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Objective:To construct oxaliplatin (L-OHP) drug-resistant cell line HCT-116/L-OHP in human colon cancer, in order to observe the reversal effect of curcumin (cur) on its drug resistance, and preliminarily explore the possible drug resistance mechanism. Method:The concentration gradient increasing method was used to gradually increase the L-OHP concentration of HCT-116 in parental colon cancer cells, and the cell line HCT-116/L-OHP resistant to L-OHP was established. The cytotoxicity of L-OHP and curcumin to HCT-116 and HCT-116/L-OHP cells was detected by cell counting kit-8(CCK-8) method to observe whether curative resistance could be reversed. Western blot was used to detect the expressions of drug-resistance-related proteins. Real-time PCR was used to detect changes in related genes. Result:Human colon cancer cell line resistant to L-OHP were successfully established and named as HCT-116/L-OHP, with a drug resistance index of 12.6.Compared with HCT-116 cell lines, the expression levels of resected and repaired cross complementation gene 1 (ERCC1) protein and gene in HCT-116/L-OHP cell lines were significantly increased (PP-1), the expression of ERCC1 decreased (PPConclusion:HCT-116/L-OHP cell lines have a stable drug resistance, and its drug resistance mechanism may be up-regulated with the expression of ERCC1, which leads to the up-regulation of Bcl-2,GST-π,MRP,P-gp,Survivin and other related proteins, and enables tumor cells to acquire drug resistance. Curcumin can reverse the drug resistance of HCT-116/L-OHP, and its mechanism may be to reduce the expression of ERCC1, thereby down-regulating the expressions of Bcl-2,GST-π,MRP,P-gp,Survivin and other drug-resistant related genes and proteins, and increase the sensitivity of tumor to L-OHP, so as to reverse the drug resistance of tumor cells.
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Objective To observe the efficacy and safety of oxcarbazepine combined with selective serotonin re-uptake inhibitor (SSRI) in the treatment of outpatients with agitated depression. Methods Thirty-two outpatients with agitated symptoms meeting CCMD-3 depression criteria were treated with oxcarbazepine combined with SSRI for 8 w: the dosage of oxcarbazepine changed dairy (1st and 2nd d, 0.3 g; 3rd d, 0.6 g; 7th and 8th, 1.2-1.5 g). The efficacy and side effects were assessed by Hamilton depression scale, Hamilton anxiety rating scale and Young manic-state rating scale. Results The mean dosage of oxcarbazepine in 32 patients was (1020±65) mg/d. Their mean effective rate and full remission rate 87.5% and 65.6%,respectively. The mean effective rate and full remission rate 1, 2, 4 and 8 w after the treatment were 28.1% (9/32) and 6.3% (2/32), 37.5% (12/32) and 12.5% (4/32), 46.9% (15/32) and 31.3% (10/32), and 90.6% (29/32) and 65.6% (21/32), respectively. The scores of the above scales 1, 2, 4 and 8 w after the treatment were significantly different with those before the treatment (P<0.05). Phase inversion was not found in these 32 patients. Conclusion The oxcarbazepine combined with SSRI maybe one of the better ways in the treatment of patients with agitated depression.
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<p><b>OBJECTIVE</b>To compare the incidences of sexual dysfunction induced by mirtazapine and SSRI in the treatment of patients with depression.</p><p><b>METHODS</b>Using key-word retrieval from the compact disks of the Chinese biological medicine (CBM) data base, we analyzed the rates of sexual dysfunction from the published clinical control trials on depression treated with mirtazapine and SSRI by applying the fixed effects model (FEM) of evidence-based medicine (EBM).</p><p><b>RESULTS</b>Among 1108 cases in 14 studies, there were 5 cases of mirtazapine-induced and 106 cases of SSRI-induced sexual dysfunction, accounting for 0.90% and 19.2% respectively, OR = 0.07 (95% CI: 0.04-0.14), Z = 8.03, P < 0.01.</p><p><b>CONCLUSION</b>SSRI is far more likely to induce sexual dysfunction than mirtazapine in the treatment of depression.</p>