K Y Jiang1, Z N Qian. 1. Department of Pharmacology, Suzhou Medical College, China.
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.
AIM: To study cerebral protective mechanism of Panax notoginsengsaponins (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.
Authors: Ye Xiong; Ling Shen; Kristina J Liu; Patrick Tso; Yuqing Xiong; Guangji Wang; Stephen C Woods; Min Liu Journal: Diabetes Date: 2010-08-03 Impact factor: 9.461