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伊里斯基因C通过调节mPGES-1表达和p38/JNK通路来抑制LPS诱导的巨细胞激活

Xin Guo¹, Yun-Da Yao², Jun-Li Kang²

¹Guangdong Provincial Hospital of Chinese Medicine, Guangdong Provincial Academy of Chinese Medical Sciences, State Key Laboratory of Dampness Syndrome of Chinese Medicine, Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangdong-Hong Kong-Macau Joint Lab on Chinese Medicine and Immune Disease Research, Guangzhou, Guangdong Province, PR China; Faculty of Chinese Medicine and State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Avenida Wailong, Taipa, Macao.

Journal of ethnopharmacology

|June 10, 2023

概括

从虹膜膜中分离出来的虹膜造蛋白C (IT24) 通过抑制微体前列腺素合成酶-1 (mPGES-1) 和p38/JNK通路,表现出抗炎作用. 这种天然化合物为治疗炎症性疾病提供了一个有希望的替代方案.

科学领域:

药理学药理学是指药理学的学科.
自然产品化学化学
免疫学免疫学免疫学

背景情况:

非类固醇抗炎药物 (NSAIDs) 广泛用于炎症状况,但有不良影响.
虹膜直径最大. 虹膜直径最大. 是一种传统的草药,对炎症和肝脏疾病具有治疗潜力.
识别来自自然来源的新型抗炎药物,如I. tectorum,对于减轻NSAID相关副作用至关重要.

研究的目的:

从Iris tectorum中分离和识别生物活性化合物.
评估隔离化合物的抗炎性质.
阐明这些化合物的抗炎作用背后的分子机制.

主要方法:

使用色谱技术 (凝,Sephadex LH-20,ODS,HPLC) 隔离化合物,并通过光谱方法 (UV,IR,MS,NMR) 进行表征.
在脂聚糖 (LPS) 刺激的RAW264.7细胞和大鼠原发性巨细胞中评估了抗炎活性.
研究的机制包括氧化 (NO),前列腺素E2 (PGE2),细胞因子水平,关键炎症媒介的蛋白质/mRNA表达 (COX,mPGES-1,NF-κB,MAPK通路) 和分子对接.

主要成果:

基因素C (IT24) 显著降低了NO和PGE2水平,但没有影响COX-1/COX-2表达.
在LPS诱导的巨细胞中,IT24降低了微体前列腺素合成酶-1 (mPGES-1) 的表达.
IT24抑制了p38/JNK酸化,但没有影响NF-κB通路;分子对接表明直接结合mPGES-1.

结论:

通过抑制mPGES-1和p38/JNK通路,IT24具有抗炎作用.
IT24显示出作为炎症疾病的治疗剂和mPGES-1抑制剂的潜力.
对IT24用于治疗mPGES-1相关疾病的进一步研究和药物开发是有必要的.

关键词:

炎症炎症是一种炎症.虹膜的构造体是虹膜的构造体.它们的分子基因C.通过MAPK路径.在mPGES-1中使用.

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