芍药苷通过调节Caspase3活性及核因子?B信号通路诱导HepG2肝癌细胞凋亡  

Paeoniflorin induces HepG2 cell apoptosis by regulating Caspase3 activation and nuclear factor kappa B signaling pathway

作　　者：白春阳[1] 王红雷[2] 

机构地区：[1]南阳市第二人民医院医务部,河南省南阳市473012 [2]南阳市第二人民医院肝胆外科,河南省南阳市473012

出　　处：《世界华人消化杂志》2015年第22期3582-3586,共5页World Chinese Journal of Digestology

摘　　要：目的:探讨芍药苷(paeoniflorin)对Hep G2肝癌细胞凋亡诱导作用,并考察其作用机制.方法:用不同浓度芍药苷(0.5、1.0、2.0 mg/mL)对Hep G2肝癌细胞进行给药,MTT法检测细胞活力,Annexin V-FITC流式细胞法检测细胞凋亡情况,酶标法检测Caspase3活性,Western blot检测核因子?B(nuclear factor kappa-B,NF-?B)信号通路相关蛋白表达.结果:与对照组比较,0.5、1.0、2.0 mg/m L芍药苷能逐渐降低Hep G2肝癌细胞活力,且在48 h,抑制率最高(P<0.05);与对照组比较,0.5、1.0、2.0 mg/m L芍药苷能逐渐促进Hep G2肝癌细胞凋亡并提高Caspase3活性(P<0.05),还能显著抑制I?B?磷酸化,从而促进细胞凋亡;并且1.0、2.0 mg/m L芍药苷能抑制细胞核内NF-?B p65磷酸化(P<0.05).结论:PF可能通过激活Caspase3活性以及抑制NF-?B p65和p I?B?表达促进Hep G2细胞凋亡.AIM：To explore the effect of paeoniflorin on apoptosis of HepG2 cells and the underlying mechanisms.METHODS：HepG2 cells were treated with different concentrations of paeoniflorin（0.5,1.0,and 2.0 mg/mL）.The viability of cells was detected by MTT assay.Apoptotic cells were detected by Annexin V-FITC flow cytometry.Caspase3 activity was measured with a colorimetric assay kit.The expression of nuclear factor kappa-B（NF-kB） related proteins was detected by Western blot.RESULTS：Compared with the control group,paeoniflorin at concentrations of 0.5,1.0,and2.0 mg/mL could reduce cell viability,and the inhibitory rate peaked at 48 h（P 〈 0.05）.Compared with the control group,paeoniflorin at concentrations of 0.5,1.0,and 2.0 mg/mL could promote cell apoptosis,increase Caspase3 activity,and suppress NF-kB p65phosphorylation（P 〈 0.05）.Paeoniflorin at concentrations of 1.0 and 2.0 mg/mL could suppress IkBα phosphorylation（P 〈 0.05）.CONCLUSION：Paeoniflorin induces apoptosis of HepG2 cells possibly via the NF-kB signal pathway.

关 键 词：芍药苷 HEPG2肝癌细胞 凋亡 核因子kB信号通路 磷酸化 

分 类 号：R285[医药卫生—中药学]