甜草Oldenlandia cantonensis How的化学成分

研究了民间草药甜草O ldenlandia cantonensisHow的化学成分。从乙醇提取物的乙酸乙酯洗脱部分得到新的五环三萜urs-12-en-29-αoic ac id-3β-ol。该化合物结构通过NMR、IR、MS等波谱数据综合解析确定。研究了urs-12-en-29-αoic ac id-3β-ol对重组人DNA拓扑异构酶Ⅰ、肝癌细胞BEL-7402和胃腺癌细胞MCG-803的抑制作用,效果显著,IC50值分别为12.0×10-6、6.5×10-6、8.0×10-6g/mL。由V(石油醚)∶V(乙酸乙酯)=20∶1洗脱得到的低极性成分进行了气相色谱-质谱分析,共鉴定60个化合物,其中长链脂肪族化合物,如烷烃、饱和及不饱和羧酸(酯)含量较丰富,占36.16%,萜类和甾体类化合物分别占6.42%和9.28%。

Effects of Oldenlandia diffusa Polysaccharides on the Structures of Chick Small Intestine Tissues

In order to explore the application effect of Oldenlandia polysaccharides(OPS)in the production of AA broilers,2007-day-old AA broilers were randomly divided into 4 groups,namely groups Ⅰ,Ⅱ,Ⅲ,and Ⅳ,each including 50 chicks.The control group(group Ⅰ)was fed with basal diet;and the 3 experimental groups were fed based on the basal diet with the addition of OPS at 0.4 g/kg(group Ⅱ),0.8 g/kg(group Ⅲ),and 1.2 g/kg(group Ⅳ)feed for 1 week,respectively,and then fed the basal diet for 4 weeks.At the ages of 14,28,and 42 d,10 chickens were put into death in the control group and the experimental groups,respectively,and the duodenum and jejunum tissue samples were collected for the analysis of the effects of OPS on the structures of chick intestines.The results showed that at the age of 14 d,the villus lengths of duodenum and jejunum in groups Ⅱ,Ⅲ,and Ⅳ were significantly greater than those in group Ⅰ(P<0.05),and the ratios of duodenal or jejunal villus length to crypt depth in groups Ⅱ and Ⅲ were significantly greater than that in group Ⅰ(P<0.05);at the age of 28 d,the villus length of duodenum in group Ⅱ was significantly greater than that in group Ⅰ(P<0.05);and at the age of 42 d,the ratios of jejunual villus length to crypt depth in groups Ⅱ,Ⅲ and Ⅳ were significantly larger than those of group I(P<0.05).It showed that OPS could promote the small intestine development of AA broilers aged 14 to 42 d.

Flavonoid-Rich Extract of Oldenlandia diffusa(Willd.)Roxb.Inhibits Gastric Cancer by Activation of Caspase-Dependent Mitochondrial Apoptosis

Objective:To evaluate the apoptosis and cycle arrest effects of Oldenlandia diffusa flavonoids on human gastric cancer cells,determine the action mechanisms in association with the mitochondrial dependent signal transduction pathway that controls production of reactive oxygen species(ROS),and evaluate the pharmacodynamics of a mouse xenotransplantation model to provide a reference for the use of flavonoids in prevention and treatment of gastric cancer.Methods:Flavonoids were extracted by an enzymatic-ultrasonic assisted method and purified with D-101 resin.Bioactive components were characterized by high-performance liquid chromatography.Cell lines MKN-45,AGS,and GES-1 were treated with different concentrations of flavonoids(64,96,128,and 160μg/mL).The effect of flavonoids on cell viability was evaluated by MTT method,and cell nuclear morphology was observed by Hoechst staining.The apoptosis rate and cell cycle phases were measured by flow cytometry,the production of ROS was detected by laser confocal microscope,the mitochondrial membrane potential(MMP)were observed by fluorescence microscope,and the expression of apoptotic proteins related to activation of mitochondrial pathway were measured by immunoblotting.MKN-45cells were transplanted into BALB/c nude mice to establish a xenograft tumor model.Hematoxylin and eosin staining was used to reveal the subcutaneous tumor tissue.The tumor volume and tumor weight were measured,the expression levels of proliferation markers proliferating cell nuclear antigen(PCNA)and Ki-67were detected by immunohistochemistry,and the expression levels of CA72-4 were measured by enzyme linked immunosorbent assay.Results:Oldenlandia diffusa flavonoids inhibited proliferation of MKN-45 and AGS human gastric cancer cells,arrested the cell cycle in G1/S phase,induced accumulation of ROS in the process of apoptosis,and altered MMP.In addition,flavonoids increased Apaf-1,Cleaved-Caspase-3,and Bax,and decreased Cyclin A,Cdk2,Bcl-2,Pro-Caspase-9,and Mitochondrial Cytochrome C(P<0.05).The MKN-45 cell mouse xenotransplantation model further clarified the growth inhibitory effect of flavonoids towards tumors.The expression levels of PCNA and Ki-67 decreased in each flavonoid dose group,the expression level of CA72-4 decreased(P<0.05).Conclusion:Flavonoids derived from Oldenlandia diffusa can inhibit proliferation and induce apoptosis of human gastric cancer cells by activating the mitochondrial controlled signal transduction pathway.

3D Microfluidic System for Evaluating Inhibitory Effect of Chinese Herbal Medicine Oldenlandia diffusa on Human Malignant Glioma Invasion Combined with Network Pharmacology Analysis

Objective:To investigate the anti-invasion efficacy of the ethanol extract of Oldenlandia diffusa Will.(EEOD) on a three-dimensional(3D) human malignant glioma(MG) cell invasion and perfusion model based on microfluidic chip culture and the possible mechanism of action of Oldenlandia diffusa Will.(OD).Methods:The comprehensive pharmacodynamic analysis method in this study was based on microfluidic chip 3D cell perfusion culture technology,and the action mechanism of Chinese medicine(CM) on human MG cells was investigated through network pharmacology analysis.First,the components of EEOD were analyzed by ultraperformance liquid chromatography with quadrupole time-of-flight mass spectrometry(UPLC-Q-TOF/MS).Then,cell viability and apoptosis were assessed to determine the optimum concentration of EEOD for invasion experiments,and two-dimensional(2D) migration and invasion abilities of U87 and U251 MG cells were evaluated using scratch wound and Transwell assays.The possible mechanism underlying the effects of EEOD on glioma was analyzed through a network pharmacology approach.Results:Thirty-five compounds of EEOD were detected by UPLC-Q-TOF/MS.EEOD suppressed the viability of MG cells,promoted their apoptosis,and inhibited their migratory and invasive potentials(all P<0.05).Network pharmacology analysis showed that OD inhibited the invasion of MG cells by directly regulating MAPK and Wnt pathways through MAPK,EGFR,MYC,GSK3B,and other targets.The anti-invasion effect of OD was also found to be related to the indirect regulation of microtubule cytoskeleton organization.Conclusion:EEOD could inhibit the invasion of human MG cells,and the anti-invasion mechanism of OD might be regulating MAPK and Wnt signaling pathways and microtubule cytoskeleton organization.

Solid-phase Extraction of β-Sitosterol from Oldenlandia diffusa Using Molecular Imprinting Polymer

The β-sitosterol imprinted polymer was prepared for selective extraction and analysis of β-sitosterol from Old-enlandia diffusa （0. diffusa） followed by HPLC with UV detection. The imprinted polymers show high affinity and selectivity to β-sitosterol. Using this molecularly imprinted polymer （MIP） cartridge as solid-phase extraction （SPE） material, the interferences could be quickly washed out and β-sitosterol was selectively retained and enriched. HPLC analysis method was used to evaluate the characteristics of this MIP material. At the condition of mobile phase composed of MeOH/H20/H3PO4 （99/1/0.1, V/V/V, pH=6.0） and the flow rate of 1.0 mL·min -1, a good linear relationship was demonstrated when the concentrations of β-sitosterol were in the range of 0.50--100.0 μg·mL-1. The recoveries ranged from 75.3% to 86.5% and the inter-day and intra-day relative standard deviations were less than 5%. This developed HPLC method was proved to be acceptable for extraction offl-sitosterol from O. diffusa.

白花蛇舌草总黄酮对人结直肠癌细胞增殖和凋亡的影响

目的:探究白花蛇舌草总黄酮对人结直肠癌细胞增殖和凋亡的影响。方法:体外培养HCT116细胞,用不同浓度白花蛇舌草总黄酮进行处理,分组:0μg/mL组、1μg/mL组、3μg/mL组、6μg/mL组、12μg/mL组。采用细胞计数试剂盒法检测24 h和48 h各组HCT116细胞的增殖能力,并计算抑制率。用苏木精-伊红染色观察细胞形态,用流式细胞术检测HCT116细胞凋亡情况,用实时荧光定量逆转录聚合酶链反应(Real-Time Fluorescence PCR,qRT-PCR)检测B淋巴细胞瘤-2(B-cell Lymphoma-2,Bcl-2)、Bcl2关联X蛋白(Bcl2 Associated X,Bax)和半胱氨酸蛋白酶3(Caspase-3)的信使核糖核酸(Messenger RNA,mRNA)表达水平,用蛋白质印迹(Western blot)法检测Bcl-2、Bax、Caspase-3和裂解的Caspase-3的蛋白表达水平。结果:不同浓度的白花蛇舌草总黄酮能明显抑制癌细胞增殖,其浓度越高,抑制率越高(均P <0.05),且处理组48 h抑制率均高于24 h(均P <0.05)。随着浓度的增加,细胞核逐渐收缩,核碎片增加,同时凋亡小体产生。与对照组相比,白花蛇舌草总黄酮也显著促进HCT116细胞的凋亡率(P <0.05)。此外,与对照组相比,白花蛇舌草总黄酮显著下调了Bcl-2和Caspase-3的表达,同时上调Bax和裂解的Caspase-3的表达,并且Bcl-2/Bax值显著降低,而裂解的Caspase-3/Caspase-3值显著升高。结论:白花蛇舌草总黄酮可抑制结直肠癌细胞的体外增殖,并通过影响Bcl-2、Bax和Caspase-3的表达诱导细胞凋亡。

白花蛇舌草总黄酮对肝细胞癌干细胞增殖及凋亡的影响

目的探讨白花蛇舌草总黄酮(FOD)对Huh7来源的肝细胞癌干细胞增殖及凋亡的影响。方法培养Huh7细胞系,通过流式分选技术筛选出Huh7细胞系中CD133阳性的干细胞(CD133^(+)-Huh7);流式分析术检测分选后CD133阳性细胞比例;Western blotting实验检测分选纯化前后细胞干性指标Nanog、Oct4、Sox2的表达。分别用0、50、100、400μg/mL FOD分别作用CD133^(+)-Huh7肝细胞癌干细胞24、48、72、96 h,应用CCK8(Cell Counting Kit-8)法检测其对细胞增殖的影响;平板克隆实验检测各组细胞增殖能力变化;Annexin V-PE/7-AAD法检测各组细胞凋亡比例,并用Western blotting法检测p53、FAS-FADD、抗凋亡蛋白Bcl-2、促凋亡蛋白Bax及凋亡指标Cleaved-Caspae3等凋亡通路蛋白的表达。结果纯化后的Huh7细胞的干性标志物Nanog、Oct4、Sox2表达更高。100μg/mL FOD刺激CD133^(+)-Huh7干细胞72 h,CCK8实验结果显示其细胞增殖较阴性对照组(0μg/mL处理组)降低(P<0.05),平板克隆实验亦显示其细胞增殖变弱;细胞凋亡比例较阴性对照组显著升高(P<0.05),抗凋亡蛋白Bcl-2表达降低而促凋亡蛋白Bax以及凋亡指标Cleaved-Caspae3的蛋白表达升高,p53、FAS、FADD通路显著上调。结论FOD可显著抑制CD133^(+)-Huh7肝细胞癌干细胞增殖,并显著促进细胞凋亡。

白花蛇舌草总黄酮对乳腺癌MDA-MB-231细胞系增殖、凋亡及干性的影响

目的探讨白花蛇舌草总黄酮(FOD)对MDA-MB-231乳腺癌细胞增殖、凋亡及干性的影响。方法培养MDA-MB-231细胞系,分别用0、100、200、400μg/mL FOD作用MDA-MB-231乳腺癌细胞不同时间(24、48、72 h),CCK8(Cell Counting Kit-8)法检测其对细胞增殖的影响;平板克隆试验检测各组MDA-MB-231细胞增殖能力变化;Annexin V-PE/7-AAD法检测各组MDA-MB-231细胞凋亡比例,并用Western blotting法检测Bcl2、Bax及凋亡指标cleaved-caspae3等凋亡通路蛋白的表达,流式细胞检测CD44+/CD24-乳腺癌细胞干性,并用Western blotting法检测干性肿瘤指标Nanog、Sox2、Oct4的表达量。结果CCK8实验显示,400μg/mL FOD作用72 h(FOD组)后细胞增殖较阴性对照组(DMSO组)受到明显抑制(P<0.05);平板克隆试验显示,药物干预组细胞增殖下降(P<0.05);经400μg/mL FOD处理的MDA-MB-231干性标志物Nanog、Oct4、Sox2表达更低(P<0.05)。流式细胞仪检测FOD组细胞凋亡比例较阴性对照组明显升高(P<0.05),抗凋亡蛋白Bcl-2表达降低,而促凋亡蛋白Bax及凋亡指标cleaved-caspae3的蛋白表达升高,FOD处理后乳腺癌细胞增殖、凋亡及干性改变,通路蛋白Akt及GSK3β磷酸化受到抑制,β-catenin表达降低。结论FOD可明显抑制MDA-MB-231乳腺癌细胞增殖及干性,促进细胞凋亡。

甜草总多酚体外抗氧化活性研究

采用总抗氧化能力、OH·清除率、DPPH·清除率来考察甜草(Oldenlandia cantonensis How)总多酚的体外抗氧化活性。结果表明,甜草总多酚总抗氧化能力略小于维生素C(VC),但甜草总多酚OH·清除率远高于VC。此外,甜草总多酚对DPPH·的IC50(22.2μg/m L)与VC相近(16.0μg/m L)。甜草总多酚是天然的抗氧化活性剂和自由基清除剂。

白花蛇舌草的免疫学调节活性和抗肿瘤活性

目的 :研究白花蛇舌草的免疫学调节活性和抗肿瘤活性。方法 :用3H介入法分析了白花蛇舌草提取物 (Oldenlandiadiffusaextract,ODE)对小鼠脾细胞的增殖活性 ;用51Cr游离实验测定了小鼠和人杀伤细胞对肿瘤细胞的特异性杀伤活性 ,用ELISA法和生物法研究了B细胞抗体的产生以及单核细胞的细胞因子产生 ,并用3H介入法分析了单核细胞对肿瘤细胞的吞噬功能 ;用层析法、蛋白酶消化法和糖分解处理(即NaIO4 处理 )分析了白花蛇舌草的化学成分。结果 :ODE对小鼠脾细胞的增殖活性有很强的促进作用 ;ODE增强小鼠和人杀伤细胞对肿瘤细胞的特异性杀伤活性 ,增强B细胞抗体的产生以及单核细胞的细胞因子产生 ,并增强单核细胞对肿瘤细胞的吞噬功能。白花蛇舌草的化学成分为 90道尔顿的糖蛋白。结论 :ODE对小鼠和人有免疫调节作用 ,并通过刺激机体的免疫系统杀伤或吞噬肿瘤细胞 ,这些活性可应用于临床调节免疫功能和治疗肿瘤等疾病。

白花蛇舌草化学成分的研究

目的:对白花蛇舌草的化学成分进行研究。方法:采用聚酰胺,Sephadex LH-20,硅胶和HPLC等多种色谱方法进行分离,理化性质,光谱数据鉴定结构。结果:分离鉴定9个化合物:2,6-二羟基-1-甲氧基-3-甲基蒽醌(1),2-羟基-1-甲氧基-3-甲基蒽醌(2),2-羟基-3-甲基蒽醌(3),quercetin-3-O-[2-O-(6-O-E-sinapoyl)-β-D-glucopyr-anos-yl]-β-glucopyranoside(4),quercetin-3-O-[2-O-(6-O-E-feru loyl)-β-D-glucopyranosyl]-β-glucop-yranoside(5),kaempferol-3-O-[2-O-(6-O-E-feru loyl)-β-D-glucopyranosyl]-β-galactopyranoside(6),quercetin-3-O-(2-O-β-D-glucopyr-anosyl)-β-D-glucopyranoside(7),芦丁(8),槲皮素(9)。结论:化合物1和8为首次从该种植物中得到,其中化合物1为新化合物。

白花蛇舌草总黄酮的抗炎及抗菌作用

目的观察白花蛇舌草总黄酮抗炎及抗菌作用。方法采用二甲苯诱导小鼠耳肿胀模型、大鼠松节油气囊肉芽增生模型、新鲜蛋清诱导大鼠足爪肿胀模型、醋酸所致小鼠毛细血管通透性增高试验和体外抗菌试验,观察白花蛇舌草总黄酮的抗炎及抗菌作用。结果白花蛇舌草总黄酮(15、30、60mg·kg-1)对二甲苯诱导的小鼠耳肿胀和醋酸所致小鼠毛细血管通透性增高有一定的抑制作用;白花蛇舌草总黄酮(12、24、48mg·kg-1)对大鼠松节油气囊肉芽增生和新鲜蛋清诱导大鼠足爪肿胀亦有明显的抑制作用;在体外,白花蛇舌草总黄酮对球菌和杆菌均具有不同程度的抑菌和杀菌作用,且对球菌的作用优于杆菌。结论白花蛇舌草总黄酮具有抗炎及抗菌作用。

白花蛇舌草提取物抗氧化作用的研究

研究了白花蛇舌草的水、乙醇、丙酮、氯仿、乙醚、石油醚提取物的抗氧化活性及其有效成分。结果表明 :在花生油中 ,这 6种溶剂的提取物均有抗氧化作用 ,以丙酮提取物的抗氧化作用最强 ,其最适使用质量分数为 0 .12 %。质量分数 0 .12 %的丙酮提取物的抗氧化活性低于质量分数 0 .0 2 %的茶多酚 ,但高于质量分数 0 .0 2 %的BHT、BHA、VC、VE。白花蛇舌草提取物的抗氧化成分以黄酮、萜类、羟基蒽醌。

白花蛇舌草总黄酮的免疫调节作用

目的 研究白花蛇舌草总黄酮(FOD)的免疫调节作用。方法 通过测定小鼠脾细胞IgM抗体形成,脾淋巴细胞的增殖反应,小鼠血清IL- 2和IFN -γ含量以及观察对小鼠白细胞数量的影响,研究白花蛇舌草总黄酮的免疫调节作用。结果 白花蛇舌草总黄酮(15、30、60mg·kg-1 )促进免疫功能低下小鼠由ConA或LPS诱导的脾淋巴细胞的增殖反应,并提高小鼠血清IL 2和IFN -γ的含量;白花蛇舌草总黄酮(60mg·kg-1 )促进免疫功能低下小鼠脾脏IgM抗体形成,并升高抗肿瘤药物(环磷酰胺或阿糖胞苷)所致的小鼠白细胞减少。结论 白花蛇舌草总黄酮具有增强机体特异性免疫功能和非特异性免疫功能的作用。

UPLC指纹图谱结合化学计量学的白花蛇舌草真伪鉴别研究

目的:建立白花蛇舌草及其伪品水线草的UPLC指纹图谱,结合化学计量学,进行真伪鉴别。方法:建立白花蛇舌草和水线草的UPLC指纹图谱,对主要色谱峰进行化学指认及快速检识,利用两者化学成分差异结合化学计量学分析,开展真伪鉴别。结果:分别建立了两者UPLC指纹图谱方法并评价了多批次的相似度;白花蛇舌草22个共有峰中的10个、水线草16个共有峰中的5个及4个非共有峰得到了指认或检识;主成分分析(PCA)可将真品、伪品分为两组;而偏最小二乘法分析(OPLS-DA)显示车叶草酸甲酯等5个色谱峰是分组的主要原因;白花蛇舌草中的(E)-6-O-阿魏酰鸡屎藤次苷甲酯、(Z)-6-O-香豆酰鸡屎藤次苷甲酯,水线草中的槲皮素-3-O-桑布双糖苷可作为两者的3个特征差异峰用于白花蛇舌草真伪鉴别。结论:将UPLC指纹图谱与化学计量学方法相结合,可用于白花蛇舌草真伪鉴别,从而为提高白花蛇舌草整体质量控制方法提供参考。

白花蛇舌草在裸鼠胶质瘤间质化疗的实验研究

目的 探讨白花蛇舌草在可移植性人脑胶质瘤间质化疗的剂量及疗效 ,并探讨其作用机制。方法 将低分化人脑胶质瘤体外细胞系SHG 4 4移植于裸小鼠 ,制作成可移植性实体瘤模型 ,用不同剂量的白花蛇舌草及以博莱霉素为对照组 ,肿瘤间质内注射药物 ,观察实体瘤的瘤重及组织细胞形态的变化。结果 将白花蛇舌草每 1ml含总黄酮以芦丁计算不少于 0 2 5mg时 ,每日 1次 ,间质注射 0 5ml持续 12日后 ,肿瘤生长有明显抑制作用 (P <0 0 5 )。结论 白花蛇舌草有明显抑制肿瘤生长的作用。

白花蛇舌草体外对人肝癌多药耐药细胞Bel-7402抗肿瘤活性的研究

目的探讨白花蛇舌草在体外对肝癌多药耐药细胞Bell-7402生长活性的抑制作用.方法 MTT法检测白花蛇舌草提取物对Bel-7402生长的抑制作用,有无逆转Bel-7402的多药耐药性;用淋巴细胞转化实验检测白花蛇舌草提取物能刺激T淋巴细胞增殖,并筛选出药物的安全剂量范围;集落形成实验观察体外抗癌药物的敏感性.结果白花蛇舌草提取物对肝癌多药耐药细胞Bel-7402的生长具有明显的抑制作用,且这种作用是剂量依赖关系.结论白花蛇舌草提取物在体外对人肝癌多药耐药细胞Be1-7402有抑制作用.

HPLC-TOFMS法对白花蛇舌草药材及其注射剂中化学成分的快速分离与鉴别

目的采用HPLC-TOFMS对白花蛇舌草药材及其注射剂中化学成分进行快速分离鉴别。方法色谱柱Ag-ilent Zorbax SB-C18柱(4.6mm×250mm,5μm),以0.3%醋酸(A)-甲醇(B)为流动相,梯度洗脱,0～30min,体积分数30%～90%B,进样量10μl,流速1.0ml/min,柱温为30℃,飞行时间质谱配有ESI离子源,质量数扫描范围m/z100～1000。结果采用HPLC-TOFMS方法对白花蛇舌草药材及其注射液制剂进行了在线化学成分分离与质谱表征,一次性在一张图谱上共鉴别出白花蛇舌草中11个化学成分,市售注射剂中6个成分,自制注射剂中2个成分。结论这可为中药白花蛇舌草及其注射剂的药效物质基础和质量控制研究奠定基础。

白花蛇舌草提取物体外抗肿瘤作用及机制研究

目的研究中药白花蛇舌草提取物对Bel-7402细胞抗肿瘤作用及其作用机制.方法采用MTT法和集落形成实验检测白花蛇舌草提取物对Bel-7402细胞生长的抑制作用;采用淋巴细胞转化实验检测白花蛇舌草提取物对小鼠脾脏T淋巴细胞增殖的刺激作用,并筛选出药物的安全剂量范围;采用透射电镜初步观察药物作用后Bel-7402细胞的形态变化.结果 1)MTT比色实验、集落形成实验的结果表明,白花蛇舌草提取物对Bel-7402细胞的生长具有明显的抑制作用,且这种作用是剂量依赖关系,IC50为1.6g/L;2)透射电镜观察表明,药物作用后的Bel-7402肿瘤细胞的体积变小,核分裂像显著减少,没有明显的凋亡现象;细胞核固缩,异染色质块状聚集浓染,线粒体变大变圆,基质变淡,线粒体嵴变短变少甚至消失,在极度肿胀时,线粒体转化为小空泡状结构,并有细胞膜破损现象.结论 1)白花蛇舌草提取物可能通过直接影响肿瘤细胞能量代谢,对Bel-7402细胞生长具有明显的抑制作用,且呈剂量依赖关系;2)白花蛇舌草提取物具有促进小鼠脾淋巴细胞增殖的作用.

白花蛇舌草化学成分研究

目的：研究白花蛇舌草水提取部位的化学成分。方法：药材水提取液用大孔吸附树脂、硅胶、MCI、Sephadex LH-20柱色谱、ODS中压液相色谱及半制备HPLC进行分离,并通过理化性质和波谱数据鉴定化合物结构。结果：从白花蛇舌草中分离得16个化合物,分别鉴定为：车叶草苷（1）、去乙酰车叶草苷（2）、京尼平苷（3）、10-去氢京尼平苷（4）、交让木苷（5）、diffusoside A（6）、diffusoside B（7）、松柏苷（8）、鸡屎藤次苷甲酯（9）、乙酰鸡屎藤次苷甲酯（10）、去乙酰车叶草酸苷甲酯（11）、羟异栀子苷（12）、水晶兰苷甲酯（13）、galioside 10-acetate（14）、地芰普内酯（15）、（＋）-neo-olivil（16）。结论：其中,化合物3、8、14~16均为首次从该植物中分离得到。