Journal of Pure and Applied MicrobiologyVol. 8 No. Special Edition Nov. 2014

Effects of Ganoderma Acid Extract on the SOD and Mitochondrion in Zero-Mg2+ Induced Epileptic Hippocampal Neurons

Junxing Liu1, Xiaoguang Liu1, Yan Liu1, Zhiwei Yang1, Fei Wu1, Lin Wang2*, Shuqiu Wang1*, Xiaorui Ma1 and Lei Liu1

1School of Basic Medical Sciences, Jiamusi University, Jiamusi 154007, P. R. China. 2The First Affiliated Hospital of Jiamusi University, Jiamusi 154003, P. R. China.

Received on 06 June 2014 and accepted on 21 October 2014



Ganoderma lucidum has been used as a traditional medicinal herb for centuries in China, and its acid extract (ganoderic acid extract, GAE) has shown some antiepileptic effects in the animal models. This was the study of the effects of GAE on the superoxide dismutase (SOD) and mitochondria in cultured primary hippocampal neurons, treated by the Mg2+ free medium, in order to aid our understanding of interactions involving GAE with the epileptiform discharge hippocampal neurons and warrant the experimental aspects for the novel anti-epilepsy agents. The SOD vigour was determined by the xanthine oxidase assay, the variations of mitochondrial membrane potential and cell apoptosis were measured by the JC-1 fluorescent staining and flow cytometry. Our results revealed that the SOD activity and mitochondrial membrane potential (117.68 U/mg pro and 244.08) of the epileptiform discharge hippocampal neurons were significantly lower than the normal ones (135.95 U/mg pro and 409.81), associated with the obvious increase of cell apoptosis (61.39 vs. 28.84). These circumstances can be reversed, with the treatment of GAE (123.86 U/mg pro, 386.92 and 14.37). It indicated that GAE can significantly improve the SOD activity and mitochondrial dysfunction, stabilize the mitochondrial membrane potential, and thereby protect the hippocampal neurons by inhibiting the apoptosis.

Keywords : Ganoderic acid extract; Epileptiform hippocampal neurons; SOD; Mitochondrial membrane potential; Cell apoptosis.