Department of Clinical Laboratory, School of Medical Laboratory Sciences, Guizhou Medical University, Guiyang 550004, China.
Department of Clinical Biochemistry, Affiliated Hospital of Guizhou Medical University, Guiyang 550004, China.
Molecules. 2017 May 6;22(5):744. doi: 10.3390/molecules22050744.
-associated gastritis is a major threat to public health and (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. -infected mouse models were established. All mice were divided into three groups: control (CG, healthy mice), model (MG, 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 ( < 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 ( < 0.01). Quercetin treatment reduced the levels of p38MAPK and BAX, and increased the levels of BCL-2 when compared with a MG group ( < 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 infection by affecting the levels of p38MAPK, BCL-2 and BAX.
-相关胃炎是威胁公众健康的主要因素，而（PC）可能对该疾病有益。然而，其分子机制尚不清楚。槲皮素从 PC 中分离出来，被发现是一种主要的生物活性化合物。通过 xCELLigence 测定了槲皮素对人胃腺癌 GES-1 细胞的影响。建立了感染的小鼠模型。所有小鼠分为三组：对照组（CG，健康小鼠）、模型组（MG，感染）和槲皮素组（QG，槲皮素处理的小鼠模型）。通过酶联免疫吸附测定（ELISA）检测白细胞介素-8（IL-8）水平。通过流式细胞术（FCM）测量细胞周期和凋亡。定量逆转录 PCR（qRT-PCR）和 Western Blot 用于检测 p38MAPK（38-kD 酪氨酸磷酸化蛋白激酶）、凋亡调节因子 BCL-2 相关蛋白 X（BAX）和 B 细胞淋巴瘤基因 2（BCL-2）的水平。与 CG 组相比，MG 组 IL-8 水平增加 8.1 倍，QG 组增加 4.3 倍。MG 组 G0-G1（细胞周期各期）% 比值高于 CG 组，而 S 期分数低于 CG 组（ < 0.01）。槲皮素治疗后，QG 组 G0-G1%比值低于 MG 组，而 S 期分数高于 MG 组（ < 0.01）。与 MG 组相比，槲皮素治疗降低了 p38MAPK 和 BAX 的水平，增加了 BCL-2 的水平（ < 0.05）。槲皮素通过影响 p38MAPK、BCL-2 和 BAX 的水平来调节胃细胞增殖和凋亡的平衡，从而保护胃免受胃炎的侵害。
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