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黄芩素通过调节巨噬细胞极化和抑制细胞焦亡发挥脂多糖诱导的肺炎症的有益作用。

Baicalein exerts beneficial effects in lipopolysaccharide-induced pulmonary inflammation by modulating macrophage polarization and inhibiting pyroptosis.

机构信息

Children's Hospital, The Second Affiliated Hospital of Shaanxi University of Chinese Medicine, Xianyang, China.

出版信息

Hum Exp Toxicol. 2024 Jan-Dec;43:9603271241249990. doi: 10.1177/09603271241249990.

Abstract

The disruption of the immune system by viral attack is a major influencing factor in the lethality of COVID-19. Baicalein is one of the key effective compounds against COVID-19. The molecular mechanisms regarding the anti-inflammatory properties of Baicalein are still unclear. In this study, we established LPS-induced mice to elucidate the role of Baicalein in the treatment of acute lung injury (ALI) and its potential molecular mechanisms. In vivo experiments showed that Baicalein could significantly ameliorate LPS-induced acute lung injury and reduce proteinous edema in lung tissue. In addition, Baicalein inhibited M1 macrophage polarization, promote M2 macrophage polarization, and regulate inflammatory responses. Furthermore, Baicalein could inhibit the expression of protein molecules associated with pyroptosis and mitigate the lung tissue injury. In summary, we revealed the therapeutic effects of Baicalein in acute lung injury, providing the theoretical basis for its clinical application.

摘要

病毒攻击导致免疫系统紊乱是 COVID-19 致死的一个主要影响因素。黄芩素是抗击 COVID-19 的关键有效化合物之一。关于黄芩素抗炎特性的分子机制尚不清楚。在这项研究中,我们建立了 LPS 诱导的小鼠模型,以阐明黄芩素在治疗急性肺损伤(ALI)及其潜在分子机制中的作用。体内实验表明,黄芩素能显著改善 LPS 诱导的急性肺损伤,减轻肺组织中的蛋白性水肿。此外,黄芩素抑制 M1 巨噬细胞极化,促进 M2 巨噬细胞极化,并调节炎症反应。此外,黄芩素可以抑制与细胞焦亡相关的蛋白分子的表达,减轻肺组织损伤。综上所述,我们揭示了黄芩素在急性肺损伤中的治疗作用,为其临床应用提供了理论依据。

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