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Nerve Protective Effect of Asiaticoside against Ischemia-Hypoxia in Cultured Rat Cortex Neurons

Tao Sun, Bin Liu, Peng Li

Department of Neurosurgery, Zaozhuang Hospital of Zaozhuang Coal Mining Group, Zaozhuang, Shangdong, China (mainland)

Med Sci Monit 2015; 21:3036-3041

DOI: 10.12659/MSM.894024

Available online:

Published: 2015-10-08

BACKGROUND: Asiaticoside is one of the main functional components of the natural plant Centella asiatica urban. Studies have reported it has several functions such as anti-depression and nerve cell protection. Asiaticoside can reduce the cerebral infarct size in acute focal cerebral ischemia in a mouse model and asiatic acid glycosides can significantly improve neurobehavioral scores. Currently, there is a lack of understanding of asiaticoside in regard to its neural protective mechanism in cerebral ischemia. This study aimed to solve this problem by using an ischemia-hypoxia cell model in vitro.
MATERIAL AND METHODS: An in vitro ischemia hypoxia cell model was successfully established by primary cultured newborn rat cortical neurons. After being treated by asiaticoside for 24 h, cell survival rate, lactate dehydrogenase release quantity, and B-cell lymphoma gene-2 (BCL-2), Bax, and caspase-3 protein expressions was detected.
RESULTS: After 10 nmol/L or 100 nmol/L of asiaticoside were given to the cells, cell survival rate increased significantly and presented concentration dependence. Asiaticoside can reduce lactate dehydrogenase release. Lactate dehydrogenase release in model cells is gradually reduced with the increase of asiaticoside concentration. The lactate dehydrogenase release in asiaticoside 10 nmol/L group, asiaticoside 100 nmol/L group and ischemia hypoxia group were 26.75±1.05, 22.36±2.87 and 52.35±5.46%, respectively (p<0.05). It was also found that asiaticoside could modulate the expression of apoptotic factors, including bcl-2, Bax, and caspase-3.
CONCLUSIONS: Asiaticoside helps to protect in vitro ischemia hypoxia neurons. This nerve cell protection may be mediated by the BCL-2 protein.

Keywords: Animals, Newborn, Animals, Apoptosis, Brain Ischemia - drug therapy, Caspase 3 - metabolism, Cell Survival, Cells, Cultured, Centella - chemistry, Cerebral Cortex - pathology, Dilazep - chemistry, Frontal Lobe - pathology, Gene Expression Regulation - drug effects, Hypoxia-Ischemia, Brain - drug therapy, L-Lactate Dehydrogenase - metabolism, Memory, Neurons - pathology, Neuroprotective Agents - chemistry, Proto-Oncogene Proteins c-bcl-2 - metabolism, Rats, Rats, Sprague-Dawley, Triterpenes - chemistry, bcl-2-Associated X Protein - metabolism