ABSTRACT
Eight pentacyclic triterpenoids including two new ones (1, 2) were isolated from the fruits of Xanthium strumarium. Their structures were elucidated by extensive spectroscopic analysis. All isolates were evaluated for in vitro cytotoxic activity on HepG2, A549, HCT116 and SW480 cancer cells. Among them, the new compound 2 was found to exhibit significant cytotoxic activity on A549, HCT116 and SW480 cancer cells with IC50 values of 9.68, 4.27 and 7.58 µM, respectively. Further, 2 was selected for cell cycle analysis and results revealed that 2 could cause HCT116 cell cycle arrest in G1 phase. In addition, Annexin V-FITC/PI staining assay showed that 2 could induce the death of HCT116 cells.
Subject(s)
Antineoplastic Agents , Xanthium , Fruit , Phytochemicals/pharmacology , Xanthium/chemistryABSTRACT
OBJECTIVE: To evaluate the value of the myocardial biochemical markers including creatine kinase MB isoenzyme (CK-MB), cardiac isoform of Tropnin-T (cTnT) and N-termimal pro-brain natriuretic peptide (NT-proBNP) and electrocardiogram (ECG) in monitoring the cardiotoxicity of recombinant human endostatin (rh-endostatin) in cancer patients. METHODS: Forty cancer patients were divided into two groups and received rh-endostatin in addition to chemotherapy (group A, n=24) or chemotherapy only (Group B, n=24). Serum CK-MB, cTnT levels and plasma NT-proBNP levels were measured and the ECG was recorded in all the patients before and after each of the two therapy cycles. RESULTS: In group A, serum CK-MB, cTnT and plasma NT-proBNP levels were significantly increased after the treatment in comparison with the baseline levels (P<0.05), but such increment was not observed in group B (P>0.05). With comparable baseline levels of CK-MB, cTnT and NT-proBNP before the treatment (P>0.05), patients in group A showed significantly higher levels of the indices than those in group B after each therapy cycle (P<0.05). Increased ECG abnormality were observed after rh-endostatin treatment in Group A (P<0.05) at a rate significantly higher than that of Group B after the second treatment cycle (P<0.05). CONCLUSION: Rh-endostatin has definite cardiotoxicity, and detection of the myocardial biochemical markers of CK-MB, cTnT and NT-proBNP may help predict the occurrence of cardiotoxicity.
Subject(s)
Biomarkers, Tumor/blood , Endostatins/therapeutic use , Lung Neoplasms/blood , Lung Neoplasms/drug therapy , Adult , Aged , Antineoplastic Agents/adverse effects , Antineoplastic Agents/therapeutic use , Carcinoma, Non-Small-Cell Lung/blood , Carcinoma, Non-Small-Cell Lung/drug therapy , Creatine Kinase, MB Form/blood , Endostatins/adverse effects , Endostatins/genetics , Female , Humans , Male , Middle Aged , Natriuretic Peptide, Brain/blood , Ovarian Neoplasms/blood , Ovarian Neoplasms/drug therapy , Peptide Fragments/blood , Recombinant Proteins/adverse effects , Recombinant Proteins/therapeutic use , Risk Assessment , Troponin T/bloodABSTRACT
OBJECTIVE: To investigate the inhibitory effects of recombinant human endostatin (rh-ES) on cell adhesion, metastatic potential and invasiveness of hepatocellular carcinoma HCCLM6 cells in vitro. METHODS: The changes in the cell proliferation status of HCCLM6 cells treated with different concentrations of rh-Endostatin in vitro was measured with MTT assay, and their invasiveness and migration were assayed using transwell cell culture chamber. The cell adhesion assay was carried out on 96-well plate precoated with matrigel. RESULTS: Rh-ES showed inhibitory effect against the proliferation of HCCLM6 cells after a 72-h treatment. The adhesion, metastatic potential and invasiveness of the cells were obviously inhibited by rh-Endostatin in a dose-dependent manner. CONCLUSION: Rh-ES inhibits the adhesion, invasiveness and migration of hepatocellular carcinoma cells in vitro, and the mechanism needs further investigation.
