Abstract

Oxidative stress, which is induced by reactive oxygen species (ROS), causes cellular damage which contributes to the pathogenesis of neurodegenerative diseases. Momordica charantia (MC), a traditional medicinal plant, is known to have a variety of health benefits, such as antidiabetic, anti-inflammatory, and antioxidant effects. However, it is unknown whether MC has protective effects against oxidative stress-induced neuronal cell death. The aim of this study was to investigate the potential action of MC on oxidative stress induced by H2O2. First, we tested whether the pretreatment of Momordica charantia ethanol extract (MCEE) attenuates H2O2-induced cell death in human neuroblastoma SK-N-MC cells. MCEE pretreatment significantly improved cell viability and apoptosis that deteriorated by H2O2. Further, MCEE ameliorated the imbalance between intracellular ROS production and removal through the enhancement of the intracellular antioxidant system. Intriguingly, the inhibition of apoptosis was followed by the blockage of mitochondria-dependent cell death cascades and suppression of the phosphorylation of the mitogen-activated protein kinase signaling (MAPKs) pathway by MCEE. Taken together, MCEE was shown to be effective in protecting against H2O2-induced cell death through its antioxidant and anti-apoptotic properties.

Highlights

  • Neurodegenerative diseases (NDs), which are commonly associated with aging, are caused by the loss of progressive neuronal function [1,2,3]

  • We demonstrate that Momordica charantia (MC) inhibits apoptosis by inhibiting the mitochondria-dependent apoptosis pathway and the mitogen-activated protein kinase signaling (MAPKs) pathway

  • Effect of the Momordica charantia ethanol extract (MCEE) on H2 O2 -Induced Cytotoxicity in SK-N-MC Cells. It is well-recognized that the human neuroblastoma SK-N-MC cell, which is induced by oxidative stress by H2 O2, is a good in vitro model of NDs due to its high stability and homogeneity [1,30]

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Summary

Introduction

Neurodegenerative diseases (NDs), which are commonly associated with aging, are caused by the loss of progressive neuronal function [1,2,3]. NDs, including Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), and amyotrophic lateral sclerosis (ALS), are characterized by the progressive loss of cognition (dementia) and motor impairment (ataxia) [4,5,6] These cognitive and motor impairments affect the life quality and life span of elderly individuals [7]. Health Organization (WHO) report (2005), the ND-related mortality rate will continue to increase to the second most common cause of death, following cardiovascular disease, by 2040 [8]. For this reason, identification of therapeutic agents for NDs is required for public health in modern society, especially considering the rapidly expanding elderly population [9].

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