Protect effects of Qingkailing injection on mitochondrion membrane potential during injury induced by hypoxia-hypoglycemia and reoxygenation in cultured rat hippocampal neurons.
- Author:
He PANG
1
;
Ling-qun ZHU
;
Fu-ling NIU
;
Wei CUI
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; drug effects; Calcium; metabolism; Cell Hypoxia; Cells, Cultured; Drug Combinations; Drugs, Chinese Herbal; administration & dosage; isolation & purification; pharmacology; Hippocampus; pathology; Hypoglycemia; pathology; Injections; Membrane Potentials; drug effects; Mitochondria; physiology; Neurons; pathology; Neuroprotective Agents; administration & dosage; isolation & purification; pharmacology; Plants, Medicinal; chemistry; Random Allocation; Rats; Rats, Wistar
- From: China Journal of Chinese Materia Medica 2005;30(23):1852-1855
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the protect effects of Qingkailing injection on mitochondrion membrane potential (MMP) during injury induced by hypoxia-hypoglycemia and reoxygenation in cultured rat hippocampal neurons.
METHODMitochondrion activity was measured by methyl thiazolyl tetrazolium (MTT) test. MMP and apoptosis were measured by flow cytometry. intracellular free calcium concentration ([Ca2+]i) was measured with confocal laser scanning microscopy.
RESULTHypoxia-hypoglycemia cultures for 5 hour and reoxygenation for 3 hour induced intracellular[Ca2+]i and apoptosis rate significantly increased. The effects were increased with the extending time of reoxygenation. MMP and mitochondrion activity declined significantly after 3 hour reoxygenation. The effects were declined with the extending time of reoxygenation. Qingkailing injection might have significantly decrease intracellular [Ca2+]i and apoptosis rate, increase MMP and mitochondrion activity.
CONCLUSIONQingkailing Injection might have significantly inhibit the decline in MMP induced by hypoxia-hypoglycemia and reoxygenation, and had effects of stable it and anti-neuronal apoptosis. The effects might be related to inhibit overload of intracellular free calcium.
