CAJ | 학술논문

目的观察不同剂量乙酰胺对毒鼠强(TET)染毒大鼠脑皮层组织抑制性氨基酸γ-氨基丁酸(GABA)和兴奋性氨基酸谷氨酸(Glu)表达的影响.方法 SPF级SD大鼠80只,随机分为5组(每组16只):生理盐水对照组、二甲基亚砜水溶液(DMSO)对照组、TET染毒组、2.8 g/kg/d乙酰胺、治疗组和5.6 g/kg/d乙酰胺治疗组.染毒组和治疗组禁食后给予TET灌胃染毒,染毒后分别肌注生理盐水和不同剂量乙酰胺,连续5d,并分别于干预后3、12、48 h和7d取材,用免疫组化方法分析各组大鼠脑颞叶皮层组织神经递质GABA和Glu的平均光密度(OD)值的变化.结果 (1)GABA表达:TET染毒组OD值于12h开始升高,48 h达峰值,7d恢复正常;2.8 g/kg/d乙酰胺治疗组与TET染毒组相比OD值在12h升高不显著,48 h时接近正常,低于染毒组,其变化更接近对照组;5.6 g/kg/d乙酰胺治疗组OD值3h即明显升高,高于染毒组(P＜0.01),12h达高峰,48 h提前恢复正常.(2)Glu表达:TET染毒组OD值3h较两对照组明显降低,12和48 h逐渐上升,至7d恢复正常;2.8 g/kg/d乙酰胺治疗组与TET染毒组OD值变化趋势大致相同,但在48 h后有向对照组接近趋势;5.6 g/kg/d乙酰胺治疗组与染毒组相比,3h时OD值高于染毒组(P＜0.01),12h时无明显差异,48 h与7d时较各组明显下降(P＜0.01).结论 TET中毒给予大量乙酰胺治疗,对TET中毒的中枢损伤似有改善作用,而给予5.6 g/kg/d乙酰胺治疗时,对神经介质表达影响复杂,治疗风险难于评估.
목적 관찰불동제량을선알대독서강(TET)염독대서뇌피층조직억제성안기산γ-안기정산(GABA)화흥강성안기산곡안산(Glu)표체적영향.방법 SPF급SD대서80지,수궤분위5조(매조16지):생리염수대조조、이갑기아풍수용액(DMSO)대조조、TET염독조、2.8 g/kg/d을선알、치료조화5.6 g/kg/d을선알치료조.염독조화치료조금식후급여TET관위염독,염독후분별기주생리염수화불동제량을선알,련속5d,병분별우간예후3、12、48 h화7d취재,용면역조화방법분석각조대서뇌섭협피층조직신경체질GABA화Glu적평균광밀도(OD)치적변화.결과 (1)GABA표체:TET염독조OD치우12h개시승고,48 h체봉치,7d회복정상;2.8 g/kg/d을선알치료조여TET염독조상비OD치재12h승고불현저,48 h시접근정상,저우염독조,기변화경접근대조조;5.6 g/kg/d을선알치료조OD치3h즉명현승고,고우염독조(P＜0.01),12h체고봉,48 h제전회복정상.(2)Glu표체:TET염독조OD치3h교량대조조명현강저,12화48 h축점상승,지7d회복정상;2.8 g/kg/d을선알치료조여TET염독조OD치변화추세대치상동,단재48 h후유향대조조접근추세;5.6 g/kg/d을선알치료조여염독조상비,3h시OD치고우염독조(P＜0.01),12h시무명현차이,48 h여7d시교각조명현하강(P＜0.01).결론 TET중독급여대량을선알치료,대TET중독적중추손상사유개선작용,이급여5.6 g/kg/d을선알치료시,대신경개질표체영향복잡,치료풍험난우평고.
Objective To investigate the effects of acetamide at different doses on the expression of inhibitory amino acids (gamma-aminobutyric acid,GABA) and excitatory amino acid (glutamate,Glu) in the cerebral cortex of rats with acute tetramine (TET) poisoning.Methods Eighty Sprague-Dawley rats (SPF) were randomly divided into five groups,with 16 rats in each group:saline control group,dimethyl sulfoxide (DMSO) control group,TET exposure group,high-dose (2.8 g/kg/d) acetamide treatment group,and superhigh-dose (5.6 g/kg/d) acetamide treatment group.Rats in the exposure group and treatment groups were exposed to TET by intragastric administration after fasting,and were then intramuscularly injected with saline or different doses of acetamide in the following 5 days.The cortex of the temporal lobe was collected at 3 h,12 h,48 h,or 7 d after treatment.The expression levels of GABA and Glu in the cortex of the temporal lobe were determined by average optical density (OD) values in immunohistochemistry.Results 1) Expression of GABA:The OD value of GABA in TET exposure group started to increase at 12 h after treatment,reached the peak at 48 h,and decreased to the normal level at 7 d.In the high-dose acetamide treatment group,the increase in OD at 12 h was not so significant as that in the TET exposure group,OD value decreased to the normal level at 48 h and was lower than that in the exposure group,and the changes were more like those in the control groups.In the super-high-dose acetamide treatment group,OD value began to increase significantly at 3 h and was significantly higher than that in the TET exposure group (P＜0.01),it reached the peak at 12 h,and was restored to the normal value at 48 h.2) Expression of Glu:The OD value of Glu in TET exposure group at 3 h after treatment was significantly lower than those in the two control groups,it increased gradually from 12 h to 48 h,and recovered to the normal level at the 7th d.The changes in the high-dose acetamide treatment group were similar to those in the TET exposure group,but became more like those in the control groups after 48 h; the OD value in super-high-dose acetamide treatment group was significantly higher than that in the TET exposure group at 3 h after treatment (P＜0.01),while no significant difference was found at 12 h; it was significantly lower than those of all other groups at 48 h and 7 d (P＜0.01).Conclusions Treatment with high dose of acetamide has some curative effect on TET poisoning-induced central nervous lesion,while the effect of superhigh-dose acetamide on expression of neurotransmitters is too complex to evaluate.