Abstract

Helicobacter pylori H. pylori is a human pathogen that can persist in the stomach of infected people for their life spans. It causes chronic gastric inflammation leading to serious gastric diseases such as gastritis, peptic ulcers, gastric cancer and mucosa-associated lymphoid tissue lymphoma. To colonize in the acidic environment of the stomach, H. pylori produces urease enzyme that catalyzes the hydrolysis of urea to yield into ammonia and carbon dioxide. This enzyme neutralizes the acidic environment of the gastric lumen, and gives the bacteria a short-term survival in this highly acidic environment. There are numerous antibiotic-based therapies for the treatment of H. pylori infection. However, antibiotic resistance has a significant impact on the failure of these treatments.Hydroxycinnamic acid derivatives are simple phenolic acids, found mainly in cereals, fruits, seeds of fruits and vegetables. Ferulic acid, Caffeic acid, p-Coumaric acid, and Sinapic acid belong to this phenolic acid group. These derivatives act as antioxidant, anti-inflammatory, antimicrobial agents and have been used for the treatment of some bacterial infections as alternatives to drugs.The objective of this study was to investigate the anti-H. pylori and urease enzyme inhibitory effects of Ferulic acid, Caffeic acid, p-Coumaric acid and Sinapic acid.The effect of hydroxycinnamic acid derivatives was tested on H. pylori standard train G27. MIC was determined by serial tube dilution method in which the final concentration ranged between 512 to 0.5 µg/ml and MBC was determined by calculating the relative proportion of live and dead bacteria with the same concentration range used in MIC. For MIC, the CLSI M07-A9and for MBC CLSI M26-A protocols were used. Urease inhibitory activity was detected by Helicheck, H. pylori-specific growth media shows urease activity by changing the color of the media. Nucleotide release was measured by spectrophotometry. The MIC was 64 µg/ml and MBC was 128 µg/ml for all compounds and they had no effect on urease enzyme. There was no detectable nucleotide release from the bacterial membrane because of the hydroxycinnamic acid derivatives damage

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