Effects of polygonum capitatum on helicobacter pylori associated gastritis through the regulation of acetyla-tion of NF-κB by SIRT-1 / 医学研究生学报

ABSTRACT

Objective The activation of NF-kappa B (NF-κB) signaling pathway plays an important role in the development of helicobacter pylori associated gastritis (HAG). The article aimed to investigate the effects of polygonum capitatum on the treatment of HAG in NF-κB signaling pathway and observe whether the regulation of NF-κB acetylation by silent information regulator 1 (SIRT1) affects the therapeutic effects of HAG. Methods The immortalized human gastric epithelial cells (GES-1) were cultured and the H.pylori stand- ard strain ATCC700392 was used for the replication of HAG cell model by 100∶1. The cells were divided into model group,drug group and normal control group. Cells were treated with 80 μg/mL in drug group,H.pylori and GES-1 were cultured together in model group and untreated GES-1 cells were taken as control group. Real time PCR was used to detect the mRNA levels of SIRT1,NF-κB/p65 and TNF-α. Western blotting was used to detect the expression levels of SIRT1,NF-κB/p65 and its acetylated protein in the total protein,as well as the expression levels of SIRT1 and NF-κB/p65 in cytoplasm and nuclear protein. Results At 12 h after the infection of H. pylori,the level of TNF-α in the supernatant was higher than that in the normal control group(P<0.05). The expression of SIRT1 de-creased in the cytoplasm of model group,while the expression levels of NF-κB/p65,acetyl-NF-κB p65(Lys310) and TNF-α in the nu-cleus increased (P<0.05). But after the treatment of polygonum capitatum,the expression of SIRT1 in the nucleus increased(P<0.05) while the expression of NF-κB/p65,acetyl-NF-κB p65(Lys310) and TNF-α decreased (P<0.05). Conclusion Polygonum capita-tum can activate the SIRT1 in the nucleus,which makes activated NF-κB/p65 in the nucleus carry out deacetylation modification in or-der to antagonize the cell damage induced by H.pylori.