芍药苷对蒙古沙鼠脑缺血后能量代谢、一氧化氮及一氧化氮合酶的影响

[Effects of paeoniflorin on cerebral energy metabolism, nitric oxide and nitric oxide synthase after cerebral ischemia in mongoliagerbils].

作者信息

Sun Rong, Lv Li-li, Liu Guo-qing

机构信息

Department of pharmacology, China Pharmaceutical University, Nanjing 210009, China.

出版信息

Zhongguo Zhong Yao Za Zhi. 2006 May;31(10):832-5.

PMID:17048669

Abstract

OBJECTIVE

To explore the effects of paeoniflorin on antagonising the delayed neuronal death (DND) induced by cerebral ischemia,and the relation between DND, cerebral tissue energy metabolism, nitric oxide (NO) and nitric oxide synthase (NOS).

METHOD

Incomplete cerebral ischemia induced was induced by ligating bilateral arteries carotis communis for 20 min followed by reperfusion 48 h in rats. The indexes including Na(+)-K(+)-ATPase activity, lactic acid content, Ca(2+)-ATPase, Mg(2+)-ATPase activity, NO content and NOS activity were determined in fore brain cortex at 48 h after reperfusion.

RESULT

Na(+)-K(+)-ATPase, Ca(2+)-ATPase and Mg(2+)-ATPase activity were lowered (P < 0.01), NO level was decreased (P < 0.01), NOS activity dropped (P < 0.01) in cerebral tissue at 48h after reperfusion, but lactic acid level had no change. Paeoniflorin could prevent reduction of Na(+)-K(+)-ATPase activity (P < 0.05, P < 0.01), increase NO level (P < 0.01), enhance NOS activity (P < 0.01) at 48h after reperfusion.

CONCLUSION

DND induced by ischemia may be concerned with energy metabolism disorder and decrease of NO formation. Paeoniflorin may play the role of antagonising cerebral ischemia by adjusting cerebral energy metabolism and nitric oxide formation.

摘要

目的

探讨芍药苷对拮抗脑缺血诱导的迟发性神经元死亡（DND）的作用，以及DND与脑组织能量代谢、一氧化氮（NO）和一氧化氮合酶（NOS）之间的关系。

方法

通过结扎大鼠双侧颈总动脉20分钟，随后再灌注48小时诱导不完全性脑缺血。在再灌注48小时后，测定前脑皮质中的Na(+)-K(+)-ATP酶活性、乳酸含量、Ca(2+)-ATP酶、Mg(2+)-ATP酶活性、NO含量和NOS活性等指标。

结果

再灌注48小时后，脑组织中Na(+)-K(+)-ATP酶、Ca(2+)-ATP酶和Mg(2+)-ATP酶活性降低（P<0.01），NO水平下降（P<0.01），NOS活性降低（P<0.01），但乳酸水平无变化。芍药苷可在再灌注48小时后防止Na(+)-K(+)-ATP酶活性降低（P<0.05，P<0.01），提高NO水平（P<0.01），增强NOS活性（P<0.01）。