核因子-κB调控老年大鼠脾淋巴细胞凋亡及淫羊藿总黄酮对其影响  

Regulatory function of nuclear factor-kappa B on spleen lymphocyte apoptosis in aged rats and effect of epimedium total flavonoids

作　　者：夏世金[1] 沈自尹[1] 刘小雨[2] 黄建华[1] 吴斌[1] 

机构地区：[1]复旦大学附属华山医院中西医结合研究所,上海200040 [2]同济大学附属第十人民医院中医科

出　　处：《中国老年学杂志》2008年第2期105-108,共4页Chinese Journal of Gerontology

基　　金：国家重点基础研究发展计划(973计划)(No2007CB507406);中国博士后科学基金(20060400578)

摘　　要：目的探讨核因子-κB(nuclear factor-kappa B,NF-кB)对老年大鼠脾淋巴细胞凋亡的调控作用及淫羊藿总黄酮(epimedium totalflavonoids,EF)对老年大鼠脾淋巴细胞凋亡的调控作用是否通过NF-κB实现。方法分别给予老年大鼠模型NF-κB抑制剂二硫代氨基甲酸吡咯烷(PDTC)和EF干预,提取大鼠脾淋巴细胞,用流式细胞仪检测细胞凋亡,Western blot检测P65蛋白表达,电泳迁移率(electrophoretic mobility shift assay,EMSA)检测NF-κB的活性。结果老年大鼠脾淋巴细胞凋亡率比青年大鼠高(P<0.01),PDTC使老年大鼠的凋亡率更高,而EF使老年大鼠的凋亡率降低,与老年组相比有显着性差异(P<0.05),且EF能拮抗PDTC诱导老年大鼠脾淋巴细胞凋亡。与青年大鼠相比老年大鼠脾淋巴细胞P65蛋白表达显著下调(P<0.01),而使用EF的老年大鼠组P65蛋白表达明显上调,表明EF诱导P65高表达。老年大鼠脾淋巴细胞NF-κB的活性弱于青年大鼠(P<0.01),而PDTC处理组的NF-κB活性最低与老年大鼠组相比差异明显(P<0.01),EF干预组的NF-κB的活性最强,与老年大鼠组相比差异非常显著(P<0.01)。相关分析表明,淋巴细胞NF-κB活性与细胞凋亡率呈负相关(r=-0.57,P<0.01)。结论NF-κB通过抑制淋巴细胞凋亡而参与老年大鼠免疫衰老调控过程;EF可能通过提高NF-κB的活性和诱导P65高表达来抑制淋巴细胞凋亡从而延缓免疫衰老进程。Objective To explore the regulatory effect of nuclear factor-kappa B （NF-κB） on spleen lymphocyte apoptosis in aged rats and whether the regulatory effect of epimedium total flavonoids （EF） on lymphocyte apoptosis is conducted through NF-κB. Methods Intervention with PDTC, a NF-κB inhibitor, and EF were given to aged rats respectively. Lymphocytes isolated from rat spleens were detected by flow cytometry, NF-κB p65 protein expression in spleen lymphocytes was measured by Western blot, and NF-κB activity in spleen lymphocytes was detected by electrophoretic mobility shift assay （EMSA）. Results The ratio of spleen lymphocyte apoptosis in aged rats was significantly higher than that in young group （ P 〈 0. 01 ）. The ratio of spleen lymphocyte apoptosis of the aged group was much lower than that of PDTC-treated group （P 〈 0. 05）, and much higher than that of EF-treated group （P 〈 0. 05）. EF inhibited the spleen lymphocyte apoptosis induced by PDTC. P65 protein expression of the aged group was much lower than that of either the young group （P 〈 0. 01 ） or EFtreated group （ P 〈 0. 05 ） , indicating higher expression of p65 induced by EF. NF-κB activity in spleen lymphocytes in aged group was significantly lower than that in young group （P 〈 0. 01 ）. NF-κB activity of EF-treated group increased significantly （P 〈 0. 01 ）, that of PDTC- treated group decreased significantly （P 〈 0. 01 ） compared with that of the aged rats. NF-κB activity showed an obviously negative correlation with apoptosis ratio（ r =-0.57, P 〈 0. 01 ）. Conclusions NF-κB participates the immunoseneseenee by positive regulation on apoptosis of lymphocytes. EF may delay immunosenescence by the way of increasing NF-κB activity and inducing p65 overexpression.

关 键 词：核因子-ΚB 淋巴细胞 凋亡 淫羊藿总黄酮 免疫衰老 

分 类 号：R339.34[医药卫生—人体生理学]