Quercetin Improves Mitochondrial Function and Inflammation in H2O2-Induced Oxidative Stress Damage in the Gastric Mucosal Epithelial Cell by Regulating the PI3K/AKT Signaling Pathway

Abstract

Functional dyspepsia (FD) is one of the most common functional gastrointestinal disorders, the therapeutic strategy of which it is limited due to its complex pathogenesis. Oxidative stress-induced damage in gastric mucosal epithelial cells is related to the pathogenesis and development of FD. Quercetin (Que) is one of the active ingredients of Zhishi that showed antioxidant, antiapoptotic, and anti-inflammatory effects. The aim of this study is to investigate the effect of Que on oxidative stress-induced gastric mucosal epithelial cells damage and its underlying molecular mechanism. The gastric mucosal epithelial cell line GES-1 was treated with 200 μM of H2O2 to construct an oxidative stress-induced damage model. The H2O2 cells were then administrated with different concentrations of Que. The results indicated that high concentration of Que (100 μM) showed cytotoxicity in H2O2-induced GES-1 cells. However, appropriate concentration of Que (25 and 50 μM) alleviated the oxidative stress damage induced by H2O2, as demonstrated by the increase of proliferation, decrease of ROS generation, apoptosis, inflammation, and alleviation of mitochondrial function and cell barrier. In addition, Que increased the activation of phosphorylation of PI3K and AKT decreased by H2O2. To investigate whether Que alleviated the oxidative stress damage in GES-1 cells by the PI3K/AKT signaling pathway, the GES-1 cells were treated with Que (25 μM) combined with and without LY294002, the PI3K inhibitor. The results showed that LY294002 suppressed the alleviation effect on Que in H2O2-induced GES-1 cells. In conclusion, the current study demonstrates that Que alleviates oxidative stress damage in GES-1 cells by improving mitochondrial function and mucosal barrier and suppressing inflammation through regulating the PI3K/AKT signaling pathway, indicating the potential therapeutic effects of Que on FD.

Protocatechuic acid and quercetin attenuate ETEC-caused IPEC-1 cell inflammation and injury associated with inhibition of necroptosis and pyroptosis signaling pathways

“…In the current experiment, consistent with improved intestinal barrier function, PCA and Que rescued the protein expression and distribution of occludin, claudin-1 and ZO-1 as measured by confocal microscopy. In accordance with our study, PCA and Que have been reported to improve protein expression of occludin, claudin-1 and ZO-1 in vivo and vitro [ 42 – 44 ]. In our present study, it is possible that PCA and Que may partially protect intestinal barrier function via improving protein expression and rescuing distribution of intestinal tight junctions.…”

Protocatechuic acid and quercetin attenuate ETEC-caused IPEC-1 cell inflammation and injury associated with inhibition of necroptosis and pyroptosis signaling pathways

“…In the current experiment, consistent with improved intestinal barrier function, PCA and Que rescued the protein expression and distribution of occludin, claudin-1 and ZO-1 as measured by confocal microscopy. In accordance with our study, PCA and Que have been reported to improve protein expression of occludin, claudin-1 and ZO-1 in vivo and vitro [34][35][36]. In our present study, it is possible that PCA and Que may partially protect intestinal barrier function via improving protein expression and rescuing distribution of intestinal tight junctions.…”

Overexpression of Laminin 5γ2 Chain Correlates with Tumor Cell Proliferation, Invasion, and Poor Prognosis in Laryngeal Squamous Cell Carcinoma

“…Synthesis of cDNA by reverse transcription was performed, and then the cDNA was analyzed by SYBR Premix Ex TaqII (Takara, RR820A). The level of the target gene was calculated by 2 −△△Ct method [ 30 ], and GAPDH was used as the internal reference. The gene primer sequences are shown in Table 2 .…”