- 期刊Histology and histopathology（Histol Histopathol）
- 发表时间2026-10-19
- 作者Zhu T, Fu W, Bai Y, Wei R, Huang J, Zeng G
- 卷期页码25156
- DOI10.14670/HH-25-156
- PMID42894930
摘要机译
【背景与目的】脊髓损伤（SCI）是一种毁灭性的神经系统疾病，以不可逆的运动和感觉功能障碍为特征，主要受氧化应激、炎症和凋亡等继发性损伤机制驱动。中药山楂叶总黄酮（TFHL）具有抗氧化和抗炎特性；
[方法]采用网络药理学方法，通过靶点预测、蛋白-蛋白相互作用分析、GO和KEGG富集分析，确定TFHL在SCI中的活性成分、潜在靶点和关键信号通路。使用大鼠SCI模型、LPS刺激的BV-2小胶质细胞和RAW264.7巨噬细胞进行实验验证。
通过BBB评分评估功能恢复，同时使用H&E染色、透射电镜、RT-qPCR和Western blotting评估组织病理学变化、超微结构改变、炎性细胞因子表达和MAPK通路激活。
[结果]网络药理学分析鉴定出15个活性化合物和69个重叠治疗靶点，主要富集于与炎症、氧化应激、凋亡和神经元存活相关的通路，包括MAPK、PI3K-Akt、TNF和NF-kB信号通路。
在体内，TFHL治疗显著改善了脊髓损伤后的运动恢复，减轻了组织学损伤，保留了线粒体结构，并降低了前炎症细胞因子的表达。在体外，TFHL显著抑制LPS诱导的小胶质细胞MAPK通路的激活。[结论]TFHL改善了SCI模型的功能和组织病理学结果，并减轻了炎症激活。
这些影响与网络药理学预测的多通路调节一致，并且至少部分支持MAPK通路抑制，需要进一步的机制和翻译研究。
展开英文摘要原文
【BACKGROUND AND OBJECTIVE】Spinal cord injury (SCI) is a devastating neurological disorder characterized by irreversible motor and sensory dysfunction, largely driven by secondary injury mechanisms including oxidative stress, inflammation, and apoptosis. Total flavonoids of hawthorn leaves (TFHL), a traditional Chinese medicine, have demonstrated antioxidant and anti-inflammatory properties; however, their therapeutic effects and mechanisms in SCI remain unclear.
【METHODS】Network pharmacology was employed to identify the active compounds, potential targets, and key signaling pathways of TFHL in SCI through target prediction, protein-protein interaction analysis, and GO and KEGG enrichment analyses. Experimental validation was performed using a rat SCI model, LPS-stimulated BV-2 microglial cells, and RAW264.7 macrophages. Functional recovery was assessed by BBB scoring, while histopathological changes, ultrastructural alterations, inflammatory cytokine expression, and MAPK pathway activation were evaluated using H&E staining, transmission electron microscopy, RT-qPCR, and western blotting.
【RESULTS】Network pharmacology analysis identified 15 active compounds and 69 overlapping therapeutic targets, mainly enriched in pathways related to inflammation, oxidative stress, apoptosis, and neuronal survival, including MAPK, PI3K-Akt, TNF, and NF-kB signaling pathways. In vivo, TFHL treatment significantly improved locomotor recovery, alleviated histological damage, preserved mitochondrial structure, and reduced the expression of pro-inflammatory cytokines following SCI. In vitro, TFHL markedly suppressed LPS-induced activation of the MAPK pathway in microglial cells.
【CONCLUSION】TFHL improves functional and histopathological outcomes in SCI models and attenuates inflammatory activation. These effects are consistent with multi-pathway regulation predicted by network pharmacology and are supported, at least in part, by MAPK pathway suppression, warranting further mechanistic and translational studies.
相关物质
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