Both baicalin (BA) and jasminoidin (JA) are active ingredients in Chinese herb medicine Scutellaria baicalensis and Fructus gardeniae, respectively. They have been shown to exert additive neuroprotective action in ischemic stroke models. In this study we used transcriptome analysis to explore the pure therapeutic mechanisms of BA, JA and their combination (BJ) contributing to phenotype variation and reversal of pathological processes. Mice with middle cerebral artery obstruction were treated with BA, JA, their combination (BJ), or concha margaritifera (CM). Cerebral infarct volume was examined to determine the effect of these compounds on phenotype. Using the hippocampus microarray and ingenuity pathway analysis (IPA) software, we exacted the differentially expressed genes, networks, pathways, and functions in positive-phenotype groups (BA, JA and BJ) by comparing with the negative-phenotype group (CM). In the BA, JA, and BJ groups, a total of 7, 4, and 11 specific target molecules, 1, 1, and 4 networks, 51, 59, and 18 canonical pathways and 70, 53, and 64 biological functions, respectively, were identified. Pure therapeutic mechanisms of BA and JA were mainly overlapped in specific target molecules, functions and pathways, which were related to the nervous system, inflammation and immune response. The specific mechanisms of BA and JA were associated with apoptosis and cancer-related signaling and endocrine and hormone regulation, respectively. In the BJ group, novel target profiles distinct from mono-therapies were revealed, including 11 specific target molecules, 10 functions, and 10 pathways, the majority of which were related to a virus-mediated immune response. The pure additive effects between BA and JA were based on enhanced action in virus-mediated immune response. This pure mechanistic analysis may provide a clearer outline of the target profiles of multi-target compounds and combination therapies.

中文翻译：

---

黄芩苷和茉莉花苷对缺血性中风小鼠的附加神经保护作用的纯机制分析。


黄芩苷（BA）和茉莉花苷（JA）分别是中草药黄芩和栀子的活性成分。它们已被证明在缺血性中风模型中发挥附加的神经保护作用。在本研究中，我们使用转录组分析来探索 BA、JA 及其组合 (BJ) 导致表型变异和病理过程逆转的纯治疗机制。大脑中动脉阻塞的小鼠接受 BA、JA、它们的组合 (BJ) 或 Concha margaritifera (CM) 治疗。检查脑梗塞体积以确定这些化合物对表型的影响。利用海马微阵列和独创性通路分析（IPA）软件，通过与阴性表型组（CM）比较，提取阳性表型组（BA、JA和BJ）中差异表达的基因、网络、通路和功能。在 BA、JA 和 BJ 组中，分别共有 7、4 和 11 个特定靶分子，1、1 和 4 个网络，51、59 和 18 个经典途径，以及 70、53 和 64 个生物功能，被识别出来。 BA和JA的纯治疗机制主要在特定靶分子、功能和通路上有重叠，与神经系统、炎症和免疫反应有关。 BA和JA的具体机制分别与细胞凋亡和癌症相关信号传导以及内分泌和激素调节有关。在 BJ 组中，揭示了与单一疗法不同的新靶点概况，包括 11 个特定靶分子、10 个功能和 10 个途径，其中大部分与病毒介导的免疫反应有关。 BA 和 JA 之间的纯累加效应是基于病毒介导的免疫反应的增强作用。这种纯粹的机制分析可以为多靶点化合物和联合疗法的靶点概况提供更清晰的轮廓。