| 百里醌对大鼠蛛网膜下腔出血后脑细胞凋亡的影响 |
| 投稿时间：2017-06-13 修订日期：2017-06-28 点此下载全文 |
| 引用本文：陈朝晖,洪溪屏,兰频,潘锋.百里醌对大鼠蛛网膜下腔出血后脑细胞凋亡的影响[J].医学研究杂志,2018,47(3):89-93 |
| DOI：
10.11969/j.issn.1673-548X.2018.03.023 |
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| 基金项目:浙江省重大科技专项基金资助项目（2013C03010） |
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| 中文摘要:目的 研究百里醌对大鼠蛛网膜下腔出血（subarachnoid hemorrhage，SAH）后脑细胞凋亡的作用及其机制。方法 采用血管内穿刺法建立SAH模型，将48只成年雄性SD大鼠采用数字表法随机分为假手术组（Sham组）、SAH组、媒介组和百里醌组，SAH造模24h后检测神经功能损伤、脑组织含水率和脑组织内依文蓝（EB）含量；Tunel法检测脑细胞凋亡；ELISA法检测脑组织中IL-13的表达；Western blot法检测脑组织中IL-13Rα2、p-PI3K、p-AKT和mTOR的表达。结果 SAH组大鼠Garcia神经功能评分、脑组织含水率和EB含量较Sham组均明显升高，脑组织中IL-13的表达上调；SAH组大鼠脑出血后细胞凋亡率显著上升，IL-13Rα2、p-PI3K、p-AKT和mTOR的表达升高；与媒介组相比较，百里醌组大鼠Garcia神经功能评分、脑组织含水率和EB含量均明显降低，IL-13在脑组织中的表达下调，细胞凋亡率显著下降，IL-13Rα2、p-PI3K、p-AKT和mTOR的表达下调。结论 百里醌可减轻大鼠SAH后脑损伤和脑细胞凋亡，其机制可能通过IL-13Rα2/PI3K/AKT/mTOR通路实现。 |
| 中文关键词:百里醌 蛛网膜下腔出血 凋亡 IL-13Rα2 |
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| Effects of Thymoquinone on Early Brain Injury and Apoptosis after Subarachnoid Hemorrhage in Rats |
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| Abstract:Objective To explore the effects of thymoquinone on early brain injury and apoptosis in rats after subarachnoid hemorrhage (SAH). Methods Total 48 adult male SD rats were randomly divided in to Sham group, SAH group, vehicle group and thymoquinone group. Neurological score, brain water content and blood-brain barrier were evaluated at 24h after SAH. Tunel staining was performed to detect cell apoptosis in rat brain tissue. ELISA method was performed for quantitative detection of IL-13. The relative levels of IL-13Rα2, p-PI3K, p-AKT and mTOR in rat brain tissue were detected by western blot. Results 24h after modeling, Garcia neurological score, brain water content and EB content of brain tissue of rats in SAH group were significantly higher than that of Sham group. ELISA analysis revealed that SAH induced a significant increase in IL-13 expression in the brain tissue. Tunel staining showed that the number of TUNEL-stained cells was increased in the subcortical brain region after SAH compared to the sham group. In addition, a higher expression of IL-13Rα2, p-PI3K, p-AKT and mTOR in rat brain were observed at 24h post-SAH. However, the neurological deficit scores, brain water content and EB content in rat brains were significantly reduced in thymoquinone group in comparison with vehicle group. The administration of thymoquinone dramatically suppressed the level of IL-13 in the rat brains. Thymoquinone treatment grossly reduced the number of TUNEL positive cells. Furthermore, thymoquinone significantly decreased the levels of IL-13Rα2, p-PI3K, p-AKT as well as mTOR. Conclusion Thymoquinone could effectively inhibit early brain injury and apoptosis following SAH in rats, which may be related to down-regulation of IL-13Rα2/PI3K/AKT/mTOR pathway. |
| keywords:Thymoquinone Subarachnoid hemorrhage Apoptosis IL-13Rα2 |
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