Abstract:

Objective　To investigate the effect of licoflavone on aspirin-induced human gastric mucosal epithelial （GES-1） cell injury and its mechanism.Methods　The study was conducted from March to November 2017.GES-1 cells were divided into 6 groups，control group （incubated with DMEM），aspirin group （incubated with 18.5 mmol/L aspirin for 24 h），low-dose，medium-dose and high-dose licoflavone groups （incubated with 18.5 mmol/L aspirin for 24 h after being pre-treated with 3，6，12 mg/L licoflavone for 2 h，respectively），PD98059 group （incubated with 18.5 mmol/L aspirin for 24 h after being pre-treated with 12 mg/L licoflavone for 2 h and with 10 μmol/L PD98059 for 1 h successively）．Proliferation inhibition rate was detected by MTT assay，apoptosis rate was measured by flow cytometry，lactate dehydrogenase （LDH），superoxide dismutase （SOD） activities，and malondialdehyde （MDA） content were determined by colorimetry，the protein expressions of p-ERK1/2，Bcl-2 and Bax were measured by western blotting.Results　 The control group showed significantly decreased proliferation inhibition rate，apoptosis rate，LDH activity，MDA content，and p-ERK1/2 and Bax expressions，but obviously increased SOD activity and Bcl-2 expression compared with other groups，as did the medium-dose and high-dose licoflavone groups and PD98059 group when compared with the aspirin group，and the PD98059 group when compared with the 3 licoflavone groups （P<0.05）．Conclusion　 Licoflavone alleviates aspirin-induced GES-1 cell injury through pro-proliferation，anti-apoptosis and anti-oxidative stress via the inhibition of ERK1/2 signaling pathway.

Key words: Epithelial cells；Licoflavone；Aspirin；Mechanotransduction, cellular

摘要： 目的　探讨甘草总黄酮对阿司匹林损伤人胃黏膜上皮细胞（GES-1）的保护作用及可能机制。方法　2017年3—11月，选取GES-1细胞株，分为6组，对照组：加DMEM培养基；阿司匹林组：阿司匹林18.5 mmol/L与GES-1共同培养24 h；甘草总黄酮低组、甘草总黄酮中组、甘草总黄酮高组：GES-1分别以甘草总黄酮（3、6、12 mg/L）预处理2 h后再加阿司匹林18.5 mmol/L共同培养24 h；PD98059组：GES-1以甘草总黄酮12 mg/L预处理2 h后，加PD98059 10 μmol/L处理1 h，再加阿司匹林18.5 mmol/L共同培养24 h。采用MTT法检测细胞增殖抑制率，采用流式细胞术检测细胞凋亡率，检测乳酸脱氢酶（LDH）、超氧化物歧化酶（SOD）活性及丙二醛（MDA）含量，采用Western blotting法检测细胞磷酸化细胞外调节蛋白激酶（p-ERK1/2）、B淋巴细胞癌2（Bcl-2）、Bcl-2相关X蛋白（Bax）表达。结果　与对照组比较，阿司匹林组、甘草总黄酮低组、甘草总黄酮中组、甘草总黄酮高组、PD98059组细胞增殖抑制率、细胞凋亡率、LDH活性、MDA含量、p-ERK1/2、Bax表达升高，SOD活性、Bcl-2表达降低（P<0.05）；与阿司匹林组比较，甘草总黄酮中组、甘草总黄酮高组、PD98059组细胞增殖抑制率、细胞凋亡率、LDH活性、MDA含量、p-ERK1/2、Bax表达降低，SOD活性、Bcl-2表达升高（P<0.05）；与甘草总黄酮低组、甘草总黄酮中组、甘草总黄酮高组比较，PD98059组细胞增殖抑制率、细胞凋亡率、LDH活性、MDA含量、p-ERK1/2、Bax表达降低，SOD活性、Bcl-2表达升高（P<0.05）。结论　甘草总黄酮可通过促增殖、抗凋亡、抗氧化应激等途径减轻阿司匹林诱导的GES-1损伤，其机制可能与抑制ERK1/2信号通路有关。

关键词: 上皮细胞, 甘草总黄酮, 阿司匹林, 动力传导, 细胞