Protective effects of salidroside on injury induced by hypoxia/hypoglycemia in cultured neurons.
- Author:
Wen-sheng ZHANG
1
;
Ling-qun ZHU
;
Fu-ling NIU
;
Rui-chun DENG
;
Chuan-xiang MA
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; drug effects; Calcium; metabolism; Cell Hypoxia; drug effects; Glucosides; isolation & purification; pharmacology; Humans; Hypoglycemia; metabolism; pathology; L-Lactate Dehydrogenase; metabolism; Neurons; pathology; Neuroprotective Agents; pharmacology; Phenols; isolation & purification; pharmacology; Plants, Medicinal; chemistry; Rhodiola; chemistry
- From: China Journal of Chinese Materia Medica 2004;29(5):459-462
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the protective effects of salidroside on injury induced by hypoxia/hypoglycemia in cultured SH-SY5Y cell.
METHODApoptosis and intracellular free calcium concentration ([Ca2+]i) were measured by flow cytometry, morphological changes and neuronal necrosis were observed with fluorescence microscope, and the lactic dehydrogenate (LDH) release was measured by LDH kits.
RESULTHypoxia/hypoglycemia cultures for 2 hours induced neuronal apoptosis and necrosis. They were 18.59% (P < 0.01) and 4.94% (P < 0.01) respectively. There were morphological changes including chromatin condensation, nuclear fragmentation and formed apoptotic bodies after exposed to hypoxia/hypoglycemia for 2, 4, 6, 12 hours. After 2 hours of hypoxia/hypoglycemia, neuronal [Ca2+]i and the release of LDH were significantly increased. They were 8.46 nmol/L (P < 0.01) and 16.59% (P < 0.01) respectively. The effects were enhanced with the extending time of hypoxia/hypoglycemia. Salidroside might have significantly decreased the percentage of neuronal apoptosis and necrosis, reduced neuronal [Ca2+]i and the release of LDH. The effects of salidroside were strengthened with the increasing of Salidroside dosage.
CONCLUSIONSalidroside has effect of anti-neuronal apoptosis. This effect might be related to its function of decreasing intracellular free calcium concentration.
