OBJECTIVE: This study aimed to identify the potential targets and regulatory mechanisms of Leo in alleviating neuronal apoptosis after ICH.
METHODS: The study employed network pharmacology, UPLC-Q-TOF-MS technique, molecular docking, pharmacodynamic studies, western blotting, and immunofluorescence techniques to explore its potential mechanisms.
RESULTS: Leo was found to assist hematoma absorption, thus improving the neurological outlook in an ICH mouse model. Importantly, molecular docking highlighted JAK as Leo\'s potential therapeutic target in ICH scenarios. Further experimental evidence demonstrated that Leo adjusts JAK1 and STAT1 phosphorylation, curbing Bax while augmenting Bcl-2 expression.
CONCLUSIONS: Leo showcases potential in mitigating neuronal apoptosis post-ICH, predominantly via the JAK/STAT mechanism.
目的:本研究旨在确定Leo减轻ICH后神经元凋亡的潜在靶点和调控机制。
方法:本研究采用网络药理学,UPLC-Q-TOF-MS技术,分子对接,药效学研究,西方印迹,和免疫荧光技术探讨其潜在机制。
结果:发现Leo辅助血肿吸收,从而改善ICH小鼠模型的神经前景。重要的是,分子对接强调JAK是ICH场景中Leo的潜在治疗靶点。进一步的实验证据表明,狮子座调节JAK1和STAT1磷酸化,抑制Bax,同时增加Bcl-2表达。
结论:Leo展示了减轻ICH后神经元凋亡的潜力,主要通过JAK/STAT机制。