苄普地尔降低左甲状腺素诱导的大鼠大脑线粒体Ca2+ Mg(2+)-ATP酶活性增强。

Bepridil reducing levothyroxine-induced enhancement of mitochondria Ca2+ Mg(2+)-ATPase activity in rat cerebrum.

作者信息

Chen D D, Dai D Z, Chu Y X

机构信息

Research Division of Pharmacology, China Pharmaceutical University, Nanjing, China.

出版信息

Zhongguo Yao Li Xue Bao. 1996 Sep;17(5):432-4.

PMID:9863167

Abstract

AIM

To study if bepridil (Bep) could affect the enhancement of activity of cerebral mitochondria Ca2+ Mg(2+)-ATPase caused by levothyroxine (Lev) in relation to ischemic overload calcium cerebrum injury.

METHODS

The experimental hyperthyroidism model with ischemic cerebrum was developed in rats by ig Lev 1 mg.kg-1.d-1 for 7 d. Ca2+ Mg(2+)-ATPase activity and its kinetic parameters were assayed.

RESULTS

The activity, Vmax and Km of cerebral mitochondria Ca2+ Mg(2+)-ATPase in control rats were 3.1 +/- 0.8, 5.1 +/- 2.3 mmol.P(i).h-1/g protein and 0.81 +/- 0.08 mmol.L-1 (ATP) respectively, whereas those of hyperthyroid rats were significantly altered to 4.6 +/- 0.5, 8.5 +/- 1.9 mmol.P(i).h-1/g protein and 0.49 +/- 0.11 mmol.L-1 (ATP) respectively. After treated with Bep 10 or 20 mg.kg-1.d-1 ig for 3 d, allabove 3 parameters of the enzyme were very significantly reduced vs those of either control or hyperthyroid.

CONCLUSION

Bep, via decreasing Ca2+ Mg(2+)-ATPase activity and increasing the affinity of Ca2+ Mg(2+)-ATPase to ATP, could prevent rat cerebrum from ATP depletion and ischemic overload calcium injury.

摘要

目的

研究苄普地尔（Bep）是否会影响左甲状腺素（Lev）引起的脑线粒体Ca2+ Mg(2+)-ATP酶活性增强，以及与缺血性脑钙超载损伤的关系。

方法

通过给大鼠腹腔注射1mg·kg-1·d-1的Lev，连续7天，建立缺血性脑实验性甲状腺功能亢进模型。测定Ca2+ Mg(2+)-ATP酶活性及其动力学参数。

结果

对照组大鼠脑线粒体Ca2+ Mg(2+)-ATP酶的活性、Vmax和Km分别为3.1±0.8、5.1±2.3mmol·P(i)·h-1/g蛋白和0.81±0.08mmol·L-1（ATP），而甲状腺功能亢进大鼠的这些参数显著改变为4.6±0.5、8.5±1.9mmol·P(i)·h-1/g蛋白和0.49±0.11mmol·L-1（ATP）。用10或20mg·kg-1·d-1的Bep腹腔注射治疗3天后，该酶的上述3个参数与对照组或甲状腺功能亢进组相比均非常显著降低。