Abstract

Oxidative stress is considered a major cause of cellular injuries, including various clinical abnormalities. Here, the neuroprotective effect of extracts from the calyx of Diospyros kaki(DCE), peel of D. kaki (DPE), and flesh of D. kaki (DFE) of Diospyros kaki on oxidative stress-induced apoptosis in PC12 cells was investigated by an 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT) reduction assay. The results showed that H₂O₂significantly decreased cell viability (50.9%), and DCE exerted the highest neuroprotective effect on H₂O₂-induced cytotoxicity. We identified that treatment with DCE of H₂O₂-stressed PC12 cells caused dose-dependent suppression of H₂O₂-induced leakage of lactate dehydrogenase (LDH) as released amount (11.1 to 30.4%); we further verified these findings by observing morphological features. H₂O₂ also induced severe apoptosis of the PC12 cells, as determined by Hoechst 33342 staining and flow cytometric analysis. DCE (100, 500 µg/ml) exerted a significantly high protective effect on PC12 cells against H₂O₂-induced cell injury, and the percentage of cells in the sub-G1 phase decreased to 3.7 and 4.6%. These results suggest that DCE can protect cells against H₂O₂-induced apoptosis, and might be a potential therapeutic agent for treating or preventing neurodegenerative diseases that are related to oxidative stress.

Key words: Apoptosis, Diospyros kaki, neurodegenerative disease, neuroprotective effect, oxidative stress.