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程序性细胞死亡5因子过表达增强雷公藤内酯醇诱导的类风湿关节炎成纤维样滑膜细胞凋亡

[Overexpression of programmed cell death 5 factor enhances triptolides-induced fibroblast-like synoviocytes apoptosis in rheumatoid arthritis].

作者信息

Chen Zhan Kun, Wang Ning, Lu Hou Shan

机构信息

Arthritis Research Center, Peking University People's Hospital, Beijing, China.

出版信息

Beijing Da Xue Xue Bao Yi Xue Ban. 2008 Dec 18;40(6):567-71.

Abstract

OBJECTIVE

To explore the effect of programmed cell death 5(PDCD5) on apoptosis of rheumatoid arthritis fibroblast-like synoviocytes(RA FLS) induced by triptolide.

METHODS

Cultured synovial cells in vitro from RA patients were transfected with Ad-PDCD5.At protein level, expression of PDCD5 in RA FLS infected with Ad-PDCD5 was detected by Western blot.RA FLS infected with Ad-PDCD5 were cultured in presence or absence of triptolide and apoptosis of RA FLS was determined by flow cytometry.

RESULTS

Infection of RA FLS with increasing concentrations of Ad-PDCD5(50-300 MOI) resulted in a does-dependent increase in the production of PDCD5. Apoptotic cells percentage for noinfection group, Ad-null group and Ad-PDCD5 group were(22.41 +/- 3.87)%, (28.77 +/- 12.97)% and (48.87 +/- 12.69)%, respectively. Alternatively, infection without addition of triptolide stimuli had no effect. The data showed that gene transfection of PDCD5 alone without addition of triptolide was not sufficient to activate RA FLS apoptosis, PDCD5 acted as an enhancer rather than inductor of apoptosis.

CONCLUSION

Overexpression of PDCD5 could enhance apoptosis of RA FLS induced by triptolide, PDCD5 may be a potential therapeutic target to RA.

摘要

目的

探讨程序性细胞死亡因子5(PDCD5)对雷公藤甲素诱导的类风湿关节炎成纤维样滑膜细胞(RA FLS)凋亡的影响。

方法

用Ad-PDCD5转染体外培养的RA患者滑膜细胞。在蛋白水平,通过蛋白质印迹法检测感染Ad-PDCD5的RA FLS中PDCD5的表达。将感染Ad-PDCD5的RA FLS在有或无雷公藤甲素的情况下培养,通过流式细胞术测定RA FLS的凋亡情况。

结果

用不同浓度(50 - 300 MOI)的Ad-PDCD5感染RA FLS,导致PDCD5的产生呈剂量依赖性增加。未感染组、Ad-空载体组和Ad-PDCD5组的凋亡细胞百分比分别为(22.41±3.87)%、(28.77±12.97)%和(48.87±12.69)%。另外,不添加雷公藤甲素刺激的感染没有影响。数据表明,单独进行PDCD5基因转染而不添加雷公藤甲素不足以激活RA FLS凋亡,PDCD5作为凋亡的增强剂而非诱导剂。

结论

PDCD5过表达可增强雷公藤甲素诱导的RA FLS凋亡,PDCD5可能是RA的一个潜在治疗靶点。

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