Vanillic Acid Inhibited the Induced Glycation Using In Vitro and In Vivo Models.

Background: Glycation is implicated in the pathophysiology of many diseases, including diabetes, cancer, neurodegenerative diseases, and aging. Several natural and synthetic compounds were investigated for their antiglycation activity. We evaluated the antiglycation effect of vanillic acid (VA) using in vitro and in vivo experimental models. Methods: In vitro, bovine serum albumin (BSA) (50 mg/ml) was incubated with glucose (50 mM) with or without VA at 1.0-100 mM for 1 week at 37°C, and then, excitation/emission fluorescence was measured at 370/440 nm to determine glycation inhibition. The cytoprotective effect of VA was evaluated using RAW 264.7 cells incubated with or without VA at 7.8-500 µM along with 100-400 µM of methylglyoxal for 48 hours, and cell viability was determined using the MTT assay. Aminoguanidine (AMG) was used as a positive control in both in vitro and cell culture experiments. In vivo, 52 streptozotocin-induced diabetic rats were randomly assigned to 4 groups and treated with 0, 1.5, 4.5, or 15 mg/kg VA for four weeks. Serum fructosamine and blood glycosylated hemoglobin (HbA1c) were then measured, and advanced glycation end-products (AGEs) were detected in the kidneys and the skin of deboned tails using an immunohistochemistry assay. Results: VA caused a concentration-dependent effect against BSA glycation (IC50 of 45.53 mM vs. 5.09 mM for AMG). VA enhanced cell viability at all concentrations of VA and methylglyoxal. VA did not affect serum fructosamine or blood HbA1c levels, although it markedly decreased AGEs in the kidney in a dose-dependent manner and decreased AGEs in the skin of deboned tail tissues. Conclusion: VA had significant antiglycation activity at cellular and long-term glycation.

Antiproliferative Activities of Lipophililic Fluoroquinolones- Based Scaffold Against a Panel of Solid and Liquid Cancer Cell Lines.

OBJECTIVES: In this work, 9 lipophilic-acid chelating FQs (fluoroquinolones) comprising chelating groups  have been prepared, characterized and screened for in vitro cytotoxicity, radical scavenging and antiinflammation propensities. METHODS: Using sulforhodamine B colorimetric bioassay vs. cisplatin; FQs-inflicted reductions' of viability against breast T47D and MCF7, Pancreatic PANC-1, colorectal HT29, HCT116, SW620, CACO2, SW480 and Leukaemia K562 cancer cell lines were examined in quadruplicates/dose/cell line. Parameters including potency, toxicity, and selectivity (potency/toxicity) have been reported along with DPPH- and NO- radicals' scavenging capacities -as their molecular action mechanism- in comparison to ascorbic acid and indomethacin respectively. Using Griess assay in Lipopolysaccharide (LPS) prompted RAW264.7 macrophages; mitigation of inflammation was investigated. RESULTS: nitroFQ 3b, unlike the rest of FQs in PANC1 and MCF7 cells, exhibited remarkably superior NO-radical scavenging/antiinflammation capacity to indomethacin with respective antiproliferative IC50 values (<50µM) 49 vs. cisplatin's 122 and 6 vs. cisplatin's 28 (p<0.01-0.001; n=4). Reduced FQ 4b of significantly dual DPPH-NO scavenging propensities exerted exceptionally substantial micromolar antiproliferation in colorectal cancer cells with respective antiproliferative IC50 values (<50µM) of HCT116 0.84< HT29 1.6

Shedding light on pharmacists' knowledge of kidney stones' etiology and treatment.

Background: The recurring nature of kidney stones (KS) makes it difficult to control and treat. Patients' education plays a part in reducing disease recurrence. Pharmacists participate in the healthcare services through educating patients with kidney stones about KS preventive measures and medications that greatly reduce the disease frequency and the treatment cost. Insufficient pharmacists' knowledge may affect the services' quality and result in misuse of KS medications. Objectives: To evaluate the pharmacists' level of knowledge to provide adequate information about KS preventive measures, medications, and treatments for patients with kidney stones in Jordan. Methods: An online descriptive survey was distributed to pharmacists to assess their knowledge about KS causes, prevention, and treatment. The results were analyzed using the SPSS software. Results: There were 393 pharmacists participated in this study. Pharmacists demonstrated an overall intermediate level of knowledge about KS. They showed an excellent level of knowledge regarding KS types and etiology, an intermediate level of knowledge about KS preventive measures and treatment, and poor knowledge about home remedies and drugs that promote KS formation. Conclusion: Pharmacists knowledge about KS management through diet and medications need to be improved. This could be through focusing on pharmacists' training for the effective implementation of knowledge in the clinical practice. Adopting guidelines by pharmacists may reduce the risk of KS recurrence and provide pharmacist-led patient education about KS management in hospitals and community pharmacies.