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黄芩苷通过抑制TLR4介导的NF-κB和MAPK信号通路减轻小鼠脂多糖诱导的乳腺炎中的炎症反应。

Baicalein attenuates inflammatory responses by suppressing TLR4 mediated NF-κB and MAPK signaling pathways in LPS-induced mastitis in mice.

作者信息

He Xuexiu, Wei Zhengkai, Zhou Ershun, Chen Libin, Kou Jinhua, Wang Jingjing, Yang Zhengtao

机构信息

College of Veterinary Medicine, Jilin University, Jilin, Changchun 130062, People's Republic of China.

College of Veterinary Medicine, Jilin University, Jilin, Changchun 130062, People's Republic of China.

出版信息

Int Immunopharmacol. 2015 Sep;28(1):470-6. doi: 10.1016/j.intimp.2015.07.012. Epub 2015 Jul 18.

Abstract

Baicalein is a phenolic flavonoid presented in the dry roots of Scutellaria baicalensis Georgi. It has been reported that baicalein possesses a number of biological properties, such as antiviral, antioxidative, anti-inflammatory, antithrombotic, and anticancer properties. However, the effect of baicalein on mastitis has not yet been reported. This research aims to detect the effect of baicalein on lipopolysaccharide (LPS)-induced mastitis in mice and to investigate the molecular mechanisms. Baicalein was administered intraperitoneally 1h before and 12h after LPS treatment. The results indicated that baicalein treatment markedly attenuated the damage of the mammary gland induced by LPS, suppressed the activity of myeloperoxidase (MPO) and the levels of tumor necrosis factor (TNF-α) and interleukin (IL-1β) in mice with LPS-induced mastitis. Besides, baicalein blocked the expression of Toll-like receptor 4 (TLR4) and then suppressed the phosphorylation of nuclear transcription factor-kappaB (NF-κB) p65 and degradation inhibitor of NF-κBα (IκBα) and, and inhibited the phosphorylation of p38, extracellular signal-regulated kinase (ERK) and c-jun NH2-terminal kinase (JNK) in mitogen-activated protein kinase (MAPK) signal pathway. These findings suggested that baicalein may have a potential prospect against mastitis.

摘要

黄芩苷是一种存在于黄芩干燥根中的酚类黄酮。据报道,黄芩苷具有多种生物学特性,如抗病毒、抗氧化、抗炎、抗血栓形成和抗癌特性。然而,黄芩苷对乳腺炎的影响尚未见报道。本研究旨在检测黄芩苷对脂多糖(LPS)诱导的小鼠乳腺炎的影响,并探讨其分子机制。在LPS处理前1小时和处理后12小时腹腔注射黄芩苷。结果表明,黄芩苷处理显著减轻了LPS诱导的小鼠乳腺损伤,抑制了LPS诱导的乳腺炎小鼠的髓过氧化物酶(MPO)活性、肿瘤坏死因子(TNF-α)和白细胞介素(IL-1β)水平。此外,黄芩苷阻断Toll样受体4(TLR4)的表达,进而抑制核转录因子-κB(NF-κB)p65的磷酸化以及NF-κBα(IκBα)的降解,并抑制丝裂原活化蛋白激酶(MAPK)信号通路中p38、细胞外信号调节激酶(ERK)和c-Jun氨基末端激酶(JNK)的磷酸化。这些发现表明黄芩苷可能对乳腺炎具有潜在的治疗前景。

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