颅脑损伤模型中S100β及AQP-4在乙醇影响下的表达
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摘要
目的通过检测颅脑损伤模型中大鼠脑组织S100β水平及AQP-4在不同浓度乙醇影响下的表达探讨其法医学意义。方法建立大鼠颅脑损伤模型,分为空白组,损伤组,低浓度乙醇组、高浓度乙醇组,(每组包括6h、12h、48h三个时间段),采用气象色谱法于大鼠血液中的乙醇浓度进行检验;采用ELISA法对于大鼠挫伤脑皮质S100β水平进行检验;免疫组化检测大鼠脑组织中AQP-4蛋白表达。结果 1)高浓度乙醇组S100β水平自6h始明显高于其他组;在12h时间段,低乙醇浓度组S100β水平显著低于另外两组。2)镜下及免疫组化研究表明高乙醇组水肿发生早于其他组。对应损伤组及空白组,高浓度乙醇组免疫组化AQP-4阳性率较高。结论颅脑损伤模型中,分析高浓度乙醇通过促进脑水肿引发脑组织中AQP-4、S100β蛋白表达上升,而低浓度乙醇摄入不会引发显著脑水肿,且挫伤脑组织S100β蛋白下调。
Objective To investigate the significance of S100β in rat brain tissue and the expression of AQP-4 under different concentrations of ethanol in the brain injury model. Methods Rat model of brain injury was established, which was divided into blank group, injury group, low concentration ethanol group and high concentration ethanol group(each group included 6 h, 12 h, 48 h three time periods). The concentrations of ethanol in the rats' blood were tested. The level of S100β in the cerebral cortex of rats was tested by ELISA. The expression of AQP-4 protein in rat brain tissue was detected by immunohistochemistry. Results 1) The S100β level in the high concentration ethanol group was significantly higher than that in the other groups from 6 h. In the 12 h time period, the S100β level in the low ethanol concentration group was significantly lower than the other two groups. 2) Microscopic and immunohistochemical studies showed that edema in the high alcohol group occurred earlier than in the other groups. Corresponding to the injury group and the blank group, the high-concentration ethanol group had a higher positive rate of AQP-4. Conclusion In the model of brain injury, the expression of AQP-4 and S100β protein in brain tissue is increased by promoting high concentration of ethanol. The low concentration of ethanol does not cause significant brain edema, and the brain tissue S100β protein is down-regulated.
Objective To investigate the significance of S100β in rat brain tissue and the expression of AQP-4 under different concentrations of ethanol in the brain injury model. Methods Rat model of brain injury was established, which was divided into blank group, injury group, low concentration ethanol group and high concentration ethanol group(each group included 6 h, 12 h, 48 h three time periods). The concentrations of ethanol in the rats' blood were tested. The level of S100β in the cerebral cortex of rats was tested by ELISA. The expression of AQP-4 protein in rat brain tissue was detected by immunohistochemistry. Results 1) The S100β level in the high concentration ethanol group was significantly higher than that in the other groups from 6 h. In the 12 h time period, the S100β level in the low ethanol concentration group was significantly lower than the other two groups. 2) Microscopic and immunohistochemical studies showed that edema in the high alcohol group occurred earlier than in the other groups. Corresponding to the injury group and the blank group, the high-concentration ethanol group had a higher positive rate of AQP-4. Conclusion In the model of brain injury, the expression of AQP-4 and S100β protein in brain tissue is increased by promoting high concentration of ethanol. The low concentration of ethanol does not cause significant brain edema, and the brain tissue S100β protein is down-regulated.
引文
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[2]Caroline Z,Reneta TA,Cristiane B,et al.Non-specific inhibitors of aquaporin-4 stimulate S100B secretion in acute hippocampal slices of rats[J].Brain Res,2013,1491:14-22.
[3]吴旭,王保捷,张国华,等.大鼠脑损伤分级自由落体打击模型的建立[J].中国法医学杂志,2005,1:1-3.
[4]王小伟,王英元.水通道蛋白-4研究进展及法医学意义[J].中国法医学杂志,2008,23(2):101-103.
[5]Alexander ST,Phillip MR,Takumi F,et al.Critical role of aquaporin-4(AQP4)in astrocytic Ca2+signaling events elicited by cerebral edema[J].Proc Natl Acad Sci U SA,2011,108(2):846-851.
[6]Matthias R,Jochen HM,Volker A.S100B in brain damage and neurodegeneration[J].Microsc Res Tech,2003,60(6):614-632.
[7]Harald W,Sophie F,Gholam P,et al.Analysis of S100calcium binding protein B serum levels in different types of traumatic intracranial lesions[J].Neurotrauma,2014,32(1):23.
[8]Goodman MD,Makley AT,Campion EM.Preinjury alcohol exposure attenuates the neuroinflammatory response to traumatic brain injury[J].J Surg Res,2013,184(2):1053-1058.