摘要
目的探讨清道夫受体A能否抑制LPS刺激RAW 264.7产生炎症因子。方法LPS诱导小鼠巨噬细胞株RAW 264.7 SR-A受体上调后,用LPS再次刺激,观察SR-A受体的上调能否抑制RAW 264.7对LPS的反应,最后采用遗传互补实验观察转染SR-A受体后能否抑制LPS活化NFκ-B。结果LPS刺激SR-A受体已上调的RAW 264.7产生的炎症因子明显下降,而遗传互补实验证实SR-A受体确实能抑制LPS通过TLR4活化NFκ-B。结论SR-A受体参与负调控LPS对RAW 264.7的活化,防止过强的炎症反应。
Objective To investigate the inhibition role of scavenger receptor A on RAW264.7 inflammatory cytokines release induced by LPS. Methods After scavenger receptor A on RAW264.7 was up-regulated by 10, 100 ng/ml, 1 μg/ml LPS for 16 h, some RAW264.7 were used for mean fluorescence intensity by flow cytometry, and some were re-stimulated by 100 ng/ml LPS for 24 h, then the concentration of both TNF-α and IL-6 in culture supernatants were detected by ELISA. Genetic complementary assay was performed to verify the inhibition role of SR-A on NF-κB induced by LPS. Results LPS of 10, 100 ng/ml and 1μg/ml could induce the SR-A expression in RAW264.7, coincident with suppression of inflammatory cytokines after re-stimulation with LPS. Genetic complementary assay showed that SR-A could reduce NF-kB activity induced by LPS for 5- folds. Conclusion SR-A could inhibit inflammatory cytokines release of RAW264.7 elicited by LPS.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2006年第6期512-514,共3页
Journal of Third Military Medical University
基金
国家自然科学基金资助项目(30400437)~~
