摘要
目的探讨PPARγ激动剂15d-PGJ2对甲状腺刺激抗体(TSAb)作用下人甲状腺细胞存活和凋亡的影响。方法应用原代培养人甲状腺细胞为研究对象,用TSAb刺激细胞24 h,不同浓度15d-PGJ2(0～40μmol/L)干预0～48 h后,MTT法测定细胞存活率;干预24 h后观察细胞凋亡形态、流式细胞技术测定细胞凋亡率。结果 15d-PGJ2呈浓度和时间依赖性抑制TSAb作用下甲状腺细胞的存活(P<0.05);5～40μmol/L15d-PGJ2对TSAb作用下甲状腺细胞有促进凋亡作用(P<0.05),并呈剂量依赖关系;10μmol/L PPARγ拮抗剂GW9662能拮抗20μmol/L15d-PGJ2对TSAb作用下甲状腺细胞的凋亡作用(P<0.05)。结论 15d-PGJ2能够引起TSAb作用下甲状腺细胞凋亡,这一效应可能主要通过PPARγ途径起作用。
Purpose To investigate the effects of peroxisome proliferator-activated receptor-γagonist 15-Deoxy-△12,14-Prostaglandin J2（15d-PGJ2） on the survival and apoptosis of thyrocytes stimulated by TSAb.Methods Making primary cultured human thyrocytes for research object.After exprosure of TSAb for 24 h,detecting effects of 15d-PGJ2 on different concentrations（0,5,10,20,40 μmol/L） and at different action time（0,12,24,48 h） on survival of thyrocytes by MMT analysis,and detecting the apoptosis rate of thyrocytes by Hochest-PI staining and flow cytometry at 24 h action time.Results 15d-PGJ2 can inhibit the survival of thyrocytes,which was dose and time-dependent in a range（P〈0.05）.5-40 μmol/L 15d-PGJ2 can promote the apoptosis of thyrocytes stimulated by TSAb in dose-dependent（P〈0.05）.The apoptosis motivated by 20 μmol/L 15d-PGJ2 could be partly reversed by 10 μmol/L PPARγ antagonist GW9662（P〈0.05）.Conclusion 15d-PGJ2 could induce the apoptosis of thyrocytes stimulated by TSAb,which was dose-dependent in a range.The effects may be mainly generated through PPARγ pathway.
出处
《中国生化药物杂志》
CAS
CSCD
北大核心
2010年第6期398-402,共5页
Chinese Journal of Biochemical Pharmaceutics
基金
福建省卫生厅青年科研基金(2006-1-15)
