The Nutraceutical Properties of Sumac (Rhus coriaria L.) against Gastritis: Antibacterial and Anti-Inflammatory Activities in Gastric Epithelial Cells Infected with H. pylori

Sumac (Rhus coriaria L.) is a spice and medicinal herb traditionally used in the Mediterranean region and the Middle East. Since we previously demonstrated Sumac biological activity in a model of tumor necrosis factor alpha (TNF-alpha)-induced skin inflammation, the present work is aimed at further demonstrating a potential role in inflammatory disorders, focusing on gastritis. For this purpose, different polar extracts (water-W, ethanol-water-EW, ethanol-E, ethanol macerated-Em, acetone-Ac, ethylacetate-EtA) were investigated in gastric epithelial cells (GES-1) challenged by TNF-alpha or H. pylori infection. The ethanolic extracts (E, EW, Em) showed the major phenolic contents, correlating with lower half maximal inhibitory concentrations (IC(50)s) on the release of interleukin-8 (IL-8, <15 mu g/mL) and interleukin-6 (IL-6, <20 mu g/mL) induced by TNF-alpha. Similarly, they inhibited IL-8 release (IC(50)s < 70 mu g/mL) during Helicobacter pylori (H. pylori) infection and exhibited a direct antibacterial activity at comparable concentrations (minimum inhibitory concentration (MIC) = 100 mu g/mL). The phenolic content and the bioactivity of EW were maintained after simulated gastric digestion and were associated with nuclear factor kappa B (NF-kappa B) impairment, considered the main putative anti-inflammatory mechanism. On the contrary, an anti-urease activity was excluded. To the best of our knowledge, this is the first demonstration of the potential role of Sumac as a nutraceutical useful in H. pylori-related gastritis.

Automated summary

Sumac is a spice and medicinal herb traditionally used in the Mediterranean region and the Middle East. This study demonstrates its potential role in inflammatory disorders, particularly gastritis. Ethanolic extracts of Sumac showed high phenolic contents and inhibited the release of interleukin-8 (IL-8) and interleukin-6 (IL-6) induced by TNF-alpha. They also exhibited antibacterial activity during H. pylori infection.