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盐酸戊乙奎醚对全脑缺血/再灌注大鼠谷氨酸释放的抑制作用及相关研究

[Penehyclidine hydrochloride inhibits glutamate release and related research in global brain ischemia/reperfusion rats].

作者信息

Shang You, Gu Pei-fei, Shang Yu, Li Yue

机构信息

Department of Anesthesiology, The First Affiliated Hospital of Liaoning Medical College, Jinzhou 121001, China.

出版信息

Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2011 Aug;27(3):353-6.

Abstract

OBJECTIVE

To investigate the effect of penehyclidine hydrochloride on glutamate (Glu)release and N-methyl-D-aspartate receptor (NMDAR)1 expression in hippocampus CA1 with global cerebral ischemia/reperfusion rats.

METHODS

Sixty male Wistar rats were randomly allocated into three groups; group A received sham operation; group B received ischemia/reperfusion; group C received penehyclidine hydrochloride treatment (2 mg/kg) before ischemia/reperfusion (n=20). Global cerebral ischemia was induced according to Pulsinelli-Brierley method. All animals were divided into two experiments: (I) Microdialysis plus HPLC/FD were used to detect Glu level after reperfusion 1 h, 3 h, 6 h. (II) After reperfusion 3 h, the animals were decapitated on ice and the brains were immediately removed to detect NMDAR1 expression in CA1 area by immunohistochemistry.

RESULTS

After penehyclidine hydrochloride treatment, extracellular Glu level in CA1 were significantly decreased compared with those of control group (P < 0.05 or 0.01); Total integrated OD, average gray value and positive-cell area of NMDAR1 in CA1 were also significantly decreased compared with those of control group (P < 0.05 or 0.01).

CONCLUSION

Penehyclidine hydrochloride might has protective effect in hippocampus CA1 on global cerebral ischemia/reperfusion animals. The protective mechanism might be involved in inhibiting Glu release and NMDAR1 expression.

摘要

目的

探讨盐酸戊乙奎醚对全脑缺血/再灌注大鼠海马CA1区谷氨酸(Glu)释放及N-甲基-D-天冬氨酸受体(NMDAR)1表达的影响。

方法

将60只雄性Wistar大鼠随机分为三组;A组接受假手术;B组接受缺血/再灌注;C组在缺血/再灌注前接受盐酸戊乙奎醚治疗(2mg/kg)(n = 20)。根据Pulsinelli-Brierley法诱导全脑缺血。所有动物分为两个实验:(I)采用微透析加高效液相色谱/荧光检测法在再灌注1h、3h、6h后检测Glu水平。(II)再灌注3h后将动物在冰上断头,立即取出大脑,通过免疫组织化学检测CA1区NMDAR1的表达。

结果

盐酸戊乙奎醚治疗后,CA1区细胞外Glu水平与对照组相比显著降低(P < 0.05或0.01);CA1区NMDAR1的总积分光密度、平均灰度值及阳性细胞面积与对照组相比也显著降低(P < 0.05或0.01)。

结论

盐酸戊乙奎醚可能对全脑缺血/再灌注动物的海马CA1区具有保护作用。其保护机制可能与抑制Glu释放及NMDAR1表达有关。

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