Bitter Bottle Gourd Toxicity

Bottle gourd (Lagenaria siceraria), colloquially known as “lauki” or “doodhi” in India, is an edible plant in the Cucurbitaceae family. Consumption of raw bottle gourd juice is common practice in India. However, little known is the fact that ingestion of raw bottle gourd juice that is extremely bitter tasting is associated with cucurbitacin toxicity. Cucurbitacin is a pheromone produced by the plant as a defense mechanism against insects and herbivores. It is responsible for imparting the bitter taste, and the associated toxicity. The exact mechanism of cucurbitacin toxicity is not well understood, however it is suspected to result in gastric erosions and increased capillary permeability, resulting in rapid onset of vomiting, diarrhea, gastrointestinal bleeding, hypotension and shock. As serum and urine concentration measurements of cucurbitacin are not readily available, bottle gourd toxicity remains a clinical diagnosis based largely on the temporal association of ingestion of unusually bitter tasting vegetable or its juice with rapid onset of symptoms. Physician awareness is therefore of paramount importance in the diagnosis of this unusual entity. We present the case of a 78-year-old woman, with no comorbid conditions, who presented to the Emergency Department (ED) with three episodes of vomiting and multiple episodes of watery loose stools soon after ingestion of extremely bitter tasting, fresh bottle gourd juice. A prompt diagnosis of cucurbitacin toxicity was made in the ED and fluid resuscitation was commenced expeditiously. However, it was noted that most physicians were unfamiliar with this entity, and therefore skeptical of the diagnosis. Our rationale in presenting this clinical case report is three-fold: 1) To create physician awareness regarding this unique clinical entity, especially among emergency physicians, as they are the first point of contact for a critically ill patient. 2) To highlight the rapid onset and progression of symptoms in cucurbitacin toxicity. 3) To emphasize aggressive fluid resuscitation and symptomatic management as the mainstay of clinical treatment.

杠板归的化学成分(英文)

采用柱层析方法从蓼科药用植物杠板归(Polygonum Perfoliatum)分离了21个化合物(1～21),通过MS与NMR数据鉴定这些化合物为α-tocopherolquinone(1),7′-dihydroxymatairesinol(2),(24S)-24-ethylcholesta-3β,5α,6α-triol(3),4-dihydroxy-5,7-dihydroxy-4-(4-hydroxyphenyl)coumarin(4),quercetin(5),cucurbitacin IIa(6),cucurbitacin U(7),iotroridoside A(8),pokeweedcerebroside5(9),bonaroside(10),helonioside A(11),helonioside B(12),lapathoside D(13),vanicoside B(14),vanicoside C(15),vanicoside F(16),asteryunnanoside F(17),saikosaponin M(18),hydropiperoside(19),quercetin-3-O-β-D-glucuronide-6″-butyl ester(20),quercetin-3-O-β-D-glucuronide-6″-methyl ester(21).化合物1～19(除4,5,12)为首次从该植物中分离得到,化合物1～11(除4,5)和17～19为首次从该属植物中分离得到.

葫芦素I(JSI-124)通过p53信号通路诱导HepG2细胞凋亡

目的研究葫芦素I(cucurbitacin I,JSI-124)诱导HepG2人肝癌细胞凋亡的机制。方法用(0.01、0.10、1.00、10.00)μmol/L JSI-124分别处理培养的HepG2细胞24、48、72 h,CCK-8法检测细胞增殖,Hoechst33258染色法观察细胞核形态变化,克隆形成实验观察集落形成能力变化,异硫氰酸荧光素标记的膜联素Ⅴ/碘化丙啶(annexinⅤ-FITC/PI)双标记结合流式细胞术检测细胞凋亡情况,实时定量PCR检测p53及其下游Bax、Fas、鼠双微体基因2(MDM2)的mRNA表达变化,Western blot法检测P53及活化caspase-3的蛋白表达变化。结果JSI-124呈浓度和时间依赖性地抑制HepG2细胞的增殖。Hoechst33258染色法显示JSI-124呈剂量及时间依赖性引起HepG2细胞核染色质的凝集。与对照组相比,流式细胞术检测结果表明1μmol/L JSI-124处理的HepG2细胞凋亡率明显增加。JSI-124显著增强p53及受其调控的下游促凋亡因子Bax和死亡受体Fas mRNA的表达,而与p53结合并抑制p53功能的MDM2的mRNA表达变化不明显。JSI-124处理HepG2细胞48 h后,p53及活化的caspase-3蛋白显著增加。结论 JSI-124通过p53及其下游的促凋亡因子诱导HepG2人肝癌细胞发生凋亡。

Advances in research on the anticancer mechanism of the natural compound cucurbitacin from Cucurbitaceae plants:a review

Cucurbitacins are highly oxidized tetracyclic triterpenoids that are widely found in plants belonging to Cucurbitaceae family and exert various pharmacological effects.Many cucurbitacin derivatives are available,of which cucurbitacins B,D,E,and I are important members of the cucurbitacin family and exert anticancer effects against various cancers.This review summarizes the advances in research on cucurbitacins B,D,E,and I in inducing tumor cell apoptosis,cytoskeletal destruction,cell cycle arrest,and autophagy and in regulating various cancer-related signaling pathways.In addition,this review summarizes the latest research on the synergistic effects of the combination of cucurbitacins and clinically approved chemotherapeutic drugs.The findings summarized in this review suggest that cucurbitacins are multi-targeting and multi-functional anticancer drugs and that their complex anticancer mechanisms should be examined in future studies.Because of their proven benefits,cucurbitacins have the potential to be used as anticancer drugs in the clinical setting.

Cucurbitacin E induces apoptosis and attenuates activation of hepatic stellate cells via PI3K/Akt-AMPK-mTOR signaling pathway

OBJECTIVE Hepatic fibrosis is a wound-healing response for injury.Activated hepatic stellate cells(HSCs)are the preferred targets of anti-hepatic fibrotic therapies.cucurbitacin E(CuE)is,one well-known natural compound derived from traditional Chinese medicine,used in Asian countries for the prevention and treatment of hepatic disease.Therefore,the present study elucidated the mechanism of CuE on inducing apoptosis and attenuating hepatic fibrosis towards activated HSCs.METHODS The murine HSC(tHSC/Cl-6)cell line were incubated in 96-well plates and treated with TNF-αand CuE at various concentrations and indicated times.Cell viability was assessed with MTT assay.Another,t-HSC/Cl-6 were incubated in 6-well plates and also treated with TNF-α,CuE,AICAR or metformin for the indicated time and concentration.Cell protein and mRNA were prepared using kit and relevant signaling were detected by Western blotting and RT-PCR.RESULTS CuE inhibited cell proliferation of activated HSC/T-6cells in concentration-and time-dependent manner.CuE triggered the activation of caspase-3,cleaved the PARP,ration of bcl-2/bax,and cytochrom c protein in a time-and concentration-dependent manner.CuE decreased p-Erk/MAPK without effects on p-p38 and p-JNK.CuE inhibited the protein and mRNA expressions ofα-SMA,TIMP-1 and collagenⅠ in activated HSC-T6.CuE broadly blocked p-PI3 K,p-Akt,p-mTOR and p-p70S6 Kexpressions.CuE significantly increased phosphorylated AMPK expression as well as AICAR and metoformin.And metformin showed significantly higher activation of AMPK than AICAR.Ability of CuE on activation of AMPK was between AICAR and metformin.It′s also found that CuE significantly decreased p-mTOR as well as AICAR and metformin.CONCLUSION CuE could modulate HSC survival and activation as a potential anti-fibrotic agent for liver fibrosis treatment.The findings demonstrate that CuE induced HSC apoptosis via ERK/MAPK and PI3K/Akt-AMPK-mTOR signaling.

Lepida Acid A from Basidiomycetes Russula lepida

A new compound, lepida acid A 1, has been isolated from the fruiting bodies of Basidiomycetes Russula lepida. Its structure was elucidated by spectral methods.

Cucurbitacin E regulates activation of hepatic stellate cells via AMPK-mTOR pathway

Hepatic fibrosis is a wound-healing response for injury. Activated hepatic stellate cells （HSCs） are the preferred targets of anti-hepatic fibrotic therapies. Cucurbitacin E （CUE） is, one well-known natural compound de- rived from Traditional Chinese Medicine, used in Asian countries for the prevention and treatment of hepatic dis- ease. Therefore, the present study elucidated the mechanism of CuE on inducing apoptosis and attenuating hepatic fibrosis towards activated HSCs. The murine hepatic stellate cells （t-HSC/C1-6） cell line were incubated in 96-well plates and treated with TNF-α and CuE at various concentrations and indicated times. Cell viability was assessed with MTT assay. Another, t-HSC/C1-6 were incubated in 6-well plates and also treated with TNF-α, CuE, AICAR or metformin for the indicated time and concentration. Cell protein and mRNA were prepared using kit and relevant signaling were detected by Western blot and RT-PCR. CuE inhibited cell proliferation of activated HSC/T-6 cells in concentration- and time-dependent manner. CuE triggered the activation of caspase-3, cleaved the PARP, ration of bcl-2/bax, and cytochrom C protein in a time- and concentration-dependent manner. CuE decreased p-Erk/MAPK without effects on p-p38 and p-JNK. CuE inhibited the protein and mRNA expressions of oL-SMA, TIMP-1 and col- lagen I in activated HSC-T6. CuE broadly blocked p-PI3K, p-Akt, p-roTOR and p-p70S6K expressions. CuE sig- nificantly increased phosphorylated AMPK expression as well as AICAR and metoformin. And metformin showed significantly higher activation of AMPK than AICAR. Ability of CuE on activation of AMPK was between AICAR and metformin. It＇s also found that CuE significantly decreased p-roTOR as well as AICAR and metformin. CuE could modulate HSC survival and activation as a potential anti-fibrotic agent for liver fibrosis treatment. The find- ings demonstrate that CuE induced HSC apoptosis via Erk/MAPK and PI3IC/Akt-AMPK-mTOR signaling.

Cucurbitacin E inhibits the proliferation of hepatoma cells in vitro and in vivo through induction of G2/M phase arrest

Objective Cucurbitacins are the highly oxygenated tetracyclic triterpenes,which are predominantly found in the Cucurbitaceae family but are also present in several other families of the plant kingdom.A number of compounds of this group have been investigated for their cytotoxic,hepatoprotective,anti-inflammatory,cardiovascular and anti-diabetic activities.In China,the cucurbitacin preparation,which contains mostly cucurbitacin B and cucurbitacin E,has been clinically used for the treatment of the primary liver carcinoma.It has been previously reported that cucurbitacin E could produce cytotoxicity against a variety of cancer cells,and various mechanisms were implicated in its cytotoxic effect.The present study is to investigate the effect of cucurbitacin E on hepatoma cells in vitro and in vivo and to study their potential mechanisms of action.Methods The MTT assay was used to assess the viability of human HepG2 and BEL7402 hepatoma cells in vitro after treatment with different concentrations of cucurbitacin E.The cell cycle distribution was determined by flowcytometric analysis after propidium iodide(PI)staining.The cell cycle-related proteins were detected using western blotting analysis.Implanted mouse hepatoma H22 model was built to evaluate the growth inhibitory effect of cucurbitacin E in vivo in mice.Results Our studies found that cucurbitacin E(10-300 nM)produced anti-proliferative effect on human HepG2 and BEL7402 hepatoma cells in vitro without cytotoxicity.According to flowcytometric analysis,cucurbitacin E arrested the cell cycle at G2/M phase in both HepG2 and BEL7402 hepatoma cells after 24 h treatment.Cucurbitacin E induced the decrease in the level of CDK1 protein and the increase in the level of p21 protein,but had no effect on the levels of cyclin A,cyclin B1 and Cdc25C protein.In in vivo anti-tumor experiment,cucurbitacin E had significant inhibitory effects on the growth of mouse H22 hepatoma cells.Conclusions Cucurbitacin E inhibited the proliferation of hepatoma cells in vitro and in vivo,at least in part,through induction of cell cycle arrest at G2/M phase,which was mediated by concomitant upregulation of p21 and downregulation of CDK1.We consider that cucurbitacin E may be useful in the treatment of liver cancer.

Human Exposure to <i>Ecballium elaterium</i>Fruit Juice: Fatal Toxicity and Possible Remedy

The human serious adverse reactions of the folkloric plant, Ecballium elaterium (EE), are well documented in the literature. This report is presenting the medical literature of 74 cases, which experienced severe adverse reactions or deaths that resulted from the administration of the plant juice. The survey of these human cases exhibits several adverse effects such as: acute rhinitis, uvular edema, soft palate, upper airway edema. In conclusion, the use of EE juice in folk medicine can cause severe adverse reactions that should not be ignored but it should be medically treated.

Review of Research Situation of Lagenaria siceraria(Molina) Standl.

Lagenaria siceraria( Molina) Standl. Var. hispisa( Thund.) Hara is an annual creeping herb of the family Cucurbitaceae. It has high nutritional value and medicinal value,and it is a high-quality vegetable with low sugar and many kinds of vitamins. This paper introduced the current research situation of L. siceraria( Molina) Standl. from medicinal value,cultivation management technology and processing technology. Besides,it discussed main points of future researches on the basis of existing research,to promote the development of L. siceraria( Molina) Standl.

Watermelon domestication was shaped by stepwise selection and regulation of the metabolome

Although crop domestication has greatly aided human civilization,the sequential domestication and regulation of most quality traits remain poorly understood.Here,we report the stepwise selection and regulation of major fruit quality traits that occurred during watermelon evolution.The levels of fruit cucurbitacins and flavonoids were negatively selected during speciation,whereas sugar and carotenoid contents were positively selected during domestication.Interestingly,fruit malic acid and citric acid showed the opposite selection trends during the improvement.We identified a novel gene cluster(CGC1,cucurbitacin gene cluster on chromosome 1)containing both regulatory and structural genes involved in cucurbitacin biosynthesis,which revealed a cascade of transcriptional regulation operating mechanisms.In the CGC1,an allele caused a single nucleotide change in Cl ERF1 binding sites(GCC-box)in the promoter of Cl Bh1,which resulted in reduced expression of Cl Bh1 and inhibition of cucurbitacin synthesis in cultivated watermelon.Functional analysis revealed that a rare insertion of 244 amino acids,which arose in C.amarus and became fixed in sweet watermelon,in Cl OSC(oxidosqualene cyclase)was critical for the negative selection of cucurbitacins during watermelon evolution.This research provides an important resource for metabolomics-assisted breeding in watermelon and for exploring metabolic pathway regulation mechanisms.

Cucurbitacin B suppresses metastasis mediated by reactive oxygen species(ROS) via focal adhesion kinase(FAK) in breast cancer MDA-MB-231 cells

Metastasis is responsible for the majority of cancer-related deaths and prevention of metastasis remains a big challenge for cancer therapy. Cucurbitacin B(Cuc B) is a natural triterpenoid with potent anticancer activities while its effect on metastasis remains unclear. In the present study, the inhibitory effect and mechanisms of Cuc B on metastasis were investigated in MDA-MB-231 breast cancer cells. The cells were treated with or without Cuc B, and the cytotoxicity was determined by MTT assay. The effect of Cuc B on metastasis was evaluated with wound healing, transwell, and adhesion assays. Furthermore, the adhesion of cancer cells to endothelial cells was determined. The protein expression was determined by Western blotting. Cuc B(< 100 nmol·L~^(-1)) showed no obvious cytotoxicity to MDA-MB-231 cells, but significantly inhibited migration, invasion, and adhesion to Matrigel, fibronectin, type I collagen, and endothelial cells. Cuc B dramatically inhibited the phosphorylation of focal adhesion kinase(FAK) and paxillin in dose-and time-dependent manners. Furthermore, Cuc B induced intracellular reactive oxygen species(ROS) generation, which could be reduced by N-acetyl-l-cysteine(NAC). In addition, NAC pretreatment could reverse Cuc B-induced suppression of migration and adhesion, expression of FAK, but showed no effect on paxillin expression. In summary, Cuc B suppressed ROS-dependent metastasis through FAK pathway in breast cancer MDA-MB-231 cells, demonstrating novel mechanisms for the anticancer effects of Cuc B.

A structural and data-driven approach to engineering a plant cytochrome P450 enzyme

Functional manipulation of biosynthetic enzymes such as cytochrome P450 s(or P450 s) has attracted great interest in metabolic engineering of plant natural products.Cucurbitacins and mogrosides are plant triterpenoids that share the same backbone but display contrasting bioactivities.This structural and functional diversity of the two metabolites can be manipulated by engineering P450 s.However,the functional redesign of P450 s through directed evolution(DE) or structure-guided protein engineering is time consuming and challenging,often because of a lack of high-throughput screening methods and crystal structures of P450 s.In this study,we used an integrated approach combining computational protein design,evolutionary information,and experimental data-driven optimization to alter the substrate specificity of a multifunctional P450(CYP87 D20)from cucumber.After three rounds of iterative design and evaluation of 96 protein variants,CYP87 D20,which is involved in the cucurbitacin C biosynthetic pathway,was successfully transformed into a P450 mono-oxygenase that performs a single specific hydroxylation at C11 of cucurbitadienol.This integrated P450-engineering approach can be further applied to create a de novo pathway to produce mogrol,the precursor of the natural sweetener mogroside,or to alter the structural diversity of plant triterpenoids by functionally manipulating other P450 s.

Arbuscular mycorrhizal fungi are necessary for the induced response to herbivores by Cucumis sativus

Aims Although ecological interactions are often conceptualized and stud-ied in a pairwise framework,ecologists recognize that the outcomes of these interactions are influenced by other members of the com-munity.Interactions(i)between plants and insect herbivores and(I)between plants and mycorrhizal fungi are ubiquitous in terrestrial ecosystems and may be linked via common host plants.Previous studies suggest that colonization by arbuscular mycorrhizal fungi(AMF)can modifty plants'induced responses to herbivore attack,but these indirect effects of fungal symbionts are poorly understood.I investigated the role of AMF in induced plant response to a gen-eralist herbivore.Methods|manipulated AMF status and herbivory in Cucumis sativus L.(cucumber,Cucurbitaceae)in a greenhouse to investigate induced responses in the presence and absence of the mycorrhi-zal fungus Glomus intraradices(Glomeraceae).Spodoptera exigua Habner(Noctuidae)were used to manipulate prior damage and later as assay caterpillars.I also measured G.intraradices and her-bivory effects on plant N and effects on plant growth.Impor tant Findings AMF status affected the induced response of C.sativus,underscor-ing the importance of incorporating the roles of plant symbionts into plant defense theory.Assay caterpillars ate significantly more leaf tissue only on mycorrhizal plants that had experienced prior damage.Despite more consumption,biomass change in these cat-erpillars did not differ from those feeding on plants with other treat-ment combinations.Leaf N content was reduced by G.intraradices but unaffected by herbivory treatments,suggesting that the observed differences in assay caterpillar feeding were due to changes in defensive chemistry that depended on AMF.

A New Flavone C-glycoside from Citrullus colocynthis

Objective To study the chemical constituents of Citrullus colocynthis. Methods The chemical constituents were isolated and purified by column chromatography on silica gel and Sephadex LH-20 and recrystallization as well. NMR spectra and physicochemical property were characterized for structural identification. Results Eleven compounds were isolated and identified as β-sitosterol (1), α-spinasterol-3-O-β-D-glucopyranoside (2), α-spinasterone (3), bis (2-ethylhexyl) phthalate (4), p-hydroxybenzoic acid (5), 6-C-p-methylbenzoylvitexin (6), dihydrocucurbitacin E (7), cucurbitacin E (8), dihydro-epi-iso-cucurbitacin D (9), dihydroisocucurbitacin B-25-acaetate (10), and cucurbitacin E 2-O-β-D-glucopyranoside (11). Conclusion Compound 6 is a novel compound. Compounds 1-5, 7, 9, and 10 are isolated from C. colocynthis for the first time.

In vitro antitumor effect of cucurbitacin E on human lung cancer cell line and its molecular mechanism

Cucurbitacin E(CuE) is previously reported to exhibit antitumor effect by several means.In this study, CuE acted as a tyrosine kinase inhibitor interfering with the epidermal growth factor receptor/mitogen-activated protein kinase(EGFR/MAPK) signaling pathway and subsequently induced apoptosis and cell cycle arrest in non-small-cell lung cancer(NSCLC) cell line A549.The apoptosis regulators, cleaved Caspases-3 and Caspases-9, were observed to be increased with the treatment of CuE.The activated transcription factor STAT3 and the apoptosis inhibitor protein survivin were also observed to be reduced.The cell cycle regulators, CyclinA2, cylinB1, CyclinD1 and CyclinE, were also investigated and the results suggested that the cell cycle was arrested at G1/G0 phase.Treatment of CuE also altered the existence status of most of the participants in the EGFR/MAPK signaling.Phosphorylation of EGFR enhanced significantly, leading to the alteration of members downstream, either total amount or phosphorylation level, notably,MEK1/2 and ERK1/2.Moreover, the results of molecular simulation brought an insight on the interaction mechanism between CuE and EGFR.In summary, CuE exhibited anti-proliferative effect against A549 cells by targeting the EGFR/MAPK signaling pathway.

Modulation of signal transduction pathways by natural compounds in cancer

Cancer is generally regarded as the result of abnormal growth of cells. According to World Health Organization, cancer is the leading cause of mortality worldwide. Mother nature provides a large source of bioactive compounds with excellent therapeutic efficacy. Numerous phytochemicals from nature have been investigated for anticancer properties. In this review article, we discuss several natural compounds, which have shown anti-cancer activity. Natural compounds induce cell cycle arrest, activate intrinsic and extrinsic apoptosis pathways, generate Reactive Oxygen Species(ROS), and down-regulate activated signaling pathways, resulting in inhibition of cell proliferation, progression and metastasis of cancer. Several preclinical studies have suggested that natural compounds can also increase the sensitivity of resistant cancers to available chemotherapy agents. Furthermore, combining FDA approved anti-cancer drugs with natural compounds results in improved efficacy. On the basis of these exciting outcomes of natural compounds against several cancer types, several agents have already advanced to clinical trials. In conclusion, preclinical results and clinical outcomes against cancer suggest promising anticancer efficacy of agents from natural sources.

Cucurbitacin B-induced G2/M cell cycle arrest of conjunctival melanoma cells mediated by GRP78-FOXM1-KIF20A pathway

Conjunctival melanoma(CM) is a rare and fatal malignant eye tumor. In this study, we deciphered a novel anti-CM mechanism of a natural tetracyclic compound named as cucurbitacin B(CuB). We found that CuB remarkably inhibited the proliferation of CM cells including CM-AS16,CRMM1, CRMM2 and CM2005.1, without toxicity to normal cells. CuB can also induce CM cells G2/M cell cycle arrest. RNA-seq screening identified KIF20A, a key downstream effector of FOXM1 pathway, was abolished by CuB treatment. Further target identification by activity-based protein profiling chemoproteomic approach revealed that GRP78 is a potential target of CuB. Several lines of evidence demonstrated that CuB interacted with GRP78 and bound with a Kdvalue of0.11 μmol/L. Furthermore, ATPase activity evaluation showed that CuB suppressed GRP78 both in human recombinant GRP78 protein and cellular lysates. Knockdown of the GRP78 gene significantly induced the downregulation of FOXM1 and related pathway proteins including KIF20A, underlying an interesting therapeutic perspective. Finally, CuB significantly inhibited tumor progression in NCG mice without causing obvious side effects in vivo. Taken together, our current work proved that GRP78-FOXM1-KIF20A as a promising pathway for CM therapy, and the traditional medicine CuB as a candidate drug to hinder this pathway.

Protecting-Group-Free One-Step Palladium-Catalyzed Coupling on C25 of Cucurbitacin B Expands Chemical Diversity with Improved Cytotoxicity against A549 Cells

The natural product cucurbitacin B has been widely studied because of its multiple biological activities,especially its potent antitumor effects.However,modifications of cucurbitacin B are mainly focused on the C2 and C16 site,studies on the C25 acetoxy group are still limited.We successfully developed a palladium-catalyzed allylic coupling of cucurbitacin B with boronic acids,providing a one-step approach to expand the chemical diversity of the C25 position.Our method was protecting-group-free,showing a good functional group tolerance and a wide substrate scope under mild reaction conditions.A library of 29 derivatives was prepared,compounds 2q and 2u showed higher cytotoxicity against A549 cells than cucurbitacin B,compounds 2n and 2o maintained potency,and the introduced hydroxyl and amino groups could be further derived.

Biological Activities and Crystal Structure of the Natural Anti-cancer Drug: Cucurbitacin Ⅱa

We isolated cucurbitacinⅡa from the rhizomes of Hemsleya pengxianensis,and tested the cytotoxicity of cucurbitacinⅡa against various cancer cell lines by the sulforhodamine B assay(SRB).At the same time,we preliminarily found that cucurbitacinⅡa has a certain inhibitory activity on kinase CDK1/cyclin B,and shows potent inhibitory activities against many cancer cell lines.The cucurbitacinⅡa was structurally characterized by specific optical rotation measurement,high-resolution mass spectroscopy and NMR spectroscopic analysis.In addition,the molecular structure of cucurbitacinⅡa was further determined by X-ray single-crystal crystallography.