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半夏泻心汤治疗减轻大鼠慢性反流性食管炎食管黏膜溃疡的严重程度。

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

作者信息

Shin Mi-Rae, Seo Bu-Il, Son Chang Gue, Roh Seong-Soo, An Hyo-Jin

机构信息

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.

Department of Herbology, College of Korean Medicine, Daegu Haany University, 136 Shinchendong-ro, Suseong-gu, Daegu 42158, Republic of Korea.

出版信息

Biomed Res Int. 2017;2017:7157212. doi: 10.1155/2017/7157212. Epub 2017 Mar 2.

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-B) activation. Taken together, these results support the fact that BHSST administration can suppress the development of esophageal mucosal ulcer regulating inflammation through the activation of the antioxidant pathway.

摘要

本研究旨在评估半夏泻心汤(BHSST)对慢性酸反流性食管炎(CRE)模型的抗氧化和抗炎活性。通过手术建立大鼠CRE模型,然后用BHSST(每天1 g/kg体重)治疗15天。使用宏观检查和苏木精/伊红染色分析食管病理变化。使用蛋白质印迹法测定抗氧化和炎症蛋白水平。BHSST给药显著降低了食管组织中血清活性氧(ROS)的过表达和硫代巴比妥酸反应性物质(TBARS)的过度形成。因此,在大体和组织学评估中,BHSST治疗的大鼠食管溃疡的严重程度低于对照大鼠。核因子红系2相关因子2(Nrf2)通过与抗氧化反应元件(ARE)结合导致抗氧化酶包括超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶1/2(GPx-1/2)和血红素加氧酶1(HO-1)的上调。此外,BHSST给药通过丝裂原活化蛋白激酶(MAPK)相关信号通路显著降低炎症蛋白的表达,并通过抑制核因子κB(NF-κB)活化显著降低炎症介质和细胞因子的蛋白表达。综上所述,这些结果支持BHSST给药可通过激活抗氧化途径调节炎症来抑制食管黏膜溃疡发展这一事实。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa6b/5352876/b0fee155e731/BMRI2017-7157212.001.jpg

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