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黄芪甲苷对颅内动脉瘤大鼠动脉血管内皮组织损伤的影响
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| 篇名： | 黄芪甲苷对颅内动脉瘤大鼠动脉血管内皮组织损伤的影响 |
| TITLE： | Effects of astragaloside Ⅳ on arterial endothelial tissue damage in rats with intracranial aneurysm |
| 摘要： | 目的 研究黄芪甲苷（AST）对颅内动脉瘤（IA）大鼠动脉血管内皮组织损伤的影响，并基于核因子κB（NF-κB）/核苷酸结合结构域富含亮氨酸重复序列和含热蛋白结构域受体3（NLRP3）信号通路探讨其作用机制。方法将大鼠分为假手术组（Sham组，灌胃并腹腔注射等体积生理盐水）、IA组（灌胃并腹腔注射等体积生理盐水）、AST低剂量组（AST-L组，灌胃40mg/kgAST）、AST高剂量组（AST-H组，灌胃80mg/kgAST）和AST-H+HY-N2485组（灌胃80mg/kg的AST并腹腔注射25mg/kg的NF-κB/NLRP3信号通路激活剂HY-N2485）。每天给药1次，连续8周。末次给药后，检测血清中炎症因子[肿瘤坏死因子α、白细胞介素18（IL-18）、IL-6]、血管内皮生长因子（VEGF）和内皮肽（ET）水平，观察IA形态，检测血管组织中血管性血友病因子（vWF）、血管细胞黏附分子1（VCAM-1）、内皮型一氧化氮合酶（eNOS）和NF-κB/NLRP3信号通路相关蛋白表达水平。结果与Sham组比较，IA组大鼠颅底动脉环有明显突起，动脉血管内皮细胞有明显损伤；血清中炎症因子和VEGF、ET水平，血管组织中vWF、VCAM-1、NLRP3蛋白表达水平以及NF-κB蛋白磷酸化水平均显著升高（P＜0.05），动脉瘤、内部弹性层破裂均显著增大（P＜0.05），eNOS蛋白表达水平显著降低（P＜0.05）；与IA组比较，AST-L组、AST-H组大鼠IA形态及上述指标水平均显著改善（P＜0.05），且AST-H组较AST-L组改善得更明显（P＜0.05）；HY-N2485可显著减轻AST对IA大鼠血管内皮组织损伤的改善作用（P＜0.05）。结论AST可能通过抑制NF-κB/NLRP3信号通路来抑制炎症因子表达，减轻炎症和血管内皮组织损伤，从而抑制IA形成。 |
| ABSTRACT： | OBJECTIVE To investigate the effect of astragaloside Ⅳ（AST） on the injury of arterial endothelial tissue in rats with intracranial aneurysms （IA）， and to explore its mechanism of action based on the nuclear factor κB （NF-κB）/nucleotide- binding domain leucine-rich repeat and pyrin domain-containing protein 3 （NLRP3） signaling pathway. METHODS Rats were divided into Sham group （intragastric administration and intraperitoneal injection of the same volume of normal saline）， IA group （intragastric administration and intraperitoneal injection of the same volume of normal saline）， AST low-dose group （AST-L group， intragastric administration of 40 mg/kg AST）， AST high-dose group （AST-H group， intragastric administration of 80 mg/kg AST）， AST-H+HY-N2485 group [intragastric administration of 80 mg/kg AST and intraperitoneal injection of 25 mg/kg HY-N2485 （activator of NF-κB/NLRP3 signaling pathway）]. They were given relevant medicine， once a day， for 8 consecutive weeks. After last medication， the levels of inflammatory factors [serum tumor necrosis factor-α （TNF-α）， interleukin-18 （IL-18）， IL-6] and vascular endothelial growth factor （VEGF） and endothelin （ET） were detected； the morphology of IA was observed； the expressions of von Willebrand factor （vWF）， vascular cell adhesion molecule-1 （VCAM-1）， endothelial nitric oxide synthase （eNOS）， and NF-κB/NLRP3 pathway related proteins in vascular tissue were also determined. RESULTS Compared with the Sham group， the basilar arterial ring of rats in the IA group had obvious protrusions， and the arterial vascular endothelial cells were significantly damaged. The levels of inflammatory factors， VEGF and ET in serum， as well as the expression levels of vWF， VCAM-1 and NLRP3 proteins and the phosphorylation level of NF-κB protein in vascular tissues were increased significantly （P＜ 0.05）. Aneurysms and ruptures of the internal elastic layer were significantly increased （P＜0.05）， while the expression level of eNOS protein was significantly decreased （P＜0.05）. Compared with IA group， the morphology of IA and the levels of above indexes were all improved significantly in AST-L and AST-H groups （P＜0.05），and the improvement in the AST-H group was more significant than that in the AST-L group （P＜0.05）； HY-N2485 could attenuate the improvement effect of AST on vascular endothelial tissue damage in IA rats （P＜0.05）. CONCLUSIONS AST may inhibit the expression of inflammatory factors， alleviate inflammation and vascular endothelial tissue damage in IA rats by inhibiting NF- κB/NLRP3 signaling pathway，thereby inhibiting the formation of IA. active_999@sina.com |
| 期刊： | 2025年第36卷第13期 |
| 作者： | 蔡强；刘柳青；唐佳宇 |
| AUTHORS： | CAI Qiang，LIU Liuqing，TANG Jiayu |
| 关键字： | 黄芪甲苷；颅内动脉瘤；NF-κB/NLRP3信号通路；血管内皮组织损伤；炎症 |
| KEYWORDS： | astragaloside Ⅳ； intracranial aneurysm； NF- |
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