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β-胡萝卜素通过抑制巨噬细胞中的NF-κB、JAK2/STAT3和JNK/p38 MAPK信号通路减轻脂多糖诱导的炎症。

β-carotene attenuates lipopolysaccharide-induced inflammation via inhibition of the NF-κB, JAK2/STAT3 and JNK/p38 MAPK signaling pathways in macrophages.

作者信息

Li Ruonan, Hong Pan, Zheng Xin

机构信息

College of Animal Science and Technology, Jilin Agricultural University, Changchun, China.

出版信息

Anim Sci J. 2019 Jan;90(1):140-148. doi: 10.1111/asj.13108. Epub 2018 Nov 20.

Abstract

β-carotene is one of the most abundant carotenoids, has potential anti-inflammatory effect, it has been reported that β-carotene could suppress LPS-induced inflammatory responses by inhibiting nuclear factor kappa B (NF-κB) translocation, but the more detailed molecular mechanisms underlying the anti-inflammatory action of β-carotene remain to be fully understood. In this study, we investigated the influence of β-carotene on the activation of JAK2/STAT3, MAPK, and NF-κB signaling pathway induced by LPS in RAW264.7 cells and peritoneal macrophages. Cells were treated with different concentrations of β-carotene for 3 hr after LPS treatment for 24 hr. The mRNA expression and the release of IL-1β, IL-6, and TNF-α were evaluated by RT-PCR and ELISA, and the level of signaling proteins of JAK2/STAT3, MAPK, and NF-κB signaling pathway were detected by Western blot. The results showed that β-carotene significantly suppressed (p < 0.05) LPS-induced release of IL-1β, IL-6, and TNF-α and their mRNA expression. LPS-induced JAK2/STAT3, IκB/NF-κB p65, JNK/p38 MAPK signal activation were significantly attenuated (p < 0.05) by β-carotene in a dose-dependent manner. In conclusion, β-carotene could attenuate LPS-induced inflammation via inhibition of the NF-κB, JAK2/STAT3, and JNK/p38 MAPK signaling pathways in macrophages.

摘要

β-胡萝卜素是最丰富的类胡萝卜素之一,具有潜在的抗炎作用。据报道,β-胡萝卜素可通过抑制核因子κB(NF-κB)易位来抑制脂多糖(LPS)诱导的炎症反应,但β-胡萝卜素抗炎作用的更详细分子机制仍有待充分了解。在本研究中,我们研究了β-胡萝卜素对LPS诱导的RAW264.7细胞和腹腔巨噬细胞中JAK2/STAT3、丝裂原活化蛋白激酶(MAPK)和NF-κB信号通路激活的影响。在LPS处理24小时后,用不同浓度的β-胡萝卜素处理细胞3小时。通过逆转录聚合酶链反应(RT-PCR)和酶联免疫吸附测定(ELISA)评估白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)的mRNA表达和释放,并通过蛋白质免疫印迹法检测JAK2/STAT3、MAPK和NF-κB信号通路的信号蛋白水平。结果表明,β-胡萝卜素显著抑制(p<0.05)LPS诱导的IL-1β、IL-6和TNF-α释放及其mRNA表达。β-胡萝卜素以剂量依赖性方式显著减弱(p<0.05)LPS诱导的JAK2/STAT3、IκB/NF-κB p65、c-Jun氨基末端激酶(JNK)/p38 MAPK信号激活。总之,β-胡萝卜素可通过抑制巨噬细胞中的NF-κB、JAK2/STAT3和JNK/p38 MAPK信号通路来减轻LPS诱导的炎症。

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