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三七总皂苷对体外培养神经元缺氧后细胞损伤的影响。

Effects of Panax notoginseng saponins on posthypoxic cell damage of neurons in vitro.

作者信息

Jiang K Y, Qian Z N

机构信息

Department of Pharmacology, Suzhou Medical College, China.

出版信息

Zhongguo Yao Li Xue Bao. 1995 Sep;16(5):399-402.

PMID:8701752
Abstract

AIM

To study cerebral protective mechanism of Panax notoginseng saponins (PNS).

METHODS

Cultured neurons of chick embryo cerebral hemisphere were used as an in vitro system for investigating the effects of PNS. The hypoxic cell damage of neurons cultured were induced by NaCN. The levels of adenosine triphosphate (ATP) were determined with HPLC. PNS was added 30 min before, beginning or after hypoxia.

RESULTS

PNS 50 and 100 mg L-1 retarded the break down of ATP of cultured neurons after 2-h hypoxia for 11.3 +/- 1.5 (P < 0.05) and 12.8 +/- 2.2 mumol/g protein (P < 0.01), respectively and accelerated the restoration of ATP during 30-min reoxygenation for 21.0 +/- 2.0 (P < 0.05) and 22.7 +/- 2.6 mumol/g protein (P < 0.01), respectively. PNS also reduced the release of creatine kinase (CK) from 75 +/- 8 kU L-1/g protein to 52 +/- 6 (P < 0.05) and 41 +/- 3 kU L-1/mg protein (P < 0.01), respectively and promoted the restoration of ATP of neurons 20 h after hypoxia when administered in the beginning of hypoxia from 13.0 +/- 0.9 mumol/g protein to 18.1 +/- 1.4 and 20.5 +/- 2.1 mumol/g protein (P < 0.01), respectively. PNS still promoted the restoration of ATP from 13.0 +/- 0.9 nmol/mg protein to 14.9 +/- 1.0 and 18.3 +/- 0.7 nmol/mg protein (P < 0.01), respectively and reduced (PNS 100 mg L-1) the CK release of neurons 20 h after hypoxia even when added in the recovery.

CONCLUSION

The protection against hypoxic damage of PNS was related to improving energy metabolism, preserving the structural integrity of neurons.

摘要

目的

研究三七总皂苷(PNS)的脑保护机制。

方法

以鸡胚大脑半球培养神经元作为体外研究系统,观察PNS的作用。用氰化钠诱导培养神经元的缺氧性细胞损伤。采用高效液相色谱法测定三磷酸腺苷(ATP)水平。在缺氧前30分钟、开始缺氧时或缺氧后加入PNS。

结果

PNS 50和100mg/L分别使培养神经元在缺氧2小时后ATP的分解延迟,其含量分别为11.3±1.5(P<0.05)和12.8±2.2μmol/g蛋白(P<0.01),并在复氧30分钟期间使ATP的恢复加速,其含量分别为21.0±2.0(P<0.05)和22.7±2.6μmol/g蛋白(P<0.01)。PNS还使肌酸激酶(CK)的释放分别从75±8kU/L/g蛋白降至52±6(P<0.05)和41±3kU/L/mg蛋白(P<0.01),并且在缺氧开始时给予PNS可促进缺氧20小时后神经元ATP的恢复,其含量分别从13.0±0.9μmol/g蛋白升至18.1±1.4和20.5±2.1μmol/g蛋白(P<0.01)。即使在恢复阶段加入PNS,它仍分别使ATP从13.0±0.9nmol/mg蛋白恢复至14.9±1.0和18.3±0.7nmol/mg蛋白(P<0.01),并使缺氧20小时后神经元的CK释放减少(PNS 100mg/L)。

结论

PNS对缺氧损伤的保护作用与改善能量代谢、维持神经元结构完整性有关。

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