CAJ | 학술논문

目的观察右美托咪定(DEX)对痫性发作大鼠海马神经细胞凋亡蛋白表达的影响.方法将36只SD大鼠随机分为3组(n=12):对照组(Control组)、右美托咪定组(DEX组)及致痫组(EP组).DEX组给予10 μg/kg剂量DEX灌胃,连续3d,至致痫当日;对照组、致痫组则分别给予等体积生理盐水灌胃.以氯化锂-匹罗卡品制作致痫模型,观察SD大鼠行为学变化;采用Westernblot检测B细胞淋巴瘤/白血病-2(bcl-2)、bcl-2相关X蛋白(bax)和半胱氨酰天冬氨酸特异性蛋白酶-3(Caspase-3)表达水平.结果 EP组大鼠均表现易激惹,DEX组反复自发性痫性发作(SRS)次数[(5.67±1.53)次]比EP组[(10.33 ±3.06)次]明显减少,且差异有统计学意义(P＜0.05).bcl-2、bax、bcl-2/bax和Caspase-3表达水平结果,对照组分别为1.0557±0.008 1、0.571 2±0.005 7、1.0870± 0.0026、0;DEX组分别为0.965 4±0.021 6、0.6920± 0.0028、1.3951±0.0328、0.676 5±0.969 7;EP组分别为0.8925±0.0063、0.7427±0.0010、1.2016±0.008 2、0.856 5±0.962 6.EP组与对照组比较,大鼠海马、bax、活化的active-Caspase-3表达水平增加,bcl-2表达水平降低,差异有统计学意义(P＜0.05),bcl-2/bax比值升高,差异有统计学意义(P＜0.05);DEX组与EP组比较,海马bcl-2表达水平、bcl-2/bax比值升高,bax、active-Caspase-3表达水平降低,差异有统计学意义(P＜0.05).结论 DEX可能作用抑制大鼠海马神经细胞Casepase-3和bax基因表达,减少SRS次数,对海马神经元产生保护作用.
목적 관찰우미탁미정(DEX)대간성발작대서해마신경세포조망단백표체적영향.방법 장36지SD대서수궤분위3조(n=12):대조조(Control조)、우미탁미정조(DEX조)급치간조(EP조).DEX조급여10 μg/kg제량DEX관위,련속3d,지치간당일;대조조、치간조칙분별급여등체적생리염수관위.이록화리-필라잡품제작치간모형,관찰SD대서행위학변화;채용Westernblot검측B세포림파류/백혈병-2(bcl-2)、bcl-2상관X단백(bax)화반광안선천동안산특이성단백매-3(Caspase-3)표체수평.결과 EP조대서균표현역격야,DEX조반복자발성간성발작(SRS)차수[(5.67±1.53)차]비EP조[(10.33 ±3.06)차]명현감소,차차이유통계학의의(P＜0.05).bcl-2、bax、bcl-2/bax화Caspase-3표체수평결과,대조조분별위1.0557±0.008 1、0.571 2±0.005 7、1.0870± 0.0026、0;DEX조분별위0.965 4±0.021 6、0.6920± 0.0028、1.3951±0.0328、0.676 5±0.969 7;EP조분별위0.8925±0.0063、0.7427±0.0010、1.2016±0.008 2、0.856 5±0.962 6.EP조여대조조비교,대서해마、bax、활화적active-Caspase-3표체수평증가,bcl-2표체수평강저,차이유통계학의의(P＜0.05),bcl-2/bax비치승고,차이유통계학의의(P＜0.05);DEX조여EP조비교,해마bcl-2표체수평、bcl-2/bax비치승고,bax、active-Caspase-3표체수평강저,차이유통계학의의(P＜0.05).결론 DEX가능작용억제대서해마신경세포Casepase-3화bax기인표체,감소SRS차수,대해마신경원산생보호작용.
Objective To observe the effect of dexmedetomidine (DEX) on apoptotic protein expression in hippocampal neurons of epileptic rats.Methods Thirty-six SD rats were randomly divided into 3 groups (n =12):control group,DEX group and epilepsy (EP) group.The DEX Group was given gavage administration of DEX (10 μg/kg) for 3 consecutive days until the date of epilepsy seizure.The control group and EP group were given gavage administration of the same volume of normal saline.Lithium chloride-pilocarpine was used to establish epileptogenic model to observe the behavioral changes of SD rats.Western blotting was adopted to detect the expression level of B cell lymphoma/lewkmia-2 (bcl-2),bcl-2 associated X protein (bax) and cysteinyl aspartate specific proteinase-3 (Caspase-3).Results Unexceptionally all the rats in EP group showed irritability.The recurrent spontaneous seizures (SRS) counts in DEX group (5.67 ± 1.53) were significantly reduced as compared with EP group (10.33 ± 3.06) (P ＜ 0.05).The expression levels of bcl-2,bax,bcl-2/bax ratio and Caspase-3 in control group were 1.055 7 ±0.008 1,0.571 2 ±0.005 7,1.087 0 ±0.002 6 and 0,those in DEX group were 0.965 4 ±0.021 6,0.692 0 ±0.002 8,1.395 1 ±0.032 8 and 0.676 5 ±0.969 7,and those in EP group were 0.892 5 ± 0.006 3,0.742 7 ± 0.001 0,1.201 6 ± 0.008 2 and 0.856 5 ± 0.962 6,respectively.As compared with control group,bax and active-Caspase-3 in the EP group were increased in the hippocampus of rats,and bcl-2 expression level was significantly reduced statistically (P ＜ 0.05).The bcl-2/bax ratio was increased statistically (P ＜ 0.05).As compared with EP group,bcl-2 expression level and bcl-2/bax ratio were increased,and the expression levels of bax and active-Caspase-3 were reduced in the hippocampus of DEX group.(P ＜ 0.05).Conclusion DEX may play a role in inhibiting the gene expression path of Caspase-3 and bax in rat hippocampal neurons and reducing the SRS counts.So it will protect the hippocampal neurons.