Quercetin from Polygonum capitatum Protects against Gastric Inflammation and Apoptosis Associated with Helicobacter pylori Infection by Affecting the Levels of p38MAPK, BCL-2 and BAX

Abstract

Helicobacter pylori-associated gastritis is a major threat to public health and Polygonum capitatum (PC) may have beneficial effects on the disease. However, the molecular mechanism remains unknown. Quercetin was isolated from PC and found to be a main bioactive compound. The effects of quercetin on human gastric cancer cells GES-1 were determined by xCELLigence. H. pylori-infected mouse models were established. All mice were divided into three groups: control (CG, healthy mice), model (MG, H. pylori infection) and quercetin (QG, mouse model treated by quercetin) groups. IL-8 (interleukin-8) levels were detected via enzyme-linked immunosorbent assay (ELISA). Cell cycle and apoptosis were measured by flow cytometry (FCM). Quantitative reverse transcription PCR (qRT-PCR) and Western Blot were used to detect the levels of p38MAPK (38-kD tyrosine phosphorylated protein kinase), apoptosis regulator BCL-2-associated protein X (BAX) and B cell lymphoma gene 2 (BCL-2). The levels of IL-8 were increased by 8.1-fold in a MG group and 4.3-fold in a QG group when compared with a CG group. In a MG group, G0–G1(phases of the cell cycle)% ratio was higher than a CG group while S phase fraction was lower in a model group than in a control group (p < 0.01). After quercetin treatment, G0–G1% ratio was lower in a QG group than a MG group while S phase fraction was higher than a MG group (p < 0.01). Quercetin treatment reduced the levels of p38MAPK and BAX, and increased the levels of BCL-2 when compared with a MG group (p < 0.05). Quercetin regulates the balance of gastric cell proliferation and apoptosis to protect against gastritis. Quercetin protects against gastric inflammation and apoptosis associated with H. pylori infection by affecting the levels of p38MAPK, BCL-2 and BAX.

Identifying potential novel drugs against Helicobacter pylori by targeting the essential response regulator HsrA

“…Quercetin inhibited vacuolation and caspase-3 activation in HeLa cells induced by the vacuolating cytotoxin A, protecting from gastric inflammation and apoptosis associated with H . pylori infection 57,58 . Kaempferol decreased transcription of type IV secretion system (T4SS) components involved in CagA injection and secretion system subunit protein A (SecA) of type V secretion system (T5SS) involved in VacA secretion, thereby producing an anti-inflammatory effect by suppressing the translocation of CagA and VacA proteins 59 .…”

Cortactin: A Major Cellular Target of the Gastric Carcinogen Helicobacter pylori

“…It might be that cortactin plays a role during endosomal trafficking of VacA from the cell membrane to the mitochondria [104], but further investigations are clearly required to unravel the detailed function of cortactin in programmed cell death. In this regard, it is interesting to note that the bioactive compound quercetin from the plant Polygonum capitatum was shown to protect against gastric inflammation and apoptosis associated with H. pylori infection in mice by affecting the expression level of p38 MAP kinase, Bcl-2 and Bax [105]. Thus, quercetin can regulate the balance between gastric cell proliferation and apoptosis in the gastric epithelium and could be a novel candidate therapeutic agent to treat H. pylori-induced gastritis and other diseases.…”

Potential Association Between Asthma, Helicobacter pylori Infection, and Gastric Cancer

“…A recent research found that quercetin has the anti-allergic properties characterized by stimulation of immune system, inhibition of histamine release, decrease in proinflammatory cytokines, and improvement in the Th1/Th2 balance ( 53 ). The experiment by Zhang et al showed that quercetin protected against gastric inflammation and apoptosis associated with HPI by affecting the levels of p38MAPK, BCL-2, and BAX ( 54 ). Thus, quercetin could act as an effective ingredient to protect against HPI and activate some pathways.…”