Lu S.-R.,Fourth Peoples Hospital of Wuxi City |
Mao Y.,Fourth Peoples Hospital of Wuxi City |
Yu H.,Fourth Peoples Hospital of Wuxi City |
Wu Y.-Y.,Fourth Peoples Hospital of Wuxi City |
And 4 more authors.
Tumor | Year: 2010
Objective:To study the effect of low molecular weight heparin (LMWH) on tumor growth, metastasis, and the expression of chemokine receptor 4 (CXCR4) in orthotopicly transplanted gastric tumor model in nude mice. Methods: The model of human gastric cancer was established by orthotopic transplantation of histologically intact tumor tissue blocks in the gastric walls of nude mice. On d 7 after transplantation all mice were randomly divided into 3 groups: control group (treated with normal saline), LMWH group (treated with low molecular weight heparin calcium), and chemotherapy group (treated with 5-fluorouracil). The drugs were given twice a week for 5 weeks. Forty two days after treatment, tumor metastatic rates and tumor volume were recorded, respectively. The expressions of CXCR4 protein and mRNA were detected by immunohistochemistry and reverse-transcriptase polymerase chain reaction (RT-PCR). Results: In comparison with that in the control group, the tumor volumes were significantly reduced in the LMWH group and chemotherapy group. The difference was significant (P <0.05). The tumor metastasis rate was significantly lower in LMWH group than that in control group (20% vs 70%, P <0.05). There was no significant difference between LMWH group and chemotherapy group (20% vs 11%, P >0.05). The expressions of CXCR4 protein and mRNA in the LMWH group were significantly decreased compared with those in the control group and chemotherapy group (P <0.05). Conclusion: LMWH has inhibitory effects on tumor growth and metastasis. The mechanism may be related with down-regulation of the expression of CXCR4 in tumor tissues.
Gao C.,Fourth Peoples Hospital of Wuxi City |
Lu Q.,Nantong University |
Guo S.,Nanjing Medical University |
Yang Z.,Nanjing Medical University |
And 3 more authors.
Asian Biomedicine | Year: 2014
Background: High plasma B-type natriuretic peptide (BNP) levels in patients with severe chronic heart failure (CHF) often indicate poor ventricular function and poor prognosis. However, in some such patients plasma BNP levels are normal. Asian BiomedicineObjective: To investigate the clinical implications of BNP levels in patients with severe CHF.Methods: Fifty-seven patients with severe CHF were divided into group A (13 normal plasma BNP level) and 44 patients (high plasma BNP levels) group B. Diuretics, angiotensin-converting enzyme inhibitors (or angiotensin II receptor antagonist, e.g., metoprolol) and digitalis were used as conventional treatment. The clinical characteristics of all patients in two groups were analyzed and compared.Results: At the first admission, left ventricular end diastolic diameter in group B was significantly lower than group A (p < 0.05), and the plasma BNP level in group B was significantly higher than group A (p < 0.05). When metoprolol was used, 6 and 5 patients in group A and B could not tolerate the initial dose. In other cases using metoprolol at average maximum tolerance dose of metoprolol 12.5 6.25 and 24.20 11.22 mg/day in group A and B, respectively, there was a significant difference between them (p < 0.05). There were no significant differences in plasma BNP levels between two groups during stable period. The plasma BNP level in group B during acute worsening stage was significantly higher than in the remission stage (962.73 165.00 ng/L vs 876.24 167.70 ng/L, p < 0.05). However, there was no significant difference between group A (74.03 11.18 ng/L) and group B (71.38 11.68 ng/L) (p > 0.05). The mobility of group A was higher than group B (11/12 vs 6/44, p < 0.05). Logistic regression analysis showed that, the plasma BNP level was the independent risk factor for predicting cardiac death (regression coefficient, 3.817; OR, 45.488; 95% CI, 5.322"388.791).Conclusion: In patients with severe CHF, normal plasma BNP level suggests depletion of BNP secretion and further deterioration of cardiac function, indicating a poor prognosis. © 2013 is published by the Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
PubMed | Fourth Peoples Hospital of Wuxi City
Type: Journal Article | Journal: Zhongguo Zhong xi yi jie he za zhi Zhongguo Zhongxiyi jiehe zazhi = Chinese journal of integrated traditional and Western medicine | Year: 2013
To observe the synergistic effect of beta-elemene Injection (betaI) combined Paclitaxel Injection (PI) on breast cancer MB-468 cells and to study possible mechanisms.Breast cancer MB-468 cells were treated with betaI (2.5, 5.0, 10.0, 20.0, 40.0, 80.0, 160.0, 320.0, and 640.0 microg/mL), PI (0.00100, 0.00200, 0.00400, 0.00800, 0.01600, 0.03125, 0.06250, 0.12500, and 0.25000 microg/mL), and betaI combined PI for 24 h and 48 h respectively. Cell proliferation was determined using SRB assay. Cell apoptosis and cell cycle phase distribution were detected using flow cytometry. The post-intervention expressions of cell cycle proteins [cyclin-dependent kinase (CDK1), cyclin-B1, P21(cip1), and P27(kip1)] were detected by Western blot.Beta-elemene or paclitaxel inhibited the growth of MB-468 cell line. The IC50 and IC20 values treated with beta-elemene for 24 h were 34.20 and 52.59 microg/mL and for 48 h were 10.15 and 17.81 microg/mL respectively, while the IC50 values treated with paclitaxel for 24 h and 48 h were 2.449 and 1.698 microg/mL respectively. Beta-elemene (20 and 40 microg/mL respectively) and Paclitaxel (0.016 and 0.008 microg/mL respectively) synergistically inhibited cell proliferation of MB-468 cells, with Q value > 1.15. Beta-elemene alone (52.59 microg/mL) apparently decreased the expression of cyclin-B1 protein. The expression of cyclin-B1 protein in the combined group was also lower than that in the PI group (1.698 microg/mL). The expression of P27(kip1) was up-regulated when compared with that in the betaI group or the PI group.Beta-elemene had synergistic effect with Paclitaxel, and its possible mechanism might be correlated with down-regulating the cell cycle protein cyclin-B1 expression and up-regulating the P27(kip1) expression.