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姜黄素可减轻脂多糖刺激的BV2小胶质细胞中促炎细胞因子的释放。

Curcumin attenuates the release of pro-inflammatory cytokines in lipopolysaccharide-stimulated BV2 microglia.

作者信息

Jin Cheng-Yun, Lee Jae-Dong, Park Cheol, Choi Yung-Hyun, Kim Gi-Young

机构信息

Department of Microbiology, College of Natural Sciences, Pusan National University, Busan 609-735, Korea.

出版信息

Acta Pharmacol Sin. 2007 Oct;28(10):1645-51. doi: 10.1111/j.1745-7254.2007.00651.x.

Abstract

AIM

Pro-inflammatory mediators, such as prostaglandin E2 (PGE2) and nitric oxide (NO), and pro-inflammatory cytokines such as interleukin (IL)-1beta, IL-6, and TNF-alpha, play pivotal roles in brain injuries. The anti-inflammatory properties are known to be associated with significant reductions in pro-inflammatory mediators in brain injuries. In the present study we investigate whether the effects of curcumin on the production of pro-inflammatory mediators in lipopolysaccharide (LPS)-stimulated BV2 microglia.

METHODS

Curcumin were administered and their effects on LPS-induced pro-inflammatory mediators were monitored by Western blotting and RT-PCR.

RESULT

Curcumin significantly inhibited the release of NO, PGE2, and pro-inflammatory cytokines in a dose-dependent manner. Curcumin also attenuated the expressions of inducible NO synthase and cyclooxygenase-2 mRNA and protein levels. Moreover, curcumin suppressed NF-kappaB activation via the translocation of p65 into the nucleus. Our data also indicate that curcumin exerts anti-inflammatory properties by suppressing the transcription of proinflammatory cytokine genes through the NF-kappaB signaling pathway.

CONCLUSION

Anti-inflammatory properties of curcumin may be useful for treating the inflammatory and deleterious effects of microglial activation in response to LPS stimulation.

摘要

目的

促炎介质,如前列腺素E2(PGE2)和一氧化氮(NO),以及促炎细胞因子如白细胞介素(IL)-1β、IL-6和肿瘤坏死因子-α,在脑损伤中起关键作用。已知抗炎特性与脑损伤中促炎介质的显著减少有关。在本研究中,我们调查姜黄素对脂多糖(LPS)刺激的BV2小胶质细胞中促炎介质产生的影响。

方法

给予姜黄素,并通过蛋白质印迹法和逆转录-聚合酶链反应监测其对LPS诱导的促炎介质的影响。

结果

姜黄素以剂量依赖性方式显著抑制NO、PGE2和促炎细胞因子的释放。姜黄素还减弱了诱导型NO合酶和环氧化酶-2 mRNA及蛋白水平的表达。此外,姜黄素通过p65向细胞核的转位抑制核因子-κB(NF-κB)的激活。我们的数据还表明,姜黄素通过NF-κB信号通路抑制促炎细胞因子基因的转录发挥抗炎特性。

结论

姜黄素的抗炎特性可能有助于治疗小胶质细胞对LPS刺激的激活所产生的炎症和有害影响。

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