古古斯特通过血氧酶-1保护免受脂多糖诱导的炎症和致命的内毒性
Bitna Kweon1, Dong-Uk Kim1, Jin-Young Oh1
1Department of Pharmacology, School of Korean Medicine, Wonkwang University, Iksan, 54538 Jeonbuk, South Korea; Hanbang Cardio-Renal Syndrome Research Center, Wonkwang University, Iksan, 54538 Jeonbuk, South Korea.
International immunopharmacology
|October 16, 2023
概括
古古斯特 (GS) 通过通过活性氧物种 (ROS) 和Nrf2激活诱导血氧酶-1 (HO-1) 来减少炎症. 这种植物在治疗炎症性疾病和内毒素症方面表现有前途.
科学领域:
- 药理学 药理学是指药理学的学科.
- 免疫学 免疫学 免疫学
- 生物化学 生物化学
背景情况:
- 古古斯特 (GS) 是一种具有已知的抗炎性质的植物.
- 基因糖对脂聚糖 (LPS) 诱导的炎症和内毒素的作用的确切机制尚不完全理解.
研究的目的:
- 为了阐明GS在LPS诱导的炎症中的抗炎机制.
- 调查血氧酶-1 (HO-1) 在GS介导的抗炎作用中的作用.
主要方法:
- 用小鼠腹巨细胞来研究GS对炎症介质的影响.
- 分析了GS诱导的HO-1表达与谷氨 (GSH) 枯竭,活性氧物种 (ROS) 生产和Nrf2转位有关.
- 在体内研究中使用了内毒性病的小鼠模型来评估GS对生存和炎症标志物的影响.
- 关键的炎症标志物包括INOS,COX-2,PGE2,IL-1β,IL-6和TNF-α被量化.
主要成果:
- GS抗炎活性主要由HO-1诱导介导,依赖于GSH耗尽和ROS生成.
- GS治疗导致GSK3β和p38的ROS依赖酸化,促进了Nrf2核转位和随后的HO-1诱导.
- GS显著抑制了iNOS,COX-2,PGE2,IL-1β,IL-6和TNF-α的表达和产生.
- 在体内,GS在内毒性小鼠中延长了生存时间,减少了肝损伤,并抑制了关键的炎症性细胞因子.
结论:
- GS通过一种ROS依赖的途径诱导HO-1,包括GSK3β/p38酸化和Nrf2激活,从而产生抗炎作用.
- 通过调节关键炎症通路,GS显示出对包括内毒素症在内的炎症状况的治疗潜力.
关键词:
末端毒性病 (Endotoxemia) 是一种导致内毒性病的疾病.在Guggulsterone中使用.血红蛋白氧化酶-1 (HO-1) 是一种脂聚糖类糖化物 脂聚糖类糖化物反应性氧物种 (ROS) 是一种反应性氧物种.更多相关视频
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