J Nutr Health.  2023 Apr;56(2):140-154. 10.4163/jnh.2023.56.2.140.

Neuroprotective effect of Deodeok (Codonopsis lanceolata) bud extracts in H2O2 -stimulated SH-SY5Y cells

  • 1Department of Agrofood Resources, National Institute of Agricultural Science, Rural Development Administration, Wanju 55365, Korea


Deodeok (Codonopsis lanceolata) is generally used in conventional medicines and is considered to have remedial properties to cure several diseases. However, application of the C. lanceolata bud as a novel food ingredient has not been fully explored. Hydrogen peroxide (H2O2) is associated with the production of oxidative damage that results in mutagenesis, carcinogenesis, and cell death. This study examines the neuroprotective effect of C. lanceolata bud extracts (CLBE) on H2O2 -stimulated apoptosis in SH-SY5Y cells.
C. lanceolata bud of length 10 to 15 cm was collected and extracted using 70% ethanol. Cytotoxicity was evaluated by the EZ-cytox reagent, measurement of lactic dehydrogenase (LDH) release and reactive oxygen species (ROS). The morphological changes of the nuclei were determined using the Hoechst 33258 dye. Enzyme activities were analyzed using the caspase activity assay kit. Related protein expressions were quantified by the Western blot immunoassay in H2O2 -stimulated SH-SY5Y cells.
Cell viability, LDH release and ROS generation, demonstrated neuroprotective effects of CLBE in H2O2-stimulated SH-SY5Y cells. The occurrence of apoptosis in H2O2-stimulated cells was confirmed by caspase activity, which was increased in H2O2-stimulated SH-SY5Y cells compared to the unexposed group. Pretreatment of CLBE was observed to inhibit the H2O2–stimulated apoptosis. In addition, exposure to CLBE resulted in increased expression of the Bcl-2 (B cell lymphoma 2) protein and decreased expression of the Bax (Bcl2 associated X) protein.
This study shows that exposure to CLBE alleviates the H2O2-stimulated neuronal damage in SH-SY5Y cells. Our results indicate the potential application of CLBE in neurodegenerative disease therapy or prevention.


neuroprotective effect; oxidative stress; neuroblastoma; apoptosis
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