Protective effect of astragalosides on anoxia/reoxygenation injury of hippocampal neuron.
- Author:
Yan-Yan YIN
1
;
Fen-Fang ZHU
;
Guo-Cui WU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Calcium; metabolism; Cell Hypoxia; drug effects; Female; Fetus; Hippocampus; cytology; Malondialdehyde; metabolism; Neurons; cytology; Neuroprotective Agents; pharmacology; Nitric Oxide; metabolism; Pregnancy; Primary Cell Culture; methods; Rats; Rats, Sprague-Dawley; Reperfusion Injury; prevention & control; Saponins; pharmacology; Superoxide Dismutase; metabolism; Triterpenes; pharmacology
- From: Chinese Journal of Integrated Traditional and Western Medicine 2010;30(11):1173-1177
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the effect of astragalosides (AST) on the anoxia/reoxygenation (A/R) injured neuron in rat.
METHODSPrimary cultured rat's hippocampal neurons were made into A/R model cells. The cell viability was detected by MTT assay and lactate dehydrogenase releasing methods; the activity of superoxide dismutase (SOD), and contents of malondialdehyde (MDA) and nitride oxide (NO) in culture supernate were detected; the apoptosis rate of hippocampal neurons after A/R was measured by flow cytometry with double-staining of Hoechst33258 and AnnexinV-PI; and intracellular calcium ion [Ca2+]i was observed with a cofocal laser-scanning microscope and determined by fluorescent probe Fluo-3/AM.
RESULTSAST enhanced the cell viability of neurons after A/R injury, increased SOD activity and decreased the MDA and NO contents in supernate, reduced the A/R-induced apoptosis and decreased the calcium overload in neurons.
CONCLUSIONAST has the protective effects on A/R injured neurons, the mechanism is possibly related with its anti-oxidation and calcium overload reducing actions.
