4.7 Article

Anti-Inflammatory Effect of Korean Propolis on Helicobacter pylori-Infected Gastric Mucosal Injury Mice Model

Journal

NUTRIENTS
Volume 14, Issue 21, Pages -

Publisher

MDPI
DOI: 10.3390/nu14214644

Keywords

Helicobacter pylori; Korean propolis; anti-inflammation; NF-kappa B; gastric mucosal injury

Funding

  1. GRRC program of Gyeonggi province [GRRC-201900830002CHA2019-B01]
  2. (Production of physiologically active substances), Republic of Korea

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Research has shown that Korean propolis (KP) has anti-inflammatory effects on gastric mucosal injury caused by Helicobacter pylori infection. KP inhibits the growth of H. pylori and reduces the expression of virulence factors. It also decreases inflammation and pathological damage by suppressing the NF-kappa B signaling pathway. These findings suggest that KP could be a natural supplement for patients with gastric mucosal injury caused by H. pylori infection.
Propolis, a natural resinous substance obtained from a variety of buds and plants, has been reported to possess various biological functions. Several recent studies have demonstrated the inhibitory effects of propolis on the growth of Helicobacter pylori (H. pylori) in vitro; however, current research efforts on Korean propolis (KP) remain insufficient especially in vivo. Our study aims to investigate the anti-inflammatory effect and molecular mechanism of KP on mouse gastric mucosa during H. pylori infection. We examined an in vivo H. pylori-induced gastric mucosal injury mice model. We found that KP inhibited the growth of H. pylori and attenuated the expression of H. pylori virulence factors such as cytotoxin-associated gene A, encoding urease A subunit, surface antigen gene and neutrophil-activating protein A. Moreover, KP reduced both gross lesions and pathological scores in H. pylori-challenged mice. In addition, KP markedly restrained the production of pro-inflammatory cytokines and nitric oxide levels compared with an untreated H. pylori-infected group. In particular, we found that KP repressed the phosphorylation of I kappa B alpha and NF-kappa B p65 subunit, and subsequently suppressed their downstream target genes. Taken together, these findings demonstrate the beneficial effects of KP on inflammation through the inhibition of NF-kappa B signaling as well as inhibition of H. pylori growth in a mouse model infected with H. pylori. This suggests the potential application of KP as a natural supplement for patient's suffering from gastric mucosal injury caused by H. pylori infection.

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