| 宇佳利,刘淼,李林桐,王少兰,冯鹏超.丁苯酞减轻缺血性脑卒中大鼠脑缺血再灌注损伤的机制.[J].中南医学科学杂志.,2026,(1):35-38, 54. |
| 丁苯酞减轻缺血性脑卒中大鼠脑缺血再灌注损伤的机制 |
| The mechanism of butylphthalide alleviating cerebral ischemia-reperfusion injury in rats with ischemic cerebral stroke |
| 投稿时间：2025-04-22 修订日期：2025-11-03 |
| DOI：10.15972/j.cnki.43-1509/r.2026.01.007 |
| 中文关键词: 丁苯酞 缺血性脑卒中 脑缺血再灌注损伤 JAK2/STAT3信号通路 氧化应激 炎症反应 |
| 英文关键词:butylphthalide ICS CIRI JAK2/STAT3 signaling pathway oxidative stress inflammatory response |
| 基金项目:河北省中医药类科研计划项目(2022424) 作者简介:宇佳利,硕士,主治医师,研究方向为脑卒中的诊治,E-mail为fdervywa39@163.com。 |
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| 中文摘要: |
| 目的探讨丁苯酞减轻缺血性脑卒中(ICS)大鼠脑缺血再灌注损伤(CIRI)的作用机制。 方法将24只健康雄性SD大鼠随机均分为假手术组、模型组和丁苯酞组。评估各组大鼠神经功能缺损评分并测定脑梗死体积及脑水肿率。采用HE染色观察脑组织病理学变化；ELISA法测定脑组织中超氧化物歧化酶(SOD)、丙二醛(MDA)、白细胞介素(IL)-6、IL-1β及肿瘤坏死因子-α(TNF-α)水平；Western blotting检测JAK2、磷酸化(p)-JAK2、信号转导和转录激活因子3(STAT3)、p-STAT3、血管内皮生长因子(VEGF)及促红细胞生成素(EPO)蛋白表达水平。 结果与假手术组相比,模型组大鼠神经功能缺损评分、脑梗死体积百分比、脑水肿率、MDA、IL-6、IL-1β、TNF-α水平以及p-JAK2/JAK2、p-STAT3/STAT3、VEGF、EPO蛋白表达水平升高(P＜0.05),脑组织中SOD水平下降(P＜0.05)。与模型组相比,丁苯酞组逆转上述指标水平(P＜0.05)。假手术组脑组织结构完整、细胞形态正常；模型组脑组织结构破坏,变性坏死明显,神经元胞核缩小、染色加深,细胞排列紊乱；丁苯酞组脑组织形态较模型组明显改善,神经细胞结构相对完整,变性和坏死程度减轻。 结论丁苯酞通过调控JAK2/STAT3信号通路减轻ICS大鼠CIRI,其机制可能与抑制氧化应激、减轻炎症反应及调节血管生成相关。 |
| 英文摘要: |
| AimTo investigate the neuroprotective mechanism of butylphthalide in cerebral ischemia-reperfusion injury (CIRI) in rats with ischemic cerebral stroke (ICS). MethodsTotally 24 healthy male SD rats were randomly divided into sham operation group, model group, and butylphthalide group. The neurological deficit scores of each group of rats were measured, and the cerebral infarction volume and cerebral edema rate were evaluated. HE staining was used to observe pathological changes in brain tissue; ELISA method was used to measure the levels of superoxide dismutase (SOD), malondialdehyde (MDA), interleukin-6 (IL-6), IL-1 β, and tumor necrosis factor-α (TNF-α) in brain tissue; Western blotting was used to detect the protein expression levels of JAK2, phosphorylated (p)-JAK2, signal transducer and activator of transcription-3 (STAT3), p-STAT3, vascular endothelial growth factor (VEGF), and erythropoietin (EPO). ResultsCompared with the sham surgery group, the model group showed an increase in neurological deficit score, the percentage of cerebral infarction volume and cerebral edema rate, MDA, IL-6, IL-1 β, TNF-α levels, as well as p-JAK2/JAK2, p-STAT3/STAT3, VEGF, and EPO protein expression levels (P＜0.05), while the SOD level in brain tissue were decreased (P＜0.05). Compared with the model group, the butylphthalide group reversed the changes of the above indicators (P＜0.05). The sham surgery group had intact brain tissue structure and normal cell morphology; The brain tissue structure of the model group was damaged, with obvious degeneration and necrosis, shrinking and deepening of neuronal nuclei, and disordered cell arrangement; The morphology of brain tissue in the butylphthalide group was significantly improved compared to the model group, with relatively intact neural cell structure and reduced degree of degeneration and necrosis. ConclusionDibenzophenone alleviates CIRI in ICS rats by regulating the JAK2/STAT3 signaling pathway, and its mechanism may be related to oxidative stress inhibition, inflammatory response reduction, and angiogenesis regulation. |
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