Abstract C079: H. pylori eradication for mitigating gastro-duodenal cancers: Modeling pharmacokinetics of levofloxacin niosomes in Sprague-Dawley rats
Abstract
Abstract Eradication of Helicobacter pylori (H. pylori) and, hence, control of its associated conditions (peptic ulcer, gastric cancer, and lymphoma) still constitute major challenge to therapeutics. H. pylori has been implicated in 60% of gastric and 90 % of duodenal ulcers and has been classified as a Class 1 carcinogen in human by the International Agency for Research on Cancer and the World health Organization (Enerson et al, 2016; Vogiatzi et al, 2007; WHO). It affects 4million people world-wide of which 0.5million is from the US and 70% are of 25-64 y/o (Chung & Shelat, 2017). Presently, gastric cancer is the second leading cause of neoplastic mortality globally (Contreras et al, 2014; Owen et al, 2018). The efficacy of currently used antibiotics (erythromycin, clarithromycin, levofloxacin, and azithromycin) in triple or quadruple combinations with proton pump inhibitor (PPI) is decreasing due to resistance development via lipopolysaccharide modification, increased drug efflux, and reduced porin pathway. Adaptive response by bacteria to specific signal due to antibacterial presence in its environment, leading to up-regulation of the efflux system (MexXY/OprM), and down-regulation of porin pathway (OprD) has been recognized as key factor in the resistance manifestation. In an earlier study, we reported that encapsulation of an anti-H. pylori drug (levofloxacin) molecules in niosomes (nano-size lipid vesicles) improved its molecular assimilation by drug-resistant E. coli…
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