Protective effect of MLIF on traumatic brain injury in rats
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摘要: 目的 研究单核细胞移动抑制因子(MLIF)对大鼠颅脑创伤(TBI)的保护作用,并初步探讨其作用机制。 方法 将大鼠随机分为5组,假手术组、模型组、MLIF低、中、高剂量组(0.33、1、3 mg/kg)。采用液压冲击法制备大鼠颅脑创伤模型,颅脑打击后30 min内完成首次尾静脉注射给药,每天给药1次,连续给药7 d。分别于给药后1、3、7 d取脑,检测大鼠脑含水量变化;采用试剂盒法检测血清超氧化物歧化酶(SOD)和丙二醛(MDA)水平;HE染色及尼氏染色观察脑组织病理改变。 结果 液压打击致大鼠颅脑创伤24 h后,MLIF低、中、高剂量组大鼠脑含水量均显著低于模型组(P<0.01),MLIF中剂量组(1 mg/kg)效果最好。与模型组比较,创伤后1、3 d,MLIF(1mg/kg)组大鼠脑含水量显著降低(P<0.01),该组大鼠血清中SOD含量明显升高(P<0.05)和MDA含量显著降低(P<0.05)。HE染色和尼氏染色结果显示,模型组大鼠脑组织病理损伤明显,呈现明显水肿、细胞固缩等;MLIF(1mg/kg)组大鼠脑组织病理损伤得到改善,水肿程度减轻。 结论 MLIF可以抑制脑损伤氧化应激及水肿反应,发挥颅脑损伤保护作用。
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关键词:
- 单核细胞移动抑制因子 /
- 颅脑损伤 /
- 脑水肿 /
- 大鼠
Abstract: Objective To study the protective effect and explore the mechanism of monocyte locomotion inhibitor factor(MLIF) on traumatic brain injury (TBI) in rats. Methods The SD rats were randomly divided into five groups:sham operation group,model group and three MLIF groups (0.33 mg/kg,1 mg/kg,3 mg/kg).Rats were made model of brain injury by fluid percussion injury.The tail vein was administered within 30 min after TBI,once every 24 hours,and rats were administered for 7 days.Brain water content,serum levels of SOD and MDA,Hematoxylin-eosin staining and Nissl staining were used to detect the rats brain tissues. Results After rats traumatic brain injury for 24h,the brain water content in rats in three MLIF groups(0.33 mg/kg,1 mg/kg and 3 mg/kg)was significantly lower than that in model group(P<0.01),The effect of MLIF (1 mg/kg) group was the best.Compared to rats traumatic brain injury for 1d and 3d,brain water content in MLIF group (1 mg/kg) was significantly lower than that in model group (P<0.01).SOD content in serum in MLIF (1 mg/kg) group was significantly increased (P <0.01) and MDA content in serum in MLIF (1 mg/kg) group was significantly decreased (P<0.05).HE staining and Nissl staining showed that the pathological changes of brain tissue in model group were obvious,and which in MLIF group were improved in brain tissue. Conclusion MLIF could inhibit oxidative stress and edema reaction of brain injury,which had protective effect on traumatic brain injury.-
Key words:
- MLIF /
- traumatic brain injury /
- brain edema /
- rats
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[1] LOANE D J,FADEN A I.Neuroprotection for traumatic brain injury:translational challenges and emerging therapeutic strategies[J].Trends Pharmacol Sci,2010,31(12):596-604. [2] RICO G,LEANDRO E,ROJAS S,et al.The effect of the monocyte locomotion inhibitory factor (MLIF) produced by Entamoeba histolytica upon nitric oxide production by human leukocytes[J].Arch Med Res,2000,31(4 Suppl):S90-S91. [3] ZHANG Y F,CHEN J,LI F,et al.A pentapeptide monocyte locomotion inhibitory factor protects brain ischemia injury by targeting the eEF1A1/endothelial nitric oxide synthase pathway[J].Stroke,2012,43(10):2764-2773. [4] 程浩,芮耀诚,章越凡,等.生物活性肽-单核细胞迁移抑制因子研究进展[J].药学实践杂志,2015,33(1):17-19,27. [5] ZHU Q Z,ZHANG Y F,LIU Y L,et al.MLIF alleviates SH-SY5Y neuroblastoma injury induced by oxygen-glucose deprivation by targeting eukaryotic translation elongation factor 1A2[J].PLoS One,2016,11(2):e0149965. [6] MCINTOSH T K,VINK R,NOBLE L,et al.Traumatic brain injury in the rat:characterization of a lateral fluid-percussion model[J].Neuroscience,1989,28(1):233-244. [7] MARKLUND N,HILLERED L.Animal modelling of traumatic brain injury in preclinical drug development:where do we go from here?[J].Br J Pharmacol,2011,164(4):1207-1229. [8] FUKUDA A M,BADAUT J.Aquaporin 4:a player in cerebral edema and neuroinflammation[J].J Neuroinflammation,2012,9:279. [9] MARMAROU A.Pathophysiology of traumatic brain edema:current concepts[J].Acta Neurochir Suppl,2003,86:7-10. [10] FEICKERT H J,DROMMER S,HEYER R.Severe head injury in children:impact of risk factors on outcome[J].J Trauma,1999,47(1):33-38. [11] DONKIN J J,VINK R.Mechanisms of cerebral edema in traumatic brain injury:therapeutic developments[J].Curr Opin Neurol,2010,23(3):293-299. [12] HALL E D,VAISHNAV R A,MUSTAFA A G.Antioxidant therapies for traumatic brain injury[J].Neurotherapeutics,2010,7(1):51-61. [13] JI X T,LIU W B,XIE K L,et al.Beneficial effects of hydrogen gas in a rat model of traumatic brain injury via reducing oxidative stress[J].Brain Res,2010,1354:196-205.
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