Veronicastrum axillare Alleviates Ethanol-Induced Injury on Gastric Epithelial Cells via Downregulation of the NF-kB Signaling Pathway.

Wei-Chun Zhao,Yan Guo,Gui-Bin Meng,Dan-Yi Wang,Gang Chen,Yan-Shan Xu

doi:10.1155/2017/7395032

Abstract

We used human gastric epithelial cells (GES-1) line in an ethanol-induced cell damage model to study the protective effect of Veronicastrum axillare and its modulation to NF-κB signal pathway. The goal was to probe the molecular mechanism of V. axillare decoction in the prevention of gastric ulcer and therefore provide guidance in the clinical application of V. axillare on treating injuries from chronic nephritis, pleural effusion, gastric ulcer, and other ailments. The effects of V. axillare-loaded serums on cell viability were detected by MTT assays. Enzyme-linked immunosorbent assay (ELISA) and Real-Time PCR methods were used to analyze the protein and mRNA expression of TNF-α, NF-κB, IκBα, and IKKβ. The results showed that V. axillare-loaded serum partially reversed the damaging effects of ethanol and NF-κB activator (phorbol-12-myristate-13-acetate: PMA) and increased cell viability. The protein and mRNA expressions of TNF-α, NF-κB, IκBα, and IKKβ were significantly upregulated by ethanol and PMA while they were downregulated by V. axillare-loaded serum. In summary, V. axillare-loaded serum has significantly protective effect on GES-1 against ethanol-induced injury. The protective effect was likely linked to downregulation of TNF-α based NF-κB signal pathway.

Highlights

Gastric ulcer is one of the most common clinical conditions of the digestive system
Our preliminary in vivo results showed that the water extract of V. axillare significantly inhibited ethanolinduced gastric epithelial cell damage [14, 15, 19]
The current study used MTT assay to examine the effect on cell viability under ethanol assault by pretreatment of GES-1 with V. axillare-loaded serum

Summary

Introduction

Gastric ulcer is one of the most common clinical conditions of the digestive system. Globally, more than 14 million people are diagnosed with gastric ulcer annually, and about 4 million people would die from related complications [1]. Human gastric epithelial tissue is in constant turn-over, maintaining a balance between cell death and new cell formation. When the damage exceeds the selfrepair capacity, the structure and function of the gastric epithelial tissue can be compromised, leading to an imbalance between cell generation and cell death, which in turn can cause gastric inflammation and ulcer. Alcohol in moderation has health benefits, elevated alcohol consumption has been linked to GI track disorders, and acute GI epithelial tissue alcohol damage is on the rise [5]. Excessive consumption of hard liquor can directly cause gastric epithelial cell damage, resulting in inflammation, congestion, edema, bleeding, erosion, and ulcer in the GI track. Alcohol has been recognized as a key pathogen in gastric epithelial tissue damage. Methods for the prevention and treatment of such damage and deduction of protective mechanisms have been the focus of many research projects [7]

Methods

Results

Conclusion