Abstract：
OBJECTIVE: This study investigates the molecular mechanisms through which Panax ginseng and Panax notoginseng saponin (PNS) mitigate neuroinflammatory damage and promote neural repair postischemic stroke, utilizing bioinformatics, and experimental approaches.
BACKGROUND: Cerebral infarction significantly contributes to disability worldwide, with chronic neuroinflammation worsening cognitive impairments and leading to neurodegenerative diseases. Addressing neuroimmune interactions is crucial for slowing disease progression and enhancing patient recovery, highlighting the need for advanced research in neuroimmune regulatory mechanisms and therapeutic strategies.
OBJECTIVE: To elucidate the effects of the traditional Chinese medicine components Panax ginseng and PNS on neuroinflammatory damage following ischemic stroke, focusing on the molecular pathways involved in mitigating inflammation and facilitating neural repair.
METHODS: The study employs single-cell sequencing and transcriptomic analysis to investigate gene expression changes associated with cerebral infarction. Gene set enrichment analysis and weighted gene co-expression network analysis are used to identify key molecular markers and core genes. Furthermore, pharmacological profiling, including functional assays, assesses the impact of Ginsenoside-Rc, a PNS derivative, on microglial cell viability, cytokine production, and reactive oxygen species (ROS) levels.
RESULTS: Our analysis revealed that MAPK14 is a critical mediator in the neuroinflammatory response to ischemic stroke. Ginsenoside-Rc potentially targets and modulates MAPK14 activity to suppress inflammation. Experimental validation showed that Ginsenoside-Rc treatment, combined with MAPK14 silencing, significantly alters MAPK14 expression and mitigates neuroinflammatory damage, evidenced by reduced microglial cell death, inflammatory factor secretion, and ROS production.
CONCLUSIONS: Ginsenoside-Rc\'s modulation of MAPK14 offers a promising therapeutic strategy for reducing neuroinflammation and potentially improving cognitive recovery post-ischemic stroke. This supports the therapeutic application of the traditional Chinese medicine Sanqi in ischemic stroke care, providing a theoretical and experimental foundation for its use.
UNASSIGNED: Future work will focus on extending these findings through clinical trials to evaluate the efficacy and safety of Ginsenoside-Rc in human subjects, aiming to translate these promising preclinical results into practical therapeutic interventions for ischemic stroke recovery.
BACKGROUND: Cerebral infarction significantly contributes to disability worldwide, with chronic neuroinflammation worsening cognitive impairments and leading to neurodegenerative diseases. Addressing neuroimmune interactions is crucial for slowing disease progression and enhancing patient recovery, highlighting the need for advanced research in neuroimmune regulatory mechanisms and therapeutic strategies.
OBJECTIVE: To elucidate the effects of the traditional Chinese medicine components Panax ginseng and PNS on neuroinflammatory damage following ischemic stroke, focusing on the molecular pathways involved in mitigating inflammation and facilitating neural repair.
METHODS: The study employs single-cell sequencing and transcriptomic analysis to investigate gene expression changes associated with cerebral infarction. Gene set enrichment analysis and weighted gene co-expression network analysis are used to identify key molecular markers and core genes. Furthermore, pharmacological profiling, including functional assays, assesses the impact of Ginsenoside-Rc, a PNS derivative, on microglial cell viability, cytokine production, and reactive oxygen species (ROS) levels.
RESULTS: Our analysis revealed that MAPK14 is a critical mediator in the neuroinflammatory response to ischemic stroke. Ginsenoside-Rc potentially targets and modulates MAPK14 activity to suppress inflammation. Experimental validation showed that Ginsenoside-Rc treatment, combined with MAPK14 silencing, significantly alters MAPK14 expression and mitigates neuroinflammatory damage, evidenced by reduced microglial cell death, inflammatory factor secretion, and ROS production.
CONCLUSIONS: Ginsenoside-Rc\'s modulation of MAPK14 offers a promising therapeutic strategy for reducing neuroinflammation and potentially improving cognitive recovery post-ischemic stroke. This supports the therapeutic application of the traditional Chinese medicine Sanqi in ischemic stroke care, providing a theoretical and experimental foundation for its use.
UNASSIGNED: Future work will focus on extending these findings through clinical trials to evaluate the efficacy and safety of Ginsenoside-Rc in human subjects, aiming to translate these promising preclinical results into practical therapeutic interventions for ischemic stroke recovery.
摘要：
目的：本研究探讨了人参和三七总皂苷（PNS）减轻中风后神经炎症损伤和促进神经修复的分子机制。利用生物信息学，和实验方法。
背景：脑梗塞在全球范围内导致残疾，慢性神经炎症加重认知障碍并导致神经退行性疾病。解决神经免疫相互作用对于减缓疾病进展和促进患者康复至关重要。强调需要在神经免疫调节机制和治疗策略方面进行高级研究。
目的：阐明中药成分人参和三七总皂苷对缺血性中风后神经炎症损伤的影响。关注减轻炎症和促进神经修复的分子途径。
方法：本研究采用单细胞测序和转录组分析来研究与脑梗死相关的基因表达变化。基因集富集分析和加权基因共表达网络分析用于识别关键分子标记和核心基因。此外，药理学分析，包括功能测定，评估人参皂苷-Rc的影响，PNS衍生物，关于小胶质细胞活力，细胞因子产生，和活性氧（ROS）水平。
结果：我们的分析显示MAPK14是缺血性卒中的神经炎症反应的关键介质。人参皂苷-Rc可能靶向并调节MAPK14活性以抑制炎症。实验验证表明，人参皂苷-Rc处理，结合MAPK14沉默，显著改变MAPK14表达并减轻神经炎症损伤，小胶质细胞死亡减少，炎症因子分泌，和ROS生产。
结论：人参皂苷-Rc对MAPK14的调节为减少缺血性卒中后神经炎症和潜在改善认知恢复提供了有希望的治疗策略。这支持了中药三七在缺血性中风护理中的治疗应用，为其使用提供了理论和实验基础。
■未来的工作将集中于通过临床试验扩展这些发现，以评估人参皂苷-Rc在人类受试者中的疗效和安全性，旨在将这些有希望的临床前结果转化为缺血性卒中恢复的实际治疗干预措施。
背景：脑梗塞在全球范围内导致残疾，慢性神经炎症加重认知障碍并导致神经退行性疾病。解决神经免疫相互作用对于减缓疾病进展和促进患者康复至关重要。强调需要在神经免疫调节机制和治疗策略方面进行高级研究。
目的：阐明中药成分人参和三七总皂苷对缺血性中风后神经炎症损伤的影响。关注减轻炎症和促进神经修复的分子途径。
方法：本研究采用单细胞测序和转录组分析来研究与脑梗死相关的基因表达变化。基因集富集分析和加权基因共表达网络分析用于识别关键分子标记和核心基因。此外，药理学分析，包括功能测定，评估人参皂苷-Rc的影响，PNS衍生物，关于小胶质细胞活力，细胞因子产生，和活性氧（ROS）水平。
结果：我们的分析显示MAPK14是缺血性卒中的神经炎症反应的关键介质。人参皂苷-Rc可能靶向并调节MAPK14活性以抑制炎症。实验验证表明，人参皂苷-Rc处理，结合MAPK14沉默，显著改变MAPK14表达并减轻神经炎症损伤，小胶质细胞死亡减少，炎症因子分泌，和ROS生产。
结论：人参皂苷-Rc对MAPK14的调节为减少缺血性卒中后神经炎症和潜在改善认知恢复提供了有希望的治疗策略。这支持了中药三七在缺血性中风护理中的治疗应用，为其使用提供了理论和实验基础。
■未来的工作将集中于通过临床试验扩展这些发现，以评估人参皂苷-Rc在人类受试者中的疗效和安全性，旨在将这些有希望的临床前结果转化为缺血性卒中恢复的实际治疗干预措施。
