创伤性脑损伤大鼠神经炎症和铁死亡的变化及干预效果  

Changes and intervention effects of neuroinflammation and iron death in rats with traumatic brain injury

作　　者：赵培超[1] 聂向飞 尹凯[1] 胡岩[1] 林文阳[1] Zhao Peichao;Nie Xiangfei;Yin Kai;Hu Yan;Lin Wenyang(Department of Neurosurgery,the First Affiliated Hospital of Zhengzhou University,Zhengzhou 450000,China)

机构地区：[1]郑州大学第一附属医院神经外科,郑州450000

出　　处：《中华实验外科杂志》2023年第12期2507-2510,共4页Chinese Journal of Experimental Surgery

摘　　要：目的探讨创伤性脑损伤大鼠神经炎症和铁死亡的变化及铁死亡抑制剂去铁胺的干预效果。方法30至SD大鼠随机数字表格法分为对照组、模型组和去铁胺组,每组10只。模型组和去铁胺组大鼠采用Feeney自由落体法建立创伤性脑损伤模型。建模成功后,去铁胺组大鼠建模前2 h腹腔注射去铁胺100 mg/kg,对照组和模型组大鼠腹腔注射等体积生理盐水。采用改良神经功能缺损评分(mNSS)评估大鼠神经功能;采用干事比重法测定脑组织水肿情况;采用酶联免疫吸附试验(ELISA)分析脑组织中肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)和白细胞介素-6(IL-6)的表达水平;生物化学酶法测定脑组织采用蛋白质免疫应激分析谷胱甘肽和铁离子水平;采用蛋白质免疫印迹分析铁死亡相关蛋白表达水平。组间比较采用单因素方差分析。结果去铁胺组大鼠神经功能缺损评分(5.80±1.14)明显低于模型组(10.20±1.55),差异有统计学意义(t=7.244,P<0.05)。去铁胺组大鼠神经功能缺损评分[(74.52±5.71)分]明显低于模型组大鼠[(87.20±3.71)分],差异有统计学意义(t=5.886,P<0.05)。去铁胺组大鼠脑组织铁离子[(0.19±0.02)mg/g]明显低于模型组[(0.27±0.01)mg/g],差异有统计学意义(t=10.36,P<0.05)。去铁胺组大鼠大鼠脑组织MDA水平[(8.61±0.49)nmol/g]明显低于模型组[(14.44±1.98)nmol/g],差异有统计学意义(t=9.045,P<0.05)。去铁胺组大鼠脑组织GSH水平[(16.23±1.37)U/g]明显低于模型组[(9.02±1.16)U/g],差异有统计学意义(t=12.330,P<0.05)。去铁胺组大鼠脑组织炎性因子TNF-α、IL-1β和IL-6[(50.49±5.44)、(40.17±3.34)、(48.60±8.59)pg/g]明显低于模型组[(85.91±6.86)、(64.58±6.48)、(72.78±9.48)pg/g],差异有统计学意义(t=12.790、10.590、5.978,P均<0.05)。去铁胺组大鼠脑组织铁死亡相关蛋白SLC7A11、FTH1和GPX4(0.40±0.07、0.46±0.09、0.40±0.05)明显高于模型组(0.73±0.05、0.68±0.06、0.66±0.06)Objective To explore the changes in neuroinflammation and iron death in rats with traumatic brain injury,and the intervention effect of iron death inhibitor desferriamine.Methods 30 to SD rats were randomly divided into a control group(10 mice),a model group(10 mice),and a deferoxamine group(10 mice)by random number table method.The model group and deferoxamine group rats were used to establish a traumatic brain injury model using the feeney free fall method.After successful modeling,rats in the deferoxamine group were intraperitoneally injected with 100 mg/kg deferoxamine 2 hours before modeling,while rats in the control and model groups were intraperitoneally injected with equal volume of physiological saline.The neural function of rats were evaluate using the modified neurological deficiency scale(mNSS);The edema of brain tissue was Measure using the specific gravity method.The expression level of tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β)and interleukin-6(IL-6)in brain tissue was analyzed by enzyme linked immunosorbent assay(ELISA).The levels of glutathione and iron ions in brain tissue was analyzed by Biochemical enzyme method.The expression level of iron death related proteins was analyzed by Western blotting.The comparison of inter group econometric data was conducted using one-way analysis of variance.Results The neurological deficit score(5.80±1.14)of the rats in the deferoxamine group was significantly lower than that of the model group rats(10.20±1.55,t=7.244,P<0.05).The neurological deficit score of rats in the deferoxamine group[(74.52±5.71)]was significantly lower than that of rats in the model group[(87.20±3.71),t=5.886,P<0.05].The iron ions in the brain tissue of rats in the deferoxamine group[(0.19±0.02)mg/g]were significantly lower than those in the model group[(0.27±0.01)mg/g,t=10.36,P<0.05].The MDA levels in the brain tissue of rats in the deferoxamine group[(8.61±0.49)nmol/g]were significantly lower than those in the model group[(14.44±1.98)nmol/g,t=9.045,P<0.05].The GSH

关 键 词：创伤性脑损伤 神经炎症 铁死亡 

分 类 号：R651.15[医药卫生—外科学]