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【bio-news】肿瘤坏死因子-α、白介素-8和地塞米松
Jee BK, Surendran S, Park KM, Lee WK, Han CW, Kim YY, Patinharayil G, Kim YH, Lee KH.
ne. 2007 Jan 1;32(1):30-5.
http://www.ncbi.nlm.nih.gov/sites/entrez
STUDY DESIGN: Human nucleus pulposus cells from intervertebral disc specimens were cultured to study the effects of tumor necrosis factor (TNF)-alpha and interleukin (IL)-8 on the focal adhesion kinase (FAK) expression by these cells. The effect of co-stimulation with dexamethasone on the FAK expression by nucleus pulposus cells was also studied.
OBJECTIVES: To evaluate the possible role of activated FAK expressed by the human nucleus pulposus cells and its correlation with inflammatory cytokines (TNF-alpha, IL-8) and dexamethasone.
SUMMARY OF BACKGROUND DATA: There have been no reported studies showing the correlation between the activated FAK expression by human nucleus pulposus cells with inflammatory cytokines and dexamethasone.
METHODS: The FAK expression in cultured human nucleus pulposus cells was studied, and Western blot and immunofluorescence analysis were performed to assess its relation to TNF-alpha, IL-8, and dexamethasone.
RESULTS: Treatments of TNF-alpha and IL-8 up-regulated the activated FAK expression. Dexamethasone attenuated the cytokine-induced FAK expression. The effects of inflammatory cytokines on the FAK expression were found to be concentration dependent, with greater correlation shown by IL-8 than TNF-alpha.
CONCLUSION: TNF-alpha and IL-8 stimulation up-regulated the FAK expression of human nucleus pulposus cells, and the coadministration of dexamethasone attenuated it. 本人已认领该文编译，48小时后若未提交译文，请其他战友自由认领。 Role of Tumor Necrosis Factor-[alpha], Interleukin-8, and Dexamethasone in the Focal Adhesion Kinase Expression by Human Nucleus Pulposus Cells.
肿瘤坏死因子-α、白介素-8和地塞米松在人类髓核细胞成簇黏附激酶表达中的作用
Abstract:
摘要:
Study Design. Human nucleus pulposus cells from intervertebral disc specimens were cultured to study the effects of tumor necrosis factor (TNF)-[alpha] and interleukin (IL)-8 on the focal adhesion kinase (FAK) expression by these cells. The effect of co-stimulation with dexamethasone on the FAK expression by nucleus pulposus cells was also studied.
研究设计：从椎间盘样本中提取人类髓核细胞进行培养，以研究肿瘤坏死因子-α (TNF-α)和白介素-8 (IL-8)在细胞成簇黏附激酶表达中的作用。同时还研究了地塞米松对人类髓核细胞成簇黏附激酶表达的共刺激效果。
Objectives. To evaluate the possible role of activated FAK expressed by the human nucleus pulposus cells and its correlation with inflammatory cytokines (TNF-[alpha], IL-8) and dexamethasone.
目标：本研究旨在评估人类髓核细胞中活化的成簇黏附激酶表达的可能作用以及其与炎性因子（TNF-α、IL-8）和地塞米松的关系。
Summary of Background Data. There have been no reported studies showing the correlation between the activated FAK expression by human nucleus pulposus cells with inflammatory cytokines and dexamethasone.
背景数据概要：关于人类髓核细胞表达的活化成簇黏附激酶与炎症因子和地塞米松之间关系的研究至今未见报道。
Methods. The FAK expression in cultured human nucleus pulposus cells was studied, and Western blot and immunofluorescence analysis were performed to assess its relation to TNF-[alpha], IL-8, and dexamethasone.
方法：研究人类髓核细胞中成簇黏附激酶的表达，并用蛋白印迹法和免疫荧光分析测定其与TNF-α、IL-8以及地塞米松的关系。
Results. Treatments of TNF-[alpha] and IL-8 up-regulated the activated FAK expression. Dexamethasone attenuated the cytokine-induced FAK expression. The effects of inflammatory cytokines on the FAK expression were found to be concentration dependent, with greater correlation shown by IL-8 than TNF-[alpha].
结果：TNF-α、IL-8的处理上调了人类髓核细胞中活化成簇黏附激酶的表达，而地塞米松则减弱了细胞因子介导的成簇黏附激酶的表达。炎症因子在成簇黏附激酶表达中的作用具有浓度依赖性，与IL-8的关系相比与TNF-α的关系更为紧密。
Conclusion. TNF-[alpha] and IL-8 stimulation up-regulated the FAK expression of human nucleus pulposus cells, and the coadministration of dexamethasone attenuated it.
结论：TNF-α、IL-8上调了人类髓核细胞中活化成簇黏附激酶的表达，同时使用地塞米松能削弱其作用。 编译：
肿瘤坏死因子-α、白介素-8和地塞米松在人类髓核细胞成簇黏附激酶表达中的作用
摘要:
研究设计：从椎间盘样本中提取人类髓核细胞进行培养，以研究肿瘤坏死因子-α (TNF-α)和白介素-8 (IL-8)在细胞成簇黏附激酶表达中的作用。同时还研究了地塞米松对人类髓核细胞成簇黏附激酶表达的共刺激效果。
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作者:admin@医学,生命科学 2010-11-06 05:11
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