根据网络药理学分析,kaempferol和ginsenoside Rg1可以改善急性低氧诱导的肺损伤
Na Li1, Yuan Cheng2, Tao Jin1
1School of Materials Science and Engineering, Southwest Jiaotong University, Chengdu, China.
Toxicology and applied pharmacology
|November 3, 2023
概括
凯姆菲罗尔和人参化物Rg1在治疗高海拔肺瘤方面表现有前途. 这些化合物减少肺炎和氧化应激,为低氧引起的肺损伤提供了潜在的治疗策略.
科学领域:
- 药理学和毒理学 药理学和毒理学
- 高度医学 高度医学
- 自然产品化学 自然产品化学
背景情况:
- 高海拔肺 (HAPE) 是一种危及生命的疾病,由急性低性缺氧引起.
- 抗炎和抗氧化疗法是减轻低氧引起的肺损伤的潜在策略.
- 来自人参的凯费醇 (KA) 和人参酶Rg1 (GRg1) 具有已知的抗炎和抗氧化特性,但它们对肺部损伤的具体影响尚不清楚.
研究的目的:
- 调查凯姆菲罗尔 (KA) 和人参化物Rg1 (GRg1) 治疗效果和潜在的药理机制,用于治疗急性低氧引起的肺损伤.
- 确定关键的分子标和信号通路,参与KA和GRg1的保护作用.
主要方法:
- 网络药理学分析被用来预测与低氧引起的肺损伤相关的KA和GRg1的潜在标.
- 使用大鼠肺组织进行动物实验,以验证预测的目标和治疗效果.
- 进行了组织病理学检查,测量了炎症性细胞因子 (IL-6,TNF-α),氧化应激标志物 (MDA,SOD,CAT) 和蛋白质/mRNA水平 (PI3K,AKT1).
主要成果:
- 网络药理学确定了AKT1,PIK3R1,PTK2,STAT3,HSP90AA1和AKT2作为关键目标,PI3K-AKT信号通路是最重要的.
- 治疗KA和GRg1显著改善了肺部组织病理学,并减少了暴露于急性低氧的老鼠的肺.
- 用KA和GRg1治疗导致炎症性细胞因子,氧化应激标志物的改善,并抑制PI3K和AKT1表达.
结论:
- 凯姆菲罗尔和人参化物Rg1在老鼠中显示出显著的保护作用,防止急性低氧诱导的肺损伤.
- 这些化合物有效地降低了肺部的水含量,改善了组织损伤,降低了促炎性细胞因子的产生,并减轻了氧化应激.
- PI3K-AKT信号通路是低氧引起的肺损伤中KA和GRg1的保护机制的关键调解者.
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