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Guilin, China

Liu Q.-H.,Guilin Medical College | Huang X.,Guilin Medical College | Xiang Q.,Scientific Research and Experiment Center | Wu J.-W.,181st Hospital of PLA | Lei X.,Guilin Medical College
Chinese Journal of Clinical Oncology | Year: 2010

Objective: To discuss the induction of (-)-epigallocatechin-3-gallate (EGCG) on the apoptosis of nasopharyngeal carcinoma (NPC) cell lines CNE-2, and the characteristics of the changes in MnSOD expression during the course. Methods: In vitro cultured CNE-2 cells were divided into the control group and another 3 experiment groups. No interventions (interfering reagent) such as EGCG were added to the control group, while the 3 experimental groups, received a EGCG concentrations in the culture solution of 10, 50 and 100 μg EGCG per ml. MTT (Thiazolyl blue) method was used to calculate the growth suppression ratio of CNE-2 cell line treated by EGCG of various concentrations at different time points, with morphological observation of the apoptosis made by fluorescence microscope. At the same time, the change in the expression of MnSOD mRNA level was measured using RT-PCR determination. Results: With increase of the EGCG drug concentration and extension of the culture time, the growth inhibition ratio of CNE-2 cells significantly rose up, that is, the survival rate of CNE-2 cells significantly decreased. Observation by a fluorescence microscope showed that the completely green and fluorescent tumor cells with normal growth could be seen in the control group. After the CNE-2 cells interacted with EGCG, the apoptotic reddish-yellow tumor cells could be seen by the fluorescence microscope. The expressions of MnSOD gene (around 700 bp) and internal-reference β-actin gene (around 500 bp) could be detected in the control and in the experimental groups. Compared with the control, however, the expression of MnSOD mRNA level notably increased (P < 0.05), after the CNE-2 cells respectively interacted with the 10, 50 and 100 μg/mL EGCG for 24h, 48h and 72h. Also, there was an up-regulation of the MnSOD mRNA expression with an increase of EGCG concentration and extension of the culture time. Conclusion: EGCG can induce the apoptosis of nasopharyngeal carcinoma cell line CNE-2 by means of up-regulating the expression of MnSOD mRNA. Source


Xiong R.,181st Hospital of PLA | Ren Q.,181st Hospital of PLA | Tian X.,181st Hospital of PLA | Tang X.,181st Hospital of PLA
Chinese Journal of Clinical Oncology | Year: 2012

Objective: The present study aims to evaluate the efficacy and side effects of nedaplatin (NDP) combined with coelom hyperthermic perfusion chemotherapy (CHPC) in treating patients with malignant pleural effusion. Methods: A total of 33 patients were randomized into two groups, namely, NDP group (n = 19) and diamminedichloroplatinum or cisplatin (DDP) group (n = 14). Pleural effusion from patients of both groups was drawn out of the thoracic cavity via the peripheral intravenous central catheter. CHPC and different drug medications were then administered. In the NDP group, 80 mg of NDP was administered to the pectoral cavity, whereas 80 mg of DDP was administered in the DDP group. Close attention was given to the patients to prevent and manage the side effects. Results: The response rate (RR) was 89.5% in the NDP group (17/19), whereas the RR was 85.7% in the DDP group (12/14). No significant differences between the RR of the two groups were observed (P > 0.05). However, different effects in the gastrointestinal reactions were observed. The gastrointestinal reaction rate was lower in the NDP group (10.5%) compared with the DDP group (42.9%). No significant differences in the side effects in the medulla, liver, and nephridium were observed between the two groups (P > 0.05). Hydration and diuresis were not needed during NDP administration. Conclusion: The regimen of NDP combined with CHPC is effective in treating patients with malignant pleural effusion. Without hydration and diuresis in the treatment, this regimen has little toxicity and can be easily used for extensive clinical applications. Source

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