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1.
China Pharmacy ; (12): 5008-5010, 2016.
Article in Chinese | WPRIM | ID: wpr-506269

ABSTRACT

OBJECTIVE:To observe clinical efficacy and safety of sertraline hydrochloride combined with esomeprazole in the treatment of patients with gastroesophageal reflux disease complicating with depression. METHODS:80 patients with gastroesopha-geal reflux disease complicating with depression selected from our hospital were divided into control group and observation group according to random number table,with 40 cases in each group. Control group received Esomeprazole magnesium enteric-coated tablets orally 40 mg,qd;observation was additionally given Sertraline hydrochloride tablets 50 mg,qd,on the basis of control group. Both groups received treatment for 1 month. Clinical efficacies of 2 groups were observed as well as clinical symptom score,gastroesophageal reflux disease diagnostic questionnaire (GERD Q scale) score,SDS score. The occurrence of ADR was compared between 2 groups. RESULTS:The total effective rate of observation group 92.50%,which was significantly higher than 77.50% of control group,with statistical significance (P0.05). After treatment,above scores of 2 groups were improved signifi-cantly,and the observation group was significantly better than the control group,with statistical significance(P0.05). CONCLUSIONS:Sertraline hydrochloride com-bined with esomeprazole shows significantly therapeutic efficacy in the treatment of patients with gastroesophageal reflux disease complicating with depression,and can effectively alleviate the clinical symptoms and improve depression with good safety.

2.
Tumor ; (12): 6-10, 2010.
Article in Chinese | WPRIM | ID: wpr-433067

ABSTRACT

Objective:To investigate the effect of ethyl acetate extract from Cortex periplocae (CPEAE) on apoptosis of human esophageal carcinoma cell line TE-13 and to elucidate its mechanism. Methods:Inhibitory effect of CPEAE on TE-13 proliferation was tested by MTT assay. The morphological changes of cell apoptosis were observed by Giemsa staining and transmission electron microscopy. Cell cycle and apoptotic ratio were tested by flow cytometry (FCM). The protein expression of CDK4 was observed by Western blotting.Results:CPEAE inhibited proliferation of TE-13 cells in a concentration-dependent and time-dependent manner, and its IC_(50) value was (2.443±0.005) μg/mL at 48 h (P<0.05). The characteristic morphological changes of apoptosis were observed in TE-13 cells after treatment with CPEAE under transmission microscope. A typical subdiploid peak was detected by flow cytometry. CPEAE decreased the expression of gene CDK4 in TE-13 cells. Conclusion:CPEAE can induce apoptosis of TE-13 cells. The effect is related with down-regulation of CDK4 expression.

3.
Chinese Journal of Cancer Biotherapy ; (6): 13-18, 2010.
Article in Chinese | WPRIM | ID: wpr-404261

ABSTRACT

Objective: To investigate the effect of cochinchina momordica seed ethanol extract (CMSEE) on the proliferation of melanoma B16 cells and the underlying mechanism. Methods: MTT and clone formation assay were used to assess the effect of CMSEE on the growth of B16 cells. Morphological changes of B16 cells were observed under phase-contrast microscope and Giemsa staining. Cell cycle and apoptosis rate were examined by flow cytometry (FCM). The effect of CMSEE on melanin production and tyrosinase activity of B16 cells was assessed by colorimetry. The effect of CMSEE on the expression of C-myc, P38, and Tyr genes was examined by RT-PCR. Results: CMSEE (10-100 mg/L) inhibited the proliferation of B16 cell in a dose-and time-dependent manner. After treatment with 10-40 mg/L CMSEE, B16 cells showed typical differentiation morphology, and melanin production and tyrosinase activity were increased. B16 cells treated with 100 mg/L CMSEE showed apoptotic morphology, decreased melanin production and tyrosinase activity. B16 cell number in G_0/G_1 phase was significantly increased (P<0.01); C-myc mRNA expression was down-regulated, and P38, Try mRNA expression was up-regulated in B16 cells after treatment with 10-40 mg/L CMSEE. Conclusion: CMSEE can markedly inhibit the proliferation of melanoma B16 cells, which is related to induction of differentiation and promotion of apoptosis of B16 cells.

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