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BioMed Research International
Volume 2017, Article ID 7157212, 10 pages
https://doi.org/10.1155/2017/7157212
Research Article

Banhasasim-Tang Treatment Reduces the Severity of Esophageal Mucosal Ulcer on Chronic Acid Reflux Esophagitis in Rats

1Department of Pharmacology, College of Korean Medicine, Sangji University, Wonju-si, Gangwon-do 26339, Republic of Korea
2Department of Herbology, College of Korean Medicine, Daegu Haany University, 136 Shinchendong-ro, Suseong-gu, Daegu 42158, Republic of Korea
3Liver and Immunology Research Center, Daejeon Oriental Hospital, Oriental Medical College, Daejeon University, 176-9 Daeheung-ro, Jung-gu, Daejeon 34929, Republic of Korea

Correspondence should be addressed to Seong-Soo Roh; rk.ca.uhd@ededd and Hyo-Jin An; rk.ca.ijgnas@najh

Received 6 December 2016; Revised 6 February 2017; Accepted 13 February 2017; Published 2 March 2017

Academic Editor: Tadayuki Oshima

Copyright © 2017 Mi-Rae Shin et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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 ulcer via regulating inflammation through the activation of the antioxidant pathway.