调而降低人肺癌细胞的活力和血管生成.

目的:建立益气逐瘀利水方的HPLC指纹图谱,并测定4种成分含量,为益气逐瘀利水方产业化开发的质量控制提供参考.方法:采用Agilent ZORBAX Eclipse XDB-C18色谱柱,乙腈-0.1％磷酸水为流动相,梯度洗脱,体积流量1.0 mL·min-1,柱温30℃,检测波长245 nm,建立10批益气逐瘀利水方指纹图谱.采用中药色谱指纹图谱相似度评价软件(2012年版)进行相似度评价,结合聚类分析(CA)、主成分分析(PCA)及正交偏最小二乘法-判别分析(OPLS-DA)模式识别技术进行质量评价,同时进行含量测定.结果:10批益气逐瘀利水方标准汤剂指纹图谱相似度均大于0.995,标定出共有峰24个,指认其中的4个共有峰(14号峰毛蕊异黄酮葡萄糖苷、15号峰阿魏酸、17号峰汉防己乙素、19号峰粉防己碱),CA、PCA及OPLS-DA将10批样品分成2类.定量分析方法学考察结果良好,10批样品中毛蕊异黄酮葡萄糖苷、阿魏酸、汉防己乙素、粉防己碱的定量结果分别为43.98～64.18、107.32～167.95、122.63～175.21、391.62～582.02 μg·g-1.结论:所建立的益气逐瘀利水方指纹图谱及定量测定方法稳定性好、重复性高,可更加全面系统地评价益气逐瘀利水方的质量.

Ulcerative colitis (UC) is a chronic inflammatory colorectal disease characterized by excessive mucosal immune response activation and dysfunction of autophagy in intestinal epithelial cells. Traditional herbal preparations, including the Huangkui lianchang decoction (HLD), are effective in UC clinical treatment in East Asia, but the underlying mechanism is unclear. This study evaluated the therapeutic effects and associated molecular mechanisms of HLD in UC in vivo and in vitro. A C57BL/6 UC mouse model was established using 2.5% dextran sulfate sodium. The effects of HLD on the colonic structure and inflammation in mice were evaluated using mesalazine as the control. The anti-inflammatory effects of HLD were assessed using disease activity index (DAI) scores, histological scores, enzyme-linked immunosorbent assay, immunohistochemistry, immunofluorescence, and western blotting. HLD displayed a protective effect in UC mice by reducing the DAI and colonic histological scores, as well as levels of inflammatory cytokines and NF-κB p65 in colonic tissues. NCM460 lipopolysaccharide-induced cells were administered drug serum-containing HLD (HLD-DS) to evaluate the protective effect against UC and the effect on autophagy. HLD-DS exhibited anti-inflammatory effects in NCM460 cells by reducing the levels of inflammatory cytokines and increasing interleukin 10 levels. HLD-DS reduced p-NF-κB p65, LC3II/I, and Beclin 1 expression, which suggested that HLD alleviated colitis by inhibiting the NF-κB pathway and autophagy. However, there was no crosstalk between the NF-κB pathway and autophagy. These findings confirmed that HLD was an effective herbal preparation for the treatment of UC.

[目的]探讨扶正胶囊提取物对免疫抑制小鼠免疫功能的调节作用.[方法]将60只昆明小鼠进行随机分组,每组10只,分为空白组、模型组、阳性对照组以及扶正胶囊提取物低、中、高剂量组.采用环磷酰胺腹腔注射建立小鼠免疫功能低下模型,检测各组小鼠的胸腺指数和脾脏指数、单核细胞吞噬能力、血清中白细胞介素-4(IL-4)、白细胞介素10(IL-10)、白细胞介素-17(IL-17)、肿瘤坏死因子-α(TNF-α)、干扰素-γ(IFN-γ)水平和脾T淋巴细胞亚群CD3+T淋巴细胞(CD3+)、CD4+T淋巴细胞(CD4+)、CD8+T淋巴细胞(CD8+)的分布与比例.[结果]扶正胶囊提取物能提升由环磷酰胺诱导的免疫低下小鼠的胸腺指数和脾脏指数,增强单核细胞吞噬功能,显著提高小鼠细胞免疫因子IL-4、IL-10、IFN-γ含量,降低IL-17、TNF-α含量,上调脾淋巴细胞亚群CD3+CD4+的表达程度和提升CD3+CD4+/CD3+CD8+比值.[结论]扶正胶囊提取物能够提升环磷酰胺所致的免疫抑制小鼠的免疫功能.

目的:建立曲酮酊中醋酸曲安奈德含量的高效液相色谱(HPLC)测定方法.方法:采用DIKMA Di-amonsilC18(5μm,250 mm×4.6 mm)色谱柱,以甲醇-水(70: 30)为流动相,流速为1.0 mL/min,柱温为30℃C,检测波长为240 nm;等度洗脱后,测定曲酮酊中醋酸曲安奈德的含量.结果:醋酸曲安奈德的线性范围为0.11～0.55 mg/mL(r=0.999 7,n=5),平均回收率为99.93％,相对标准偏差(relative standard deviation,RSD)为1.28％;近2年生产的5批次曲酮酊中醋酸曲安奈德的百分含量(按40 mg/mL为100％计算)在88.73％～97.36％之间,有4批次含量大于90％.结论:该测定方法简便、快捷、准确,适用于自制制剂中曲酮酊的含量测定,为其质量标准的建立提供参考.

Activation of hepatic stellate cells (HSCs) is a pivotal event in liver fibrosis, characterized by enhanced retinoic acid signals. Although up-regulated retinoic acid signal responds further to maintain HSC activation, the underlying molecular mechanisms are largely unknown. In this study, we sought to investigate the role of lncRNA-H19 in regulation of retinoic acid signals, and to further examine the underlying mechanism in this molecular context. We found that lncRNA-H19 upregulation could enhance retinoic acid signals to induce HSC activation, whereas lncRNA-H19 knockdown completely disturbed retinoic acid signals. Moreover, the activation of retinoic acid signals impaired the lncRNA-H19 knockdown mediated HSC inactivation. Interestingly, we also found that enhanced retinoic acid signals by lncRNA-H19 was associated with a coordinate increase in retinol metabolism during HSC activation. Increased retinol metabolism contributed to obvious lipid droplet consumption. Importantly, we identified that alcohol dehydrogenase III (ADH3) was essential for lncRNA-H19 to enhance retinoic acid signals. The inhibition of ADH3 completely abrogated the lncRNA-H19 mediated retinoic acid signals and HSC activation. Of note, we identified dihydroartemisinin (DHA) as a natural inhibitor for lncRNA-H19. Treatment with DHA significantly decreased the expression of lncRNA-H19, reduced the expression of ADH3, blocked retinoic acid signals, and in turn, inhibited HSC activation. Overall, these results provided novel implications to reveal the molecular mechanism of increased retinoic acid signals during HSC activation, and identify lncRNA-H19/ADH3 pathway as a potential target for the treatment of liver fibrosis.

目的:建立羌菊感冒颗粒HPLC指纹图谱,并测定其中7种成分的含量.方法:采用ZORBAX Eclipse XDB-C18(250 mm×4.6 mm,5 μm)色谱柱;流动相为乙腈-0.1％磷酸溶液,梯度洗脱;流速为1.0 mL/min;柱温为35℃;检测波长为254 nm;建立HPLC指纹图谱;并在254、325 nm波长下测定样品中7种成分的含量.结果:建立羌菊感冒颗粒的指纹图谱,共标定26个共有峰,指认出7种成分,10批样品的相似度均＞0.950.聚类分析将样品大致分为2类.绿原酸、升麻素苷、阿魏酸、异绿原酸B、5-O-甲基维斯阿米醇苷、蒙花苷、甘草酸在相应的浓度范围内线性关系良好(r≥0.9992),平均加样回收率为98.40％ ～ 101.48％,RSD为0.92％～ 2.03％.结论:该方法简便、准确、重复性好,可以用于羌菊感冒颗粒的质量控制.

目的:建立高效液相色谱法(HPLC)同时测定三黄洗剂中5种成分(盐酸小檗碱、黄芩苷、汉黄芩苷、芦荟大黄素和大黄酸)的含量.方法:采用ZORBAX Eclipse XDB-C18色谱柱(4.6 mm×250 mm,5μm);甲醇-0.1％磷酸溶液为流动相梯度洗脱,流速1.0 mL/min;检测波长265 nm;柱温30℃;进样量10μL.结果:盐酸小檗碱、黄芩苷、汉黄芩苷、芦荟大黄素和大黄酸分别在28.56～171.36μg/mL,27.26～163.56μg/mL,8.84～53.04μg/mL,1.508～9.048μg/mL,0.642～3.852μg/mL(r均≥0.9998)范围内呈良好的线性关系,平均加样回收率(n=6)及相应的RSD分别为98.70％(1.60％),98.61％(1.72％),99.09％(1.97％),98.16％(4.23％),99.71％(2.84％).结论:该实验建立的高效液相色谱法简便快速,结果准确,稳定性良好,为科学评价和有效控制三黄洗剂的质量提供可靠依据.

目的 建立抗病毒颗粒(金银花、连翘、蒲公英等)HPLC指纹图谱,并同时测定新绿原酸、绿原酸、隐绿原酸、咖啡酸、木犀草苷、异绿原酸B、3,5-二咖啡酰奎宁酸、4,5-二咖啡酰奎宁酸、蒙花苷的含有量.方法 该药物水提液的分析采用ZORBAX Eclipse XDB-C18色谱柱(4.6 mm×250 mm,5μm);流动相乙腈-水(含0.1％甲酸),梯度洗脱,体积流量1.0 mL/min;检测波长320 nm;柱温30℃.结果 12批样品指纹图谱中有17个共有峰,并指认出其中10个,相似度大于0.97,无明显分类.9种成分在各自范围内线性关系良好(R2＞0.9990),平均加样回收率97.34％ ～ 102.69％,RSD 0.79％ ～2.20％.结论 该方法准确、重复性好,可用于抗病毒颗粒的质量控制.