3-Pentylcatechol, a Non-Allergenic Urushiol Derivative, Displays Anti-Helicobacter pylori Activity In Vivo.

Hang Yeon Jeong,Jae-Hak Moon,Sueun Lee,Tae-Il Jeon,Changjong Moon,Xuan Trong Truong,Ju Gyeong Kim,Tae Ho Lee

doi:10.3390/ph13110384

Abstract

We previously reported that 3-pentylcatechol (PC), a synthetic non-allergenic urushiol derivative, inhibited the growth of Helicobacter pylori in an in vitro assay using nutrient agar and broth. In this study, we aimed to investigate the in vivo antimicrobial activity of PC against H. pylori growing in the stomach mucous membrane. Four-week-old male C57BL/6 mice (n = 4) were orally inoculated with H. pylori Sydney Strain-1 (SS-1) for 8 weeks. Thereafter, the mice received PC (1, 5, and 15 mg/kg) and triple therapy (omeprazole, 0.7 mg/kg; metronidazole, 16.7 mg/kg; clarithromycin, 16.7 mg/kg, reference groups) once daily for 10 days. Infiltration of inflammatory cells in gastric tissue was greater in the H. pylori-infected group compared with the control group and lower in both the triple therapy- and PC-treated groups. In addition, upregulation of cytokine mRNA was reversed after infection, upon administration of triple therapy and PC. Interestingly, PC was more effective than triple therapy at all doses, even at 1/15th the dose of triple therapy. In addition, PC demonstrated synergism with triple therapy, even at low concentrations. The results suggest that PC may be more effective against H. pylori than established antibiotics.

Highlights

Helicobacter pylori infection is a major public health concern worldwide
Inoculation, the colonization of pylori and associated gastric disorders in mouse gastric tissue were confirmed via quantitative polymerase chain associated gastric disorders in mouse gastricThe tissue were confirmed via quantitative polymerase chain reaction
These results and catarrhal inflammation in the gastric tissue of the infected group. These results indicate erosion, and catarrhal inflammation in the gastric tissue of the infected group. These results indicate that H. pylori successfully colonized the stomachs of mice after inoculation and induced that pylori successfully colonized the stomachs of mice after inoculation and induced gastric disorders

Summary

Introduction

Helicobacter pylori infection is a major public health concern worldwide. This infection occurs in the gastric mucosa of more than 50% of the world’s population [1] and it is directly associated with gastrointestinal disorders, including chronic gastritis, peptic ulcer disease, mucosa-associated lymphoid tissue (MALT) lymphoma, and gastric cancer [2,3,4,5]. H. pylori infection is associated with numerous extra-gastric disorders, such as cardiovascular, neurologic, hematologic, dermatologic, head and neck, and urogynecologic diseases, as well as diabetes mellitus and metabolic syndrome [7,8]. The success rates of these H. pylori

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