黄芩苷通过PI3K-Akt-mTOR通路诱导淋巴瘤细胞凋亡和自噬  

Baicalin induces apoptosis and autophagy in lymphoma cells via PI3K-Akt-mTOR pathway

作　　者：雷晓红[1] 高树丽 岳云霄[3] 史存真 LEI Xiaohong;GAO Shuli;YUE Yunxiao;SHI Cunzhen(Department of Pharmacy,the First People’s Hospital of Pingdingshan,Pingdingshan 467000,China;Clinical Pharmacy Department,the First People’s Hospital of Pingdingshan,Pingdingshan 467000,China;Department of Oncology,the First Affiliated Hospital of Zhengzhou University,Zhengzhou 450000,China)

机构地区：[1]平顶山市第一人民医院药学部,平顶山467000 [2]平顶山市第一人民医院药学部药剂科,平顶山467000 [3]平顶山市第一人民医院药学部临床药学室,平顶山467000 [4]郑州大学第一附属医院肿瘤科,郑州450000

出　　处：《西北药学杂志》2022年第4期70-75,共6页Northwest Pharmaceutical Journal

基　　金：河南省科技攻关项目(编号:LHGJ20190010)。

摘　　要：目的基于PI3K-Akt-mTOR通路探究黄芩苷(C_(21)H_(18)O_(11))对淋巴瘤细胞增殖及自噬的作用机制。方法用CCK-8和细胞计数法检测不同质量浓度(0、50、100、200、400、800μg·mL^(-1))黄芩苷对淋巴瘤细胞系Raji细胞增殖的抑制作用,通过Annexin V-FITC/PI双染法及DAPI染色法观察细胞凋亡及自噬过程,用蛋白印迹实验检测黄芩苷对细胞凋亡和自噬过程上游机制的影响。结果黄芩苷能够显著抑制磷脂酰肌醇3-激酶(phosphatidyl inositol3-kinase,PI3K)、蛋白激酶B(alkaline protein kinases,Akt)、雷帕霉素靶蛋白(mammal target of rapamycin,mTOR)蛋白的磷酸化,即显著降低p-PI3K、p-Akt和p-mTOR的表达水平(P<0.01);黄芩苷能显著上调LC3-Ⅰ和LC3-Ⅱ蛋白的表达水平,抑制p62蛋白的表达(P<0.01),进而诱导Raji细胞的凋亡和自噬。结论黄芩苷可能通过抑制PI3K-Akt-mTOR信号通路抑制淋巴瘤细胞的生长,并通过提高LC3-Ⅰ和LC3-Ⅱ蛋白的表达水平从而抑制p62的表达,进而促进Raji细胞的凋亡和自噬过程。Objective To explore the mechanism of baicalin(C_(21)H_(18)O_(11))in the proliferation and autophagy of lymphatic carcinoma cells by PI3 K-Akt-mTOR pathway.Methods The inhibitory effect of baicalin(0,50,100,200,400,800μg·mL^(-1))on the proliferation of lymphoma cell line Raji was observed with CCK-8 and cell counting methods.Annexin V-FITC/PI double staining and DAPI staining were used to observe the process of apoptosis and autophagy.The effect of baicalin on the upstream mechanism of apoptosis and autophagy was detected by Western blot.Results Baicalin can significantly inhibit the growth and proliferation of Raji cell line,promote the apoptosis and autophagy of Raji cells,and significantly inhibit the phosphorylation of PI3K,Akt and mTOR,i.e.,significantly reduce the expression of p-pi3k,p-Akt and p-mTOR(P<0.01).Further experiments showed that baicalin couldsignificantly up regulate the expression of LC3-Ⅰand LC3-Ⅱprotein,inhibit the expression of p62 protein(P<0.01),and then induce the apoptosis and autophagy of Raji cells.Conclusion Baicalin may inhibit the growth of lymphoma cells by inhibiting PI3K-Akt-mTOR signaling pathway,and inhibit the expression of p62 by increasing the protein expression of LC3-Ⅰand LC3-Ⅱ,so as to promote the apoptosis and autophagy of Raji cells.

关 键 词：黄芩苷 淋巴瘤 PI3K-Akt-mTOR信号通路 

分 类 号：R965[医药卫生—药理学]