摘要
目的探讨阿司匹林抑制肝癌细胞HepG2增殖及其机制。方法用人肝癌细胞HepG2,将其分为观察组1、观察组2、观察组3和对照组,3组观察组分别使用终浓度为5,10和20 mmol·L^(-1)的阿司匹林进行治疗,对照组给予等量的生理盐水,观察阿司匹林对HepG2细胞增殖的抑制作用、不同浓度阿司匹林对HepG2细胞周期和凋亡的影响、HepG2细胞中X的蛋白质(Bax)和B淋巴细胞瘤bai-2基因(Bcl-2)的mRNA及蛋白相对表达量的对比。结果不同浓度的阿司匹林作用24和48 h后,对HepG2细胞增殖的抑制作用显著高于对照组(P<0.05),随着药物浓度的增加,抑制作用也随之升高;不同浓度的阿司匹林作用48 h后对HepG2细胞增殖的抑制作用高于24 h(P<0.05);不同浓度的阿司匹林G0/G1期的细胞百分比均高于对照组(P<0.05),不同浓度的阿司匹林的凋亡率也高于对照组(P<0.05),随着剂量的升高,HepG2细胞周期也被明显抑制,其凋亡率逐渐增加(P<0.05);Bax mRNA和蛋白的相对表达量依次为:观察组3>观察组2>观察组1>对照组(P<0.05);Bcl-2 mRNA和蛋白的相对表达量依次为:观察组3<观察组2<观察组1<对照组(P<0.05)。结论阿司匹林可抑制肝癌细胞HepG2的增殖,其机制可能与Bcl-2与Bax的动态失衡有关,通过Bax的过表达来促进肝癌细胞HepG2的凋亡及其对HepG2细胞增殖的抑制作用。
Objective To investigate the effects of aspirin on the proliferation of HepG2 cells and its mechanism.Methods Human liver cancer cells HepG2 were divided into observation group 1,observation group 2,observation group 3 and control group.The observation group was treated with aspirin at a final concentration of 5,10 and 20 mmol·L-1.The drug was administered to observe the inhibitory effect of aspirin on the proliferation of HepG2 cells,and the effect of aspirin at different concentrations on the cell cycle and apoptosis of HepG2 cells.The Bax and Bcl-2 mRNA and protein expression in HepG2 cells was compared.Results After 24 and 48 h of aspirin at different concentrations,the inhibitory effect on the proliferation of HepG2 cells was significantly higher than that of the control group(P<0.05).As the drug concentration increased,the inhibitory effect also increased;the inhibitory effect of aspirin on the proliferation of HepG2 cells after 48 h of action was higher than that of 24 h of action(P<0.05);the percentage of G0/G1 phase of aspirin with different concentrations was higher than that of the control group(P<0.05).Aspirin had a higher apoptotic rate than the control group(P<0.05).As the dose increased,the more obvious the HepG2 cell cycle was inhibited,the apoptotic rate also gradually increased(P<0.05);the relative expression of Bax mRNA and protein expression was in order as:observation group 3>observation group 2>observation group 1>control group(P<0.05);the relative expression levels of Bcl-2 mRNA and protein expression were in order as:observation group 3<observation group 2<observation group 1<control group(P<0.05).Conclusion Aspirin can inhibit the proliferation of HepG2 cells.The mechanism may be related to the dynamic imbalance of Bcl-2 and Bax.Overexpression of Bax can promote the apoptosis of HepG2 cells and its inhibitory effect on HepG2 cells.
作者
马颖
马明
马玲
MA Ying;MA Ming;MA Ling(Medical Laboratory Center,the First Affiliated Hospital of Xinjiang Medical University,Urumqi 830054,China;Department of Hepatobiliary Surgery,Xinjiang Uygur Autonomous Region People′s Hospital,Urumqi 830001,China;Chest Hospital of Xinjiang Uygur Autonomous Region,Urumqi 830001,China)
出处
《西北药学杂志》
CAS
2020年第6期860-863,共4页
Northwest Pharmaceutical Journal
基金
新疆维吾尔自治区自然科学基金资助项目(编号:2018D01C186)。
关键词
阿司匹林
肝癌
细胞增殖
aspirin
liver cancer
cell proliferation
