RESUMO
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 IKKß. 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 IKKß 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.
RESUMO
OBJECTIVE: To study the antiulcer effects and the mechanism of Veronicastrum axillare (Sieb. et Zucc) Yamazaki (VAY) on ethanol induced gastric ulcer rats. METHODS: Totally 48 healthy SD rats were randomly divided into 6 groups, i.e., the normal group, the model group, the ranitidine group, the high dose VAY group, the medium dose VAY group, and the low dose VAY group, 8 in each group. Rats in the normal group and the model group were administered with normal saline respectively. Rats in the ranitidine group were administered with 0.18% ranitidine suspension (at the daily dose of 0.027 g/kg) by gastrogavage. Those in the high dose VAY group, the medium dose VAY group, and the low dose VAY group were administered with VAY at the daily dose of 2.8 g/kg, 1.4 g/kg, and 0.7 g/kg by gastrogavage, once daily for 14 consecutive days. The gastric ulcer model was established using absolute ethanol after the last gastrogavage. The ulcer index and the ulcer inhibitory rate were compared. The concentrations of malonyldialdehyde (MDA), nitric oxide (NO), epidermal growth factor (EGF), and the activity of superoxide dismutase (SOD) in the serum and the homogenate of the gastric mucosa tissue were detected. RESULTS: Compared with the model group, the gastric ulcer index in the rest groups obviously decreased (P < 0.01). The ulcer index was dose-dependent with VAY (P < 0.01), with the highest gastric ulcer index shown in the high dose VAY group (P < 0.01). Compared with the normal group, the concentrations of MDA and NO significantly increased in the serum and the gastric mucosa tissue, the activity of SOD and the EGF content in the gastric mucosa tissue of rats in the model group significantly decreased (P < 0.01). Compared with the model group, the MDA concentrations in the serum and the gastric mucosa tissue decreased, the serum NO content increased, the NO content in the gastric mucosa tissue decreased, the serum SOD activity increased, the EGF content in the gastric mucosa tissue increased in the rest groups, all showing statistical difference (P < 0.05, P < 0.01). CONCLUSIONS: The water extract of VAY had significant effects on ethanol induced gastric ulcer. Its mechanisms might lie in reducing the generation of free radicals, promoting the oxygen free radical clearance, restraining lipid peroxidation, regulating and controlling the in vivo contents of NO and EGF.
