Helicobacter pylori 유발 위 손상에 대한 Lactobacillus paracasei HP7의 위 염증완화 및 점막 보호 효과 = Protective effects of Lactobacillus paracasei HP7 against Helicobacter pylori induced gastric inflammation and mucosal injury

다국어 초록 (Multilingual Abstract)

pylori is a major gastric pathogen that colonizes the gastric mucosa and can lead to chronic gastritis, peptic ulcer disease, and gastric cancer. This study aimed to evaluate the anti-inflammatory and gastroprotective effects of HP7 in a H. pylori–infected C57BL/6 mouse model. H. pylori infection was confirmed using the CLO test, in which all mice in the HP group showed a rapid color change within 2 hours, whereas HP7-treated mice exhibited a noticeably slower reaction. Serum IgG titers were elevated by approximately 49% in the HP group, while HP7 administration markedly reduced IgG levels by 32.5% and 13.4% in the respective treatment groups.
Histopathological analysis revealed severe epithelial damage and inflammatory cell infiltration in the HP group, whereas HP7 treatment alleviated these lesions, consistent with the corresponding histological scores. Gastric inflammatory responses were further examined through the expression of IL-6, IL-8, and TNF-α. All cytokines were significantly upregulated in the HP group compared with the normal control, while HP7 supplementation significantly reduced their expression, with IL-8 showing the greatest reduction (approximately 59–62%). MUC1 expression decreased by 46% in the HP group (p < 0.001) but increased by more than 50% following HP7 treatment(p < 0.001). PGE2, a mediator of gastric inflammation and pain, increased by 74% in the HP group (p < 0.05) and was reduced by over 40% in HP7-treated mice (p < 0.01). Furthermore, gastric acid–related factors including gastrin, CCK2R, and histamine were decreased in the HP7 group to 45%, 50%, and 34% of HP-induced levels, respectively.
Collectively, these findings indicate that L. paracasei HP7 effectively mitigates H. pylori–induced gastric inflammation and mucosal damage, suggesting its potential application as a functional food ingredient with anti-inflammatory and gastroprotective properties.

목차 (Table of Contents)

• Ⅰ. 서론 1
• 연구목적 8
• Ⅱ. 재료 및 방법 9
• 2.1. H.pylori 의 배양 9
• 2.2. 시험물질 9
• 2.3. 동물실험 디자인 9
• 2.4. H.pylori 감염확인 13
• 2.5. Campylobacter-like organism(CLO) test 13
• 2.6. 식이효율 측정 14
• 2.7. H.pylori IgG 항체가 측정 13
• 2.8. 위 점막의 조직학적 분석 15
• 2.9. Enzyme-linked immunosorbent assay(ELISA) 16
• 2.10. Quantitative Polymerase Chain Reaction (qPCR) Assay 16
• 2.11. Statistical analysis 19
• Ⅲ. 결과 및 고찰 20
• 3.1. 실험동물의 체중 및 장기 무게 20
• 3.2. CLO test를 이용한 pylori 감염확인 23
• 3.3 H. pylori 혈청 IgG 항체 검사 결과 25
• 3.4. H.pylori 감염 마우스에서 위 점막 조직의 병리학적 변화 27
• 3.5. H. pylori 감염 마우스에서 TLR4 mRNA 발현 수준 변화 30
• 3.6. H.pylori 감염에 따른 염증성 사이토카인 mRNA 발현 변화 33
• 3.7. H.pylori 감염에 따른 항염증성 사이토카인의 mRNA 수준 변화 35
• 3.8. H.pylori 감염 마우스에서 MUC1 의 mRNA 수준 변화 37
• 3.9. H.pylori 감염 마우스에서 PGE2 의 mRNA 수준 변화 39
• 3.10. H.pylori 감염에 따른 위산분비 관련인자 mRNA 수준변화 41
• Ⅳ. 요약 및 결론 44
• 참고문헌 46
• ABSTRACT 56