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논문 기본 정보

자료유형
학술저널
저자정보
Kim Jun-Young (Department of Laboratory Animal Medicine College of Veterinary Medicine Konkuk University Seoul 05029 Republic of KoreaGC Biopharma Corporation Gyeonggi-do 16924 Republic of Korea) Seo Sun-Min (Department of Laboratory Animal Medicine College of Veterinary Medicine Konkuk University Seoul 05029 Republic of Korea) Kim Han-Woong (Department of Laboratory Animal Medicine College of Veterinary Medicine Konkuk University Seoul 05029 Republic of KoreaRegenerative Dental Medicine Institute Hysensbio Gyeonggi-do 13814 Republic of Ko) Lee Woo-Jong (CONNEXT Co. Ltd Daegu 41061 Republic of Korea) 최양규 (건국대학교)
저널정보
한국미생물생명공학회 Journal of Microbiology and Biotechnology Journal of Microbiology and Biotechnology 제33권 제1호
발행연도
2023.1
수록면
35 - 42 (8page)
DOI
10.4014/jmb.2209.09048

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This study aimed to identify the therapeutic ability of a novel toll-like receptor (TLR) 5 agonist, KMRC011, on ulcerative colitis induced by Citrobacter rodentium and dextran sulfate sodium in a C57BL/6N mouse model. Ulcerative colitis was induced in the mice by the oral administration of 1% dextran sulfate sodium in sterile drinking water for seven days ad libitum, followed by C. rodentium infection on the seventh day by intra-gastric administration (DSS-CT group). KMRC011 was administered intramuscularly at both 24 h and 15 min before (Treatment 1 group), and at both 15 min and 24 h after (Treatment 2 group) the C. rodentium infection. The length of the large intestine and histopathological counts were significantly greater and mucosal thickness was significantly thinner in the Treatment 1 group compared to the DSS-CT and Treatment 2 groups. Il-6 and Il-10 mRNA expression levels were upregulated, while Ifn-γ and Tnf-α mRNA expression levels were significantly downregulated in the Treatment 1 group, compared to the DSS-CT group. NF-κB p65 expression level was elevated due to ulcerative colitis in the DSS-CT group, but was significantly downregulated in the Treatment 1 group. Overall, KMRC011 showed protective effects against murine colitis by inhibiting NF-κB signaling.

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