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人参皂苷RB3对缺氧缺血性脑损伤的保护作用及其机制

[Protective effects of ginsenoside RB3 on hypoxic/ischemic brain injury and involved mechanisms].

作者信息

Shen Hong-mei, Zhang Zhi-jun, Jiang Shang, Jiang Zheng-lin

机构信息

Department of Basic Medicine, School of Medicine, Soozhow University, Suzhou 215123, China.

出版信息

Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2006 Aug;22(3):302-6.

Abstract

AIM

To observe protective effects and involved mechanism of ginsenoside Rb3 on hypoxic/ischemic brain injury, using cultured hippocampal neurons, rat hippocampal slices and intact animals.

METHODS

(1) Mice were tightly closed in glasses of 150 ml, and then survival time of them was observed. (2) During simulated ischemia and after reoxygenation, changes of orthodromic population spikes (OPS) in the area CA1 of hippocampal slice were investigated. (3) By using histochemistry, the expressions of NOS in CA1 area of rat hippocampus after hypoxic exposure were observed. (4) Using LDH detection, tests of total NOS, iNOS and cNOS activity, the protective effects of ginsenoside Rb3 were investigated on cultured hippocampal neurons treated with hypoxia.

RESULTS

(1) Given ginsenoside Rb3 (10 mmol/L), mice survived significantly longer than that of control group. (2) The occurrence of HIP (hypoxic injury potentials) decreased after administration of ginsenosides Rb3 (60 micromol/L) in many slices, while the recovery rate and amplitude of OPS after reoxygenation were significantly higher than those of the control group. (3) In CA1 area of rat hippocampus, NOS-positive neurons increased at the end of 24 h hypoxia and further 24 h reoxygenation, while the number of NOS-positive neurons decreased after treatment with ginsenoside Rb3. (4) The LDH leakage rate of cultured rat hippocampal neurons increased at the end of hypoxia, while it decreased after treatment with Rb3. Moreover the total NOS, especially iNOS activity of these neurons also decreased.

CONCLUSION

Ginsenoside Rb3 has a significant protective effect on hypoxic-ischemic injury of neurons, and this involves the stabilization of the cell membrane, the inhibition of the expression and activity of NOS, especially iNOS activity.

摘要

目的

采用培养的海马神经元、大鼠海马脑片和整体动物,观察人参皂苷Rb3对缺氧缺血性脑损伤的保护作用及其机制。

方法

(1) 将小鼠密闭于150 ml玻璃瓶中,观察其存活时间。(2) 在模拟缺血及复氧过程中,研究海马脑片CA1区顺向群体峰电位(OPS)的变化。(3) 采用组织化学方法,观察缺氧暴露后大鼠海马CA1区一氧化氮合酶(NOS)的表达。(4) 采用乳酸脱氢酶(LDH)检测、总NOS、诱导型NOS(iNOS)和组成型NOS(cNOS)活性检测,研究人参皂苷Rb3对缺氧处理的培养海马神经元的保护作用。

结果

(1) 给予人参皂苷Rb3(10 mmol/L)后,小鼠存活时间显著长于对照组。(2) 给予人参皂苷Rb3(60 μmol/L)后,许多脑片中缺氧损伤电位(HIP)的发生率降低,而复氧后OPS的恢复率和幅度显著高于对照组。(3) 在大鼠海马CA1区,缺氧24 h末及再复氧24 h后,NOS阳性神经元增多,而人参皂苷Rb3处理后NOS阳性神经元数量减少。(4) 缺氧结束时,培养的大鼠海马神经元LDH漏出率升高,而Rb3处理后降低。此外,这些神经元的总NOS,尤其是iNOS活性也降低。

结论

人参皂苷Rb3对神经元缺氧缺血损伤具有显著的保护作用,其机制可能与稳定细胞膜、抑制NOS尤其是iNOS的表达和活性有关。

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