| 王朝晨,张 浩,崔 健,王 钢,雍晓莉.盐酸氟桂利嗪对脑出血大鼠氧化应激、炎症因子表达以及神经功能的影响及机制探索[J].现代生物医学进展英文版,2025,(3):419-427,467. |
| 盐酸氟桂利嗪对脑出血大鼠氧化应激、炎症因子表达以及神经功能的影响及机制探索 |
| Effects and Mechanisms of Flunarizine Hydrochloride on Oxidative Stress, Inflammatory Factor Expression, and Neurological Function in Rats with Cerebral Hemorrhage |
| Received:June 26, 2024 |
| DOI：10.13241/j.cnki.pmb.2025.03.003 |
| 中文关键词: 盐酸氟桂利嗪 脑出血 氧化应激 炎症 NF-κB信号通路 |
| 英文关键词: Flunarizine hydrochloride Cerebral hemorrhage Oxidative stress Inflammation NF-κB signaling pathway |
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| 中文摘要: |
| 摘要 目的：研究盐酸氟桂利嗪对脑出血大鼠氧化应激、炎症因子表达以及神经功能的影响并对其作用机制进行初步探索。方法：大鼠分成假手术组、模型组（脑出血大鼠模型）、低剂量治疗组（脑出血大鼠模型，予0.6 mg/kg盐酸氟桂利嗪治疗）、中剂量治疗组（脑出血大鼠模型，予1.2 mg/kg盐酸氟桂利嗪治疗）、高剂量治疗组（脑出血大鼠模型，予2.4 mg/kg盐酸氟桂利嗪治疗）。干预后，首先对各组大鼠进行神经功能评分，随后测定脑组织含水量，并分别用试剂盒检测脑组织中SOD、MDA、GSH-PX水平，采用流式细胞术检测脑组织中神经细胞的凋亡水平，采用qRT-PCR法检测脑组织中TNF-α、IL-6、IL-1β的mRNA水平，采用Western blot法检测脑组织中Bax、Bcl-2、NF-κBp65蛋白表达水平。结果：与假手术组比较，模型组大鼠神经功能评分降低，脑组织含水量升高，脑组织中SOD、GSH-PX水平降低，MDA水平升高，细胞凋亡增多，TNF-α、IL-6、IL-1β mRNA水平升高，Bax、NF-κBp65蛋白表达水平升高，Bcl-2蛋白表达水平降低。与模型组比较，低剂量治疗组、中剂量治疗组、高剂量治疗组大鼠神经功能评分升高，脑组织含水量降低，脑组织中SOD、GSH-PX水平升高，MDA水平降低，细胞凋亡减少，TNF-α、IL-6、IL-1β mRNA水平降低，Bax、NF-κBp65蛋白表达水平降低，Bcl-2蛋白表达水平升高，且其中以高剂量治疗组的干预效果最优。结论：盐酸氟桂利嗪可改善脑出血大鼠脑组织的氧化应激、减少炎症因子释放、减少细胞凋亡，进而降低脑组织含水量、改善大鼠神经功能，其作用机制可能与抑制NF-κB信号通路有关。 |
| 英文摘要: |
| ABSTRACT Objective: The aim of this study was to investigate the effects of Flunarizine hydrochloride on oxidative stress, expression of inflammatory factors, and neurological function in rats with cerebral hemorrhage, as well as to explore its preliminary mechanisms of action. Methods: Rats were divided into the sham surgery group, model group (rats with cerebral hemorrhage), low-dose treatment group (rats with cerebral hemorrhage, treated with 0.6 mg/kg of Flunarizine hydrochloride), medium-dose treatment group (rats with cerebral hemorrhage, treated with 1.2 mg/kg of Flunarizine hydrochloride), and high-dose treatment group (rats with cerebral hemorrhage, treated with 2.4 mg/kg of Flunarizine hydrochloride). After intervention, neurological function was first assessed using a neurological function score. Subsequently, brain tissue water content was measured, and the levels of SOD, MDA, and GSH-PX in brain tissue were detected using assay kits. Flow cytometry was used to evaluate neuronal apoptosis, qRT-PCR was performed to measure TNF-α, IL-6, and IL-1β mRNA levels in brain tissue, and Western blotting was conducted to assess the protein expression levels of Bax, Bcl-2, and NF-κBp65 in brain tissue. Results: Compared with the sham surgery group, rats in the model group showed decreased neurological function scores, increased brain tissue water content, decreased SOD and GSH-PX levels, increased MDA levels, increased neuronal apoptosis, elevated mRNA levels of TNF-α, IL-6, and IL-1β, and increased protein expression levels of Bax and NF-κBp65, along with reduced Bcl-2 protein expression. In comparison to the model group, rats in the low-dose, medium-dose, and high-dose treatment groups exhibited improved neurological function scores, reduced brain tissue water content, increased SOD and GSH-PX levels, decreased MDA levels, reduced neuronal apoptosis, lowered mRNA levels of TNF-α, IL-6, and IL-1β, and decreased protein expression levels of Bax and NF-κBp65, while Bcl-2 protein expression was increased. Notably, the high-dose treatment group showed the most significant intervention effects. Conclusion: The Flunarizine hydrochloride ameliorates oxidative stress, reduces the release of inflammatory factors, and attenuates neuronal apoptosis in rats with cerebral hemorrhage, thereby lowering brain tissue water content and improving neurological function. The mechanism could be potentially associated with the inhibition of the NF-κB signaling pathway. |
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