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作 者:于洪丹 郁盛雪 左中夫 Yu Hongdan;Yu Shengxue;Zuo Zhongfu(Liaoning Province Key Laboratory of Diabetic Cognitive Dysfunction,Jinzhou Medical University;Department of Human Anatomy,Jinzhou Medical University,Jinzhou 121000 China)
机构地区:[1]锦州医科大学辽宁省糖尿病感知功能障碍重点实验室 [2]锦州医科大学人体解剖学教研室,辽宁锦州121000
出 处:《锦州医科大学学报》2022年第2期7-11,共5页Journal of Jinzhou Medical University
基 金:辽宁省自然科学基金项目,项目编号:2019-ZD-0807。
摘 要:目的探讨姜黄素通过HMGB1介导的炎症反应对人HepG2肝癌细胞增殖、迁移和凋亡的影响。方法选择终浓度为0、5、10、20μg/mL的姜黄素处理人HepG2肝癌细胞48 h。通过CCK-8试剂盒检测HepG2肝癌细胞的增殖情况,划痕实验观察HepG2肝癌细胞的迁移能力,Annexin V-FITC/PI双染法通过流式细胞仪分析HepG2肝癌细胞的凋亡率,Western blot检测凋亡和炎症相关蛋白的表达水平。结果姜黄素对HepG2肝癌细胞的增殖抑制作用表现为剂量依赖性,48 h姜黄素的半数抑制浓度(IC_(50))为10μg/mL;HepG2肝癌细胞的迁移能力随姜黄素浓度的增加而明显降低;与对照组(0μg/mL)相比,5μg/mL的姜黄素未能明显诱导HepG2肝癌细胞凋亡(P>0.05),10μg/mL和20μg/mL的姜黄素能显著诱导HepG2肝癌细胞发生凋亡(P<0.05);Western blot结果表明姜黄素上调凋亡相关蛋白Bax/Bcl-2、p53及p-p53(ser315)的表达,下调炎症相关蛋白HMGB1、IL-6、NF-κB、p-NF-κB(ser536)的表达。结论本研究表明,姜黄素能抑制人HepG2肝癌细胞的增殖,促进其凋亡的发生,其机制可能与姜黄素抑制促炎因子HMGB1的表达而降低炎症反应,进而诱导HepG2肝癌细胞的凋亡。Objective To investigate the effects of curcumin on the proliferation,migration and apoptosis of human HepG2 hepatoma cells through HMGB1 mediated inflammatory response.Methods HepG2 cells were treated with differently final concentrations(0,5,10,20μg/mL)of curcumin for 48 hours.Cell Counting Kit-8(CCK-8)assay and Annexin V-FITC/PI double staining method by flow cytometry(FCM)was used to evaluate the effects of curcumin on cell proliferation and apoptosis.Scratch experiment was to investigate the cell migration ability.Western blot analysis was performed to analyze the levels of apoptosis and inflammation associated proteins.Results The inhibitory effect of curcumin on the proliferation of HepG2 hepatoma cells was dose-dependent,and the IC_(50) of curcumin at 48 h was 10μg/mL;the migration ability of HepG2 hepatoma cells decreased with the increase of curcumin concentration;compared with the control group(0μg/mL),5μg/mL curcumin could not induce apoptosis of HepG2 hepatoma cells(P>0.05),10μg/mL and 20μg/mL curcumin could significantly induce apoptosis of HepG2 hepatoma cells(P<0.05);Western blot showed that curcumin up-regulated the expression of apoptosis related proteins Bax/Bcl-2,p53 and p-p53(Ser315),and down-regulated the expression of inflammatory related proteins HMGB1,IL-6,NF-κB and p-NF-κB(Ser536).Conclusion This study showed that curcumin can inhibit the proliferation and promote the apoptosis of human HepG2 hepatoma cells.The mechanism may be that curcumin inhibits the expression of pro-inflammatory factor HMGB1 and reduces the inflammatory response,thus inducing the apoptosis of HepG2 hepatoma cells.
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