上海交通大学学报（医学版）
上海交通大學學報（醫學版）
상해교통대학학보（의학판）
JOURNAL OF SHANGHAI JIAOTONG UNIVERSITY(MEDICAL SCIENCE)
2010年
4期
394-398
,共5页
代谢型谷氨酸受体%匹罗卡品%mRNA%癫(癎)动物模型
代謝型穀氨痠受體%匹囉卡品%mRNA%癲(癎)動物模型
대사형곡안산수체%필라잡품%mRNA%전(간)동물모형
metabotropic glutamate receptor%pilocarpine%mRNA%epilepsy animal model
目的 观察匹罗卡品诱导的颞叶癫(癎)大鼠海马CA1区代谢型谷氨酸受体(mGluR)1、4、7的表达变化.方法 56只SD大鼠随机分为对照组、癫(癎)状态(SE)2 h组、SE 12 h组、SE 24 h组、SE 72 h组、SE 7 d组和SE 14 d组,每组8只.SE各组腹腔注射325 mg/kg匹罗卡品建立癫(癎)模型,对照组注射等量生理盐水.采用RT-PCR和免疫组织化学方法检测各组大鼠海马CA1 区mGluR1、4、7 mRNA和mGluR1蛋白的表达.结果 RT-PCR检测显示,SE 24 h组mGluR1 mRNA表达较对照组显著降低,而SE 7 d组则显著增加(P<0.05);SE各组mGluR4 mRNA表达与对照组差异无统计学意义(P>0.05);SE 12 h组、SE 24 h组、SE 72 h组和sE 14 d组mGluR7 mRNA表达较对照组显著降低(P<0.05).免疫组织化学检测显示,mGluRl蛋白主要存在于细胞膜上,其表达变化规律与mGluR1 mRNA一致.结论 mGluR1、4、7可能参与难治性癫(癎)的发病过程.
目的 觀察匹囉卡品誘導的顳葉癲(癎)大鼠海馬CA1區代謝型穀氨痠受體(mGluR)1、4、7的錶達變化.方法 56隻SD大鼠隨機分為對照組、癲(癎)狀態(SE)2 h組、SE 12 h組、SE 24 h組、SE 72 h組、SE 7 d組和SE 14 d組,每組8隻.SE各組腹腔註射325 mg/kg匹囉卡品建立癲(癎)模型,對照組註射等量生理鹽水.採用RT-PCR和免疫組織化學方法檢測各組大鼠海馬CA1 區mGluR1、4、7 mRNA和mGluR1蛋白的錶達.結果 RT-PCR檢測顯示,SE 24 h組mGluR1 mRNA錶達較對照組顯著降低,而SE 7 d組則顯著增加(P<0.05);SE各組mGluR4 mRNA錶達與對照組差異無統計學意義(P>0.05);SE 12 h組、SE 24 h組、SE 72 h組和sE 14 d組mGluR7 mRNA錶達較對照組顯著降低(P<0.05).免疫組織化學檢測顯示,mGluRl蛋白主要存在于細胞膜上,其錶達變化規律與mGluR1 mRNA一緻.結論 mGluR1、4、7可能參與難治性癲(癎)的髮病過程.
목적 관찰필라잡품유도적섭협전(간)대서해마CA1구대사형곡안산수체(mGluR)1、4、7적표체변화.방법 56지SD대서수궤분위대조조、전(간)상태(SE)2 h조、SE 12 h조、SE 24 h조、SE 72 h조、SE 7 d조화SE 14 d조,매조8지.SE각조복강주사325 mg/kg필라잡품건립전(간)모형,대조조주사등량생리염수.채용RT-PCR화면역조직화학방법검측각조대서해마CA1 구mGluR1、4、7 mRNA화mGluR1단백적표체.결과 RT-PCR검측현시,SE 24 h조mGluR1 mRNA표체교대조조현저강저,이SE 7 d조칙현저증가(P<0.05);SE각조mGluR4 mRNA표체여대조조차이무통계학의의(P>0.05);SE 12 h조、SE 24 h조、SE 72 h조화sE 14 d조mGluR7 mRNA표체교대조조현저강저(P<0.05).면역조직화학검측현시,mGluRl단백주요존재우세포막상,기표체변화규률여mGluR1 mRNA일치.결론 mGluR1、4、7가능삼여난치성전(간)적발병과정.
Objective To observe the expression of metabotropic glutamate receptor (mGluR) 1, 4, 7 in CA1 region of hippocampus in rats with pilocarpine-induced temporal lobe epilepsy. Methods Fifty-six SD rats were randomly divided into control group, status epilepticus (SE) 2 h group, SE 12 h group, SE 24 h group, SE 72 h group, SE 7 d group and SE 14 d group, with 8 rats in each group. Temporal lobe epilepsy models were established in SE 2 h group, SE 12 h group, SE 24 h group, SE 72 h group, SE 7 d group and SE 14 d group by intraperitoneal injection of 325 mg/kg pilocarpine, and rats in control group were injected with same amount of normal saline. RT-PCR and immunohistochemistry were employed to detect the expression of mGluRl, 4, 7 mRNA and mGluRl protein in CA1 region of hippocampus in each group. Results It was revealed by RT-PCR that the expression of mGluRl mRNA was significantly lower in SE 24 h group than that in control group, while the expression of mGluRl mRNA was significantly higher in SE 7 d group than that in control group (P<0.05). There was no significant difference in the expression of mGluR4 mRNA among groups (P > 0. 05). The expression of mGluR7 mRNA in SE 12 h group, SE 24 h group, SE 72 h group and SE 14 d group was significantly lower than that in control group (P <0.05). Immunohistochemical examination demonstrated that mGluRl protein mainly existed on cell membrane, and the changes of expression of mGluRl protein were in line with those of mGluRl mRNA. Conclusion mGluR 1, 4, 7 may be involved in the pathogenesis of intractable temporal lobe epilepsy.
