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The Effects of Mannyeon-hwan on Acetic Acid-induced Ulcerative Colitis in Rats

흰쥐에서 acetic acid로 유발된 궤양성 대장염에 대한 만년환의 효과

  • Won-ho Kong (Dept. of Korean Internal Medicine, College of Korean Medicine, Dong-eui University) ;
  • Bum-hoi Kim (Dept. of Anatomy, College of Korean Medicine, Dong-eui University) ;
  • Won-ill Kim (Dept. of Korean Internal Medicine, College of Korean Medicine, Dong-eui University)
  • 공원호 (동의대학교 한의과대학 비계내과학교실) ;
  • 김범회 (동의대학교 한의과대학 해부학교실) ;
  • 김원일 (동의대학교 한의과대학 비계내과학교실)
  • Received : 2024.08.29
  • Accepted : 2024.10.14
  • Published : 2024.09.30

Abstract

Objectives: This study was designed to verify the effects of Mannyeon-hwan (MNH) on acetic acid-induced ulcerative colitis in rats. Methods: Ulcerative colitis was induced in male Sprague-Dawley rats weighing approximately 250 g by injecting acetic acid through the anus. Rats were classified into four groups: normal group, control group (acetic-acid, AA), low concentration group (AA+MNH(L)), and high concentration group (AA+MNH(H)). Body weight, visual evaluation of the colonic mucosa, anatomical histological changes, and changes in the expression of proteins in colon tissue were compared and analyzed. Results: Compared to the control group, the MNH groups showed significant recovery from weight loss and mucosal damage. The expression of inflammatory proteins such as TNF-α, IL-6, IL-1β, NF-κB p65, MPO, and COX-2 were significantly decreased in the MNH groups compared to those in the AA group. In the MNH groups, significant changes in proteins involved in apoptosis such as caspase-3, BAX, and Bcl-2 were observed compared to those in the AA group. Additionally, changes in the expression of TNF-α, IL-6, IL-1β, NF-κB p65, BAX, and Bcl-2 were greater in the MNH(H) group than those in the MNH(L) group. Conclusion: Mannyeon-hwan was found to be effective in suppressing inflammation of the colonic mucosa in ulcerative colitis, inhibiting the expression of inflammation-related proteins, and suppressing damage to the colonic mucosa by regulating the expression of apoptosis-related proteins.

Keywords

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