Neuroprotective effects of Momordica charantia extract against hydrogen peroxide-induced cytotoxicity in human neuroblastoma SK-N-MC cells.
10.4163/jnh.2017.50.5.415
- Author:
Kkot Byeol KIM
1
;
Seonah LEE
;
Jae Hyeok HEO
;
Jung Hee KIM
Author Information
1. Research Institute, Seoul Medical Center, Seoul 02053, Korea. nostoi72@naver.com
- Publication Type:Original Article
- Keywords:
Momordica charantia ethanol extract (MCE);
antioxidant;
MAPK pathway;
apoptosis;
SK-N-MC
- MeSH:
Apoptosis;
Blotting, Western;
Caspase 3;
Catechin;
Cell Death;
Cell Survival;
Down-Regulation;
Ethanol;
Gallic Acid;
Gene Expression;
Humans*;
Hydrogen*;
MAP Kinase Signaling System;
Mitogen-Activated Protein Kinases;
Momordica charantia*;
Momordica*;
Neuroblastoma*;
Neurons;
Neuroprotective Agents*;
Oxidative Stress;
Phenol;
Phosphorylation;
Reactive Oxygen Species;
Real-Time Polymerase Chain Reaction;
RNA, Messenger;
Sincalide
- From:Journal of Nutrition and Health
2017;50(5):415-425
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: Many studies have suggested that neuronal cells protect against oxidative stress-induced apoptotic cell death by polyphenolic compounds. We investigated the neuroprotective effects and the mechanism of action of Momordica charantia ethanol extract (MCE) against H₂O₂-induced cell death of human neuroblastoma SK-N-MC cells. METHODS: The antioxidant activity of MCE was measured by the quantity of total phenolic acid compounds (TPC), quantity of total flavonoid compounds (TFC), and 2,2-Diphenyl-1-pycrylhydrazyl (DPPH) radical scavenging activity. Cytotoxicity and cell viability were determined by CCK-8 assay. The formation of reactive oxygen species (ROS) was measured using 2,7-dichlorofluorescein diacetate (DCF-DA) assay. Antioxidant enzyme (SOD-1,2 and GPx-1) expression was determined by real-time PCR. Mitogen-activated protein kinases (MAPK) pathway and apoptosis signal expression was measured by Western blotting. RESULTS: The TPC and TFC quantities of MCE were 28.51 mg gallic acid equivalents/extract g and 3.95 mg catechin equivalents/extract g, respectively. The IC₅₀ value for DPPH radical scavenging activity was 506.95 µg/ml for MCE. Pre-treatment with MCE showed protective effects against H₂O₂-induced cell death and inhibited ROS generation by oxidative stress. SOD-1,2 and GPx-1 mRNA expression was recovered by pre-treatment with MCE compared with the presence of H₂O₂. Pre-treatment with MCE inhibited phosphorylation of p38 and the JNK pathway and down-regulated cleaved caspase-3 and cleaved PARP by H₂O₂. CONCLUSION: The neuroprotective effects of MCE in terms of recovery of antioxidant enzyme gene expression, down-regulation of MAPK pathways, and inhibition apoptosis is associated with reduced oxidative stress in SK-N-MC cells.
