NR4A1介导黄芩苷对人胶质瘤U251细胞的作用机制  

Mechanism of Baicalin on Human Glioma U251 Cells Mediated by NR4A1

作　　者：龚杰 周明华 Gong Jie;Zhou Minghua(Jinzhou Medical University,Jinzhou 121000 China;Hanjiang Normal University,Shiyan 442000 China)

机构地区：[1]锦州医科大学,辽宁锦州121000 [2]汉江师范学院,湖北十堰442000

出　　处：《锦州医科大学学报》2023年第5期26-32,共7页Journal of Jinzhou Medical University

摘　　要：目的 探讨NR4A1介导黄芩苷对人胶质瘤U251细胞增殖与凋亡的作用。方法 采用不同浓度的黄芩苷(50、100、150μM)干预U251细胞24、48、72 h,利用CCK8法检测黄芩苷对U251细胞生长的抑制作用。不同浓度的黄芩苷(50、100、150μM)干预U251细胞24 h,流式细胞术法检测U251细胞的凋亡情况,qRT-PCR法检测NR4A1、PRDX1、BCL2、BAX、KI67和PCNA相关基因的表达情况。选用浓度为150μM黄芩苷和10μmol/L DIM-C-pPhOH(NR4A1拮抗剂)分别干预U251细胞24 h,利用流式细胞术检测U251细胞凋亡情况,qRT-PCR法检测NR4A1、PRDX1、BCL2、BAX、KI67和PCNA相关基因的表达情况。结果 黄芩苷对人胶质瘤U251细胞的增殖具有抑制作用,且呈时间、浓度依赖性(P<0.05)。不同浓度的黄芩苷作用于人胶质瘤U251细胞24 h后,U251细胞凋亡率显著增高(P<0.01);黄芩苷剂量依赖性抑制NR4A1、PRDX1、BCL2、KI67和PCNA的表达,然而剂量依赖性上调BAX的表达。150μM黄芩苷和DIM-C-pPhOH分别抑制NR4A1、PRDX1、BCL2、KI67和PCNA的表达,然而上调BAX的表达(P<0.05)。结论 黄芩苷抑制人胶质瘤U251细胞的生长,并诱导其凋亡。其机制可能是通过抑制NR4A1基因的表达进而抑制PRDX1、BCL2、KI67、PCNA基因和上调BAX基因的表达有关。Objective To investigate the effect of baicalin on proliferation and apoptosis of human glioma U251 cells mediated by NR4A1.Methods Different concentrations of baicalin(50μM,100μM and 150μM)were used to interfere with U251 cells for 24 h,48 h and 72 h,and the inhibitory effect of baicalin on U251 cell growth was detected by CCK8 method.Different concentrations of baicalin(50μM,100μM and 150μM)interfered with U251 cells for 24 h.The apoptosis of U251 cells was detected by flow cytometry,and the expression of NR4A1,PRDX1,BCL2,BAX,KI67 and PCNA related genes were detected by qRT-PCR.Baicalin with concentration of 150μM and 10μMol/L DIM-C-pPhOH(NR4A1 antagonist)were selected to interfere with U251 cells for 24 hours respectively.The apoptosis of U251 cells was detected by flow cytometry,and the expression ofNR4A1,PRDX1,BCL2,BAX,KI67 and PCNA related genes were detected by qRT-PCR.Results Baicalin inhibited the proliferation of human glioma U251 cells in a time-dependent and concentration-dependent manner(P<0.05).The apoptosis rate of human glioma U251 cells was significantly increased(P<0.01)after 24 hours of baicalin treatment with different concentrations;baicalin inhibited the expression of NR4A1,PRDX1,BCL2,KI67 and PCNA in a dose-dependent manner,while the expression of BAX was up-regulated in a dose-dependent manner.150μM mbaicalin and DIM-C-pPhOH inhibited the expression of NR4A1,PRDX1,BCL2,KI67 and PCNA respectively,but up-regulated the expression of BAX(P<0.05).Conclusion Baicalin can inhibit the growth of human glioma U251 cells and induce its apoptosis.The mechanism may be related to the inhibition of PRDX1,BCL2,KI67,PCNA and up-regulation of BAX expression by inhibiting the expression of NR4A1.

关 键 词：黄芩苷 U251细胞 DIM-C-pPhOH NR4A1 

分 类 号：R965.2[医药卫生—药理学]