Fuente: PubMed "rice" NPJ Sci Food. 2026 Jun 20. doi: 10.1038/s41538-026-00956-8. Online ahead of print.ABSTRACTThe aim of this study was to investigate the effect of PVLWGVPKG (PV9) on gastric mucosa cell damage induced by Helicobacter pylori infection. PV9 intervention could significantly reduce the number of Helicobacter pylori adhering to GES-1 cells (p <0.05). Molecular docking showed that PV9 and its degraded fragments could bind to Helicobacter pylori adhesins, and hydrogen bonds might be the main driving force. Dot blot assays confirmed the binding between PV9 and adhesins SabA and BabA in vitro. The protective mechanism of PV9 against Helicobacter pylori infection-induced GES-1 damage cells was analyzed. It was found that PV9 could accelerate the clearance of reactive oxygen species, reduce mitochondrial membrane potential, improve cell cycle arrest, and prevent apoptosis. In addition, PV9 can also significantly improve the antioxidant capacity of cells (SOD, GSH-Px, and CAT), reducing the content of pro-inflammatory factors (IL-1β, IL-6, IL-8, IL-18, and TNF-α) and increasing the content of anti-inflammatory factors (IL-10). The results of qRT-PCR showed that PV9 could protect GES-1 cells by regulating the expression of apoptotic factors. Moreover, the TLR4/MyD88/NF-κB signaling pathways may play a significant role in this process. This study provides a new idea for antagonizing Helicobacter pylori infection with active peptide components.PMID:42323355 | DOI:10.1038/s41538-026-00956-8