title: Banhasasim-Tang Treatment Reduces the Severity of Esophageal Mucosal Ulcer on Chronic Acid Reflux Esophagitis in Rats.
abstract: The present study was conducted to evaluate both antioxidant and anti-inflammatory activity of Banhasasim-tang (BHSST) on chronic acid reflux esophagitis (CRE) model. Rat CRE model was established operatively and then treated with BHSST (1 g/kg body weight per day) for 15 days Esophageal pathological changes were analyzed using macroscopic examination and hematoxylin/eosin staining. The antioxidant and inflammatory protein levels were determined using Western blotting. The administration of BHSST significantly reduced both the overexpression of serum reactive oxygen species (ROS) and an excessive formation of thiobarbituric acid-reactive substances (TBARS) in esophagus tissue. Thus, the severity of esophageal ulcer was lower in BHSST treated rats than control rats on the gross and histological evaluation. Nuclear factor-erythroid 2-related factor 2 (Nrf2) led to the upregulation of antioxidant enzyme including SOD, GPx-1/2, and HO-1 by binding to antioxidant response element (ARE). Moreover, BHSST administration markedly reduced the expression of inflammatory proteins through mitogen-activated protein kinase- (MAPK-) related signaling pathways and decreased significantly the protein expressions of inflammatory mediators and cytokines by inhibition of nuclear factor-kappa B (NF-κB) activation. Taken together, these results support the fact that BHSST administration can suppress the development of esophageal mucosal ulcerviaregulating inflammation through the activation of the antioxidant pathway.
authors.affiliation: Department of Pharmacology, College of Korean Medicine, Sangji University, Wonju-si, Gangwon-do 26339, Republic of Korea; Department of Herbology, College of Korean Medicine, Daegu Haany University, 136 Shinchendong-ro, Suseong-gu, Daegu 42158, Republic of Korea.
authors.forename: Mi-Rae
authors.identifier: 0000-0002-4365-6988
authors.initials: MR
authors.lastname: Shin
authors.affiliation: Department of Herbology, College of Korean Medicine, Daegu Haany University, 136 Shinchendong-ro, Suseong-gu, Daegu 42158, Republic of Korea.
authors.forename: Bu-Il
authors.identifier: 0000-0002-9149-6560
authors.initials: BI
authors.lastname: Seo
authors.affiliation: Liver and Immunology Research Center, Daejeon Oriental Hospital, Oriental Medical College, Daejeon University, 176-9 Daeheung-ro, Jung-gu, Daejeon 34929, Republic of Korea.
authors.forename: Chang Gue
authors.identifier: 0000-0002-6963-5229
authors.initials: CG
authors.lastname: Son
authors.affiliation: Department of Herbology, College of Korean Medicine, Daegu Haany University, 136 Shinchendong-ro, Suseong-gu, Daegu 42158, Republic of Korea.
authors.forename: Seong-Soo
authors.identifier: 0000-0002-4162-6849
authors.initials: SS
authors.lastname: Roh
authors.affiliation: Department of Pharmacology, College of Korean Medicine, Sangji University, Wonju-si, Gangwon-do 26339, Republic of Korea.
authors.forename: Hyo-Jin
authors.identifier: 0000-0002-2937-874X
authors.initials: HJ
authors.lastname: An
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage* / Q000378:metabolism; D051546:Cyclooxygenase 2 / Q000096:biosynthesis; D004195:Disease Models, Animal; D000071041:Esophageal Mucosa / Q000187:drug effects / Q000378:metabolism; D004947:Esophagus / Q000187:drug effects / Q000473:pathology; D005764:Gastroesophageal Reflux / Q000188:drug therapy* / Q000235:genetics / Q000473:pathology; D005786:Gene Expression Regulation / Q000187:drug effects; D005978:Glutathione / Q000096:biosynthesis; D006801:Humans; D007249:Inflammation / Q000188:drug therapy* / Q000235:genetics / Q000473:pathology; D051267:NF-E2-Related Factor 2 / Q000096:biosynthesis; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D000975:Antioxidants; D051267:NF-E2-Related Factor 2; D017382:Reactive Oxygen Species; D051546:Cyclooxygenase 2; D005978:Glutathione