Li Ruonan, Hong Pan, Zheng Xin
College of Animal Science and Technology, Jilin Agricultural University, Changchun, China.
Anim Sci J. 2019 Jan;90(1):140-148. doi: 10.1111/asj.13108. Epub 2018 Nov 20.
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.
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。