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tigar在脑出血中的作用与机制研究
首发时间：2024-05-28
摘要：目的：本文旨在探究tigar（tp53诱导的糖酵解和细胞凋亡调控因子）在脑出血损伤中的作用及其潜在机制。 方法：采用脑立体定向将胶原酶注射到8-10周龄雄性c57小鼠的右侧纹状体中以建立脑出血（ich）模型。在 ich 后的不同时间点收集脑组织。通过蛋白质印迹法评估 ich 后 tigar 的蛋白质水平。应用野生型小鼠，tigar过表达小鼠和tigar敲除小鼠，通过脑血肿体积检测，神经功能缺损评分和前肢放置实验观察tigar对脑出血损伤的作用。western blot和实时荧光定量pcr（qpcr）技术检测nod 样受体热蛋白结构域蛋白 3 (nlrp3)，半胱氨酸蛋白酶-1(caspase1)和白介素6 (il-6)及白介素1β (il-1β)的表达。结果：在ich后，tigar蛋白水平显著升高，特别是在ich后6小时。此外，ich 后炎症反应增强，表现为nlrp3、cleaved-caspase1、il-1β 和il-6水平升高。tigar过表达可减轻ich 后神经功能缺损和减少血肿体积。相反，tigar 敲除加剧神经损伤并增加血肿体积。tigar抑制了炎症小体nlrp3和caspase1表达，减少炎症因子il-1β，il-6的mrna水平。结论：tigar在ich后表达上调。tigar可通过降低炎症反应来减轻脑出血损伤。
关键词： 炎症
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the role and mechanism of tigar in intracerebral hemorrhage
abstract：this study aimed to investigate the role of tigar (tp53-induced glycolysis and apoptosis regulator) in intracerebral hemorrhage (ich) injury and the underlying mechanisms.methods:ich was induced by injecting collagenase into the right striatum of 8-10-week-old male c57 mice using brain stereotactic techniques. brain tissues were collected at various time points after ich. the protein levels of tigar following ich were assessed through western blotting. wild-type mice, tigar overexpression (tg) mice and tigar knockout (ko) mice were utilized to evaluate the effect of tigar on ich injury by measuring cerebral hematoma volume, neurological deficit score and forelimb placement experiment. additionally, western blotting along with real-time quantitative fluorescent pcr (qpcr) techniques were employed to measure the expression levels of nod-like receptor thermal protein domain protein 3 (nlrp3), cysteine protease-1 (caspase1), interleukin-6 (il-6), and interleukin-1β (il-1β). results: tigar protein levels are markedly elevated, particularly at 6 hours post-ich. in addition, inflammatory response were enhanced after ich as evidenced by elevated levels of nlrp3, cleaved-caspase-1, il-1β and il-6. tigar overexpression attenuated neurological deficits and decreasing hematoma volume following ich. conversely, tigar knockout exacerbated neurological deficits and increases hematoma volume. additonally, tigar inhibited the expression of inflammasome nlrp3 and cleaved-caspase1, and reduced the mrna levels of inflammatory cytokines il-1β and il-6. conclusions: tigar protein levels are upregulated post-ich. tigar may attenuate ich injury by inflammation.
keywords： inflammation
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