RESUMO
This study synthesized a La2O3@snowflake-like Cu2S composite to fabricate an electrochemical sensor for sensitively simultaneous detection of diclofenac and chlorzoxazone exploiting an easy hydrothermal approach, followed by analysis with XRD, FE-SEM, and EDX methods. According to voltammetric studies, the electrocatalytic diclofenac and chlorzoxazone oxidations on the electrode modified with La2O3@SF-L Cu2S composites were increased, with greater oxidation currents, as well as the oxidation potential was significantly decreased due to synergetic impact of La2O3@SF-L Cu2S composites when compared with the pure SF-L Cu2S NS-modified electrode. The differential pulse voltammetry findings showed wide straight lines (0.01-900.0 µM) for La2O3 NP@SF-L Cu2S NS-modified electrode with a limit of detection (LOD) of 1.7 and 2.3 nM for the detection of diclofenac and chlorzoxazone, respectively. In addition, the limit of quantification was calculated to be 5.7 and 7.6 nM for diclofenac and chlorzoxazone, respectively. The diffusion coefficient was calculated to be 1.16 × 10-5and 8.4 × 10-6 cm2/s for diclofenac and chlorzoxazone oxidation on the modified electrode, respectively. Our proposed electrode was examined for applicability by detecting diclofenac and chlorzoxazone in real specimens.
RESUMO
BACKGROUND AND PURPOSE: Doxorubicin (DOX) is an effective agent for the treatment of many neoplastic diseases. Cardiotoxicity is the major side effect of this drug and limits its use. Vanillic acid (VA) is a pharmaceutical compound from the phenolic acids family. The present study is an attempt to investigate the possible helpful effects of VA against DOX-induced cardiotoxicity in rats. EXPERIMENTAL APPROACH: For induction of cardiotoxicity, male Wistar rats received total of six doses of DOX (2.5 mg/kg i.p.) three times per week from days 14 to 28. Treatment groups received daily oral doses of VA (10, 20, and 40 mg/kg) two weeks before DOX injection and then plus DOX for 2 weeks. At the end of experiment, systolic blood pressure (SBP) and heart rate (HR) were detected using tail-cuff method. Lactate dehydrogenase (LDH), creatine phosphokinase-MB (CK-MB), serum glutamic oxaloacetic transaminase (SGOT), malondialdehyde (MDA), and ferric reducing antioxidant power (FRAP) were measured in serum samples. Troponin-I and toll-like receptor 4 (TLR4) were measured in cardiac tissue. All the measurements processed spectrophotometrically using commercial ELISA kits. Cardiac tissue was also processed for histopathological examination. FINDINGS / RESULTS: Treatment with VA significantly increased SBP compared to the DOX group and restored HR near to the normal level. Administration of VA at all of doses, decreased serum levels of LDH, SGOT, CK-MB, MDA, cardiac troponin-I, cardiac TLR4 and increased FRAP value. CONCLUSION AND IMPLICATIONS: These results suggest that VA may exert cardioprotective effects against DOX-induced cardiotoxicity by decreasing oxidative stress and biomarkers of cardiotoxicity, suppression of TLR4 signaling and consequently inflammation pathway.
