脑出血（ICH）可诱发强烈的氧化应激、神经炎症和脑细胞凋亡。然而，传统的脑出血治疗方法有很多缺点。迫切需要副作用最小的替代有效疗法。采用药效学实验、分子对接、网络药理学、代谢组学等方法探讨荆防颗粒（JFG）治疗脑出血的作用及其机制。在这项研究中，我们通过行为、脑含水量和磁共振成像实验研究了 JFG 对 ICH 的治疗效果。然而，JFG 的关键活性成分和目标仍然未知。这里我们验证了JFG对于改善ICH后的脑损伤是有益的。网络药理学分析表明，JFG 的抗炎作用主要是通过木犀草素、( )-Anomalin 和 Phaseol 激活磷脂酰肌醇 3-激酶 (PI3K)/AKT 通路以及靶向 AKT1、肿瘤坏死因子 α 介导的。 TNF-α) 和白介素-1β (IL-1β)。分子对接分析显示平均亲和力为-8.633 kcal/mol，表明结合强度小于-5 kcal/mol。代谢组学分析表明，JFG通过调节牛磺酸和亚牛磺酸的代谢、缬氨酸、亮氨酸和异亮氨酸的生物合成等代谢途径发挥对ICH的治疗作用。总之，我们证明 JFG 通过激活 PI3K/Akt 信号通路减轻 ICH 后的神经炎症和 BBB 损伤。

Intracerebral hemorrhage (ICH) can induce intensive oxidative stress, neuroinflammation, and brain cell apoptosis. However, conventional methods for ICH treatment have many disadvantages. There is an urgent need for alternative, effective therapies with minimal side effects. Pharmacodynamics experiment, molecular docking, network pharmacology, and metabolomics were adopted to investigate the treatment and its mechanism of Jingfang Granules (JFG) in ICH. In this study, we investigated the therapeutic effects of JFG on ICH using behavioral, brain water content and Magnetic resonance imaging experiments. However, the key active component and targets of JFG remain unknown. Here we verified that JFG was beneficial to improve brain injury after ICH. A network pharmacology analysis revealed that the anti-inflammatory effect of JFG is predominantly mediated by its activation of the phosphatidylinositol 3-kinase (PI3K)/AKT pathway through Luteolin, (+)-Anomalin and Phaseol and their targeting of AKT1, tumor necrosis factorα (TNF-α), and interleukin-1β (IL-1β). Molecular docking analyses revealed an average affinity of -8.633 kcal/mol, indicating a binding strength of less than -5 kcal/mol. Metabolomic analysis showed that JFG exerted its therapeutic effect on ICH by regulating metabolic pathways, such as the metabolism of taurine and hypotaurine, biosynthesis of valine, leucine, and isoleucine. In conclusion, we demonstrated that JFG attenuated neuroinflammation and BBB injury subsequent to ICH by activating the PI3K/Akt signaling pathway.