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Anti-inflammatory effects of TP1 in LPS-induced Raw264.7 macrophages
Applied Biological Chemistry ( IF 3.2 ) Pub Date : 2024-02-15 , DOI: 10.1186/s13765-024-00873-y
Minji Kim , Jangeun An , Seong-Ah Shin , Sun Young Moon , Moonsu Kim , Seyeon Choi , Huiji Kim , Kim-Hoa Phi , Jun Hyuck Lee , Ui Joung Youn , Hyun Ho Park , Chang Sup Lee

Inflammation is an essential defense mechanism in health; however, excessive inflammation contributes to the pathophysiology of several chronic diseases. Although anti-inflammatory drugs are essential for controlling inflammation, they have several side effects. Recent findings suggest that naturally derived compounds possess physiological activities, including anti-inflammatory, antifungal, antiviral, anticancer, and immunomodulatory activities. Therefore, this study aimed to investigate the anti-inflammatory effects and molecular mechanisms of 2,5,6-trimethoxy-p-terphenyl (TP1), extracted from the Antarctic lichen Stereocaulon alpinum, using in vitro models. TP1 treatment decreased the production of nitric oxide (NO) and reactive oxygen species (ROS) in LPS-stimulated Raw264.7 macrophages. Additionally, TP1 treatment significantly decreased the mRNA levels of pro-inflammatory cytokines (IL-1β, TNF-α, IL-6) and the mRNA and protein levels of the pro-inflammatory enzymes (inducible nitric oxide synthase and cyclooxygenase-2). Moreover, TP1 suppressed lipopolysaccharide-induced phosphorylation of the NF-κB and MAPK signaling pathways in Raw264.7 macrophages. Conclusively, these results suggest that TP1 ameliorates inflammation by suppressing the expression of pro-inflammatory cytokines, making it a potential anti-inflammatory drug for the treatment of severe inflammatory diseases.

中文翻译:

TP1 在 LPS 诱导的 Raw264.7 巨噬细胞中的抗炎作用

炎症是健康的重要防御机制;然而,过度炎症会导致多种慢性疾病的病理生理学。尽管抗炎药物对于控制炎症至关重要,但它们也有一些副作用。最近的研究结果表明,天然衍生的化合物具有生理活性,包括抗炎、抗真菌、抗病毒、抗癌和免疫调节活性。因此,本研究旨在利用体外模型研究从南极地衣 Stereocaulon alpinum 中提取的 2,5,6-三甲氧基对三联苯 (TP1) 的抗炎作用和分子机制。 TP1 处理降低了 LPS 刺激的 Raw264.7 巨噬细胞中一氧化氮 (NO) 和活性氧 (ROS) 的产生。此外,TP1 治疗显着降低促炎细胞因子(IL-1β、TNF-α、IL-6)的 mRNA 水平以及促炎酶(诱导型一氧化氮合酶和环氧合酶-2)的 mRNA 和蛋白质水平。此外,TP1 抑制 Raw264.7 巨噬细胞中脂多糖诱导的 NF-κB 和 MAPK 信号通路的磷酸化。总之,这些结果表明TP1通过抑制促炎细胞因子的表达来改善炎症,使其成为治疗严重炎症性疾病的潜在抗炎药物。
更新日期:2024-02-15
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