Journal of Nutrition and Health  2015;48(5):451-456

doi:10.4163/jnh.2015.48.5.451

Anti-apoptotic effect of fermented Citrus sunki peel extract on chemical hypoxia-induced neuronal injury.

Woon Chul KO 1 ; Sun Ryung LEE

Affiliations

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Keywords

Citrus sunki; apoptosis; hypoxia; stroke; neuronal cells

Country

Republic of Korea

Language

Korean

MeSH

Abstract

PURPOSE: Neuronal apoptotic events induced by aging and hypoxic/ischemic conditions is an important risk factor in neurodegenerative diseases such as ischemia stroke and Alzheimer's disease. The peel of Citrus sunki Hort. ex Tanaka has long been used as a traditional medicine, based on multiple biological activities including anti-oxidant, anti-inflammation, and anti-obesity. In the current study, we examined the actions of fermented C. sunki peel extract against cobalt chloride (CoCl2)-mediated hypoxic death in human neuroblastoma SH-SY5Y cells. METHODS: Cell viability was measured by trypan blue exclusion. Expression of apoptosis related proteins and release of cytochrome c were detected by western blot. Production of intracellular reactive oxygen species (ROS) and apoptotic morphology were examined using 2',7'-dichlorofluorescin diacetate (DCF-DA) and 4',6-diamidino-2-phenylindole (DAPI) staining. RESULTS: Exposure to CoCl2, a well-known mimetic agent of hypoxic/ischemic condition, resulted in neuronal cell death via caspase-3 dependent pathway. Extract of fermented C. sunki peel significantly rescued the CoCl2-induced neuronal toxicity with the cell viability and appearance of apoptotic morphology. Cytoprotection with fermented C. sunki peel extract was associated with a decrease in activities of caspase-3 and cleavage of poly (ADP ribose) polymerase (PARP). In addition, increase in the intracellular ROS and release of cytochrome c from mitochondria to the cytosol were inhibited by treatment with extract of fermented C. sunki peel. CONCLUSION: Based on these data, fermented C. sunki peel extract might have a protective effect against CoCl2-induced neuronal injury partly through generation of ROS and effectors involved in mitochondrial mediated apoptosis.