摘要
目的:探讨三七总皂甙(PNS)的脑保护作用机制.方法:体外培养鸡胚脑神经细胞,用氰化钠造成缺氧,作为试验PNS作用的模型,细胞内三磷酸腺苷(ATP)和培养液中肌酸激酶浓度作为观察指标,分别用HPLC-UV和全自动生化分析仪定量.结果:缺氧前30min将PNS 50和100 mg L^(-1)加入到培养液中能明显延缓缺氧2h细胞内ATP的耗竭(分别为11.3±1.5和12.8±2.2μmol/g protein),促进再给氧30min时细胞内ATP的恢复(分别为21.0±2.0和22.7±2.6 μmol/g protein).PNS于缺氧开始或再给氧时给予,仍能促进再给氧期细胞内ATP的恢复,减少神经细胞内肌酸激酶的释放. 结论:PNS对培养神经细胞缺氧性损伤具有保护作用,其机制可能与改善能量代谢,保护细胞结构完整性有关.
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 μmol/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. 6μmol/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 μmol/g protein to 18- 1 ± 1.4 and 20. 5 ± 2. 1 μmol/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 recoverv.CONCLUSION: The protection against hypoxic damage of PNS was related to improving energy metabolism, preserving the structural integrity of neurons.
出处
《中国药理学报》
CSCD
1995年第5期399-402,共4页
Acta Pharmacologica Sinica
关键词
三七
人参
神经元
缺氧症
腺苷三磷酸
肌酸激酸
Panax notoginseng
ginseng
saponins
cultured cells
neurons
anoxia
adenosine triphosphate
creatine kinase