Fu J-D, Yao J-J, Wang H, Cui W-G, Leng J, Ding L-Y, Fan K-Y
Department of Digestive Disease, People's Hospital of Rizhao, Affiliated Clinical Hospital of Jining Medical Univerity, Jining Medical University, Rizhao, Shandong, China.
Eur Rev Med Pharmacol Sci. 2019 Jan;23(1):155-161. doi: 10.26355/eurrev_201901_16759.
To investigate the effects of epigallocatechin-3-gallate (EGCG) on proliferation and apoptosis of human gastric cancer SGC7901 cells under a hypoxic state.
Human gastric cancer SGC7901 cells were sub-cultured, and the cobalt chloride (CoCl2) hypoxia model was established. The blank control group (normoxia group), hypoxia control group (hypoxia group) and hypoxia + different concentrations of EGCG subgroups (20, 40, 60, 80, 100 μg/mL EGCG) were set up. Cell viability was detected via methyl thiazolyl tetrazolium (MTT) assay, apoptosis was detected via flow cytometry, and expressions of hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) were detected via reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting.
Relatively low concentrations of EGCG (20-80 μg/mL) presented no significant inhibiting effect on SGC7901 cell growth within a short time (24 h) (p>0.05). The increasing concentration of EGCG inhibited cell proliferation under a hypoxia state (p<0.05). EGCG induced apoptosis in a dose-dependent manner under hypoxia (p<0.05). EGCG could significantly impede expressions of HIF-1α and VEGF proteins (p<0.05), and down-regulate the level of VEGF mRNA (p<0.05), but it showed no significant effect on the HIF-1α mRNA expression (p>0.05).
EGCG inhibited cell proliferation under hypoxia via the downregulation of HIF-1α and its downstream target gene VEGF levels, providing a theoretical basis for the early diagnosis and treatment of gastric cancer in clinic.
探讨表没食子儿茶素-3-没食子酸酯（EGCG）对缺氧状态下人胃癌SGC7901细胞增殖和凋亡的影响。
对人胃癌SGC7901细胞进行传代培养，建立氯化钴（CoCl2）缺氧模型。设置空白对照组（常氧组）、缺氧对照组（缺氧组）和缺氧+不同浓度EGCG亚组（20、40、60、80、100μg/mL EGCG）。通过甲基噻唑基四氮唑（MTT）法检测细胞活力，通过流式细胞术检测细胞凋亡，通过逆转录-聚合酶链反应（RT-PCR）和蛋白质印迹法检测缺氧诱导因子-1α（HIF-1α）和血管内皮生长因子（VEGF）的表达。
较低浓度的EGCG（20 - 80μg/mL）在短时间（24小时）内对SGC7901细胞生长无显著抑制作用（p>0.05）。EGCG浓度增加可抑制缺氧状态下的细胞增殖（p<0.05）。EGCG在缺氧条件下呈剂量依赖性诱导细胞凋亡（p<0.05）。EGCG可显著抑制HIF-1α和VEGF蛋白的表达（p<0.05），下调VEGF mRNA水平（p<0.05），但对HIF-1α mRNA表达无显著影响（p>0.05）。
EGCG通过下调HIF-1α及其下游靶基因VEGF水平抑制缺氧状态下的细胞增殖，为临床胃癌的早期诊断和治疗提供了理论依据。
