A simple, sensitive, and selective square-wave voltammetric method was developed for the determination of pantoprazole. The influence of the nature of the supporting electrolyte solution, pH, modulation amplitude, frequency, and scan increment was examined by square-wave voltammetric method for pantoprazole. The best results were obtained in Britton-Robinson buffer of pH 5.0. The peak currents were measured with hanging mercury drop electrode at 2987 mV vs. Ag/ AgCI. The calibration curve for pantoprazole was found as linear at a concentration range from 0.15 to 25.23 mg mL 21 . The limit of detection and the limit of quantification of pantoprazole were 0.048 mg mL 21 and 0.15 mg mL 21 , respectively. The validation parameters of the proposed method were evaluated. The method was applied to the pharmaceutical formulation and to both spiked plasma and the plasma of patients orally administered pantoprazole. A spectrophotometric method reported in the literature was utilized as a comparison method. There were no significant differences between the results obtained by two methods.

No abstract

No abstract

No abstract

Background: Ankaferd Blood Stopper® is a commercially available herbal extract with potent blood-stopping property and is clinically used to treat immediate dental, dermal, external and internal bleeding. Its possible anti-neoplastic effect or whether it ingenerates drug resistance in cells has not been previously scrutinized. Objective: In the present study HEPG2 hepatocellular carcinoma cell line was exposed to clinically used dose (8 μL/mL) of the blood stopper for 24 h and the behavioral changes were investigated on both proteomic and genomic levels. Method: Cell culture experiments were performed by using Ankaferd® application in HepG2 cell line. Cytotoxic activity experiments with MTT, oncoproteomic studies with 2d gel electrophoresis, genomic studies were performed with RT-PCR. Results: It was seen that the agent did not significantly inhibit cell viability subsequent to 24 h of the treatment meanwhile, it clearly deducted cell viability after 72 h. Although reduction of HEPG2 cell proliferation was not witnessed as a response to 24 h of treatment with Ankaferd®, genomic and oncoproteomic analysis demonstrated diversification. Conclusion: It was established that protein processing networks in endoplasmic reticulum which regulate protein folding, relocation and degradation were effected. Additionally, it was proved that along with the elongation of the exposure period, mitochondrial apoptotic pathway may be activated due to hnRNP F-p53 interaction. Given to the fact that the agent did not inclined P-glycoprotein-dependent drug resistance unlike many clinically used chemotherapeutic agents, it also can be considered for combination treatment. Overall, these findings suggest that Ankaferd® offers a novel promising approach against hepatocellular carcinoma which needs further investigation.