Neurosupportive Role of Vanillin, a Natural Phenolic Compound, on Rotenone Induced Neurotoxicity in SH-SY5Y Neuroblastoma Cells

Chinnasamy Dhanalakshmi, Thamilarasan Manivasagam, Jagatheesan Nataraj, Arokiasamy Justin Thenmozhi, Musthafa Mohamed Essa

Research output: Contribution to journalArticle

32 Citations (Scopus)

Abstract

Vanillin, a phenolic compound, has been reported to offer neuroprotection against experimental Huntington's disease and global ischemia by virtue of its antioxidant, anti-inflammatory, and antiapoptotic properties. The present study aims to elucidate the underlying neuroprotective mechanism of vanillin in rotenone induced neurotoxicity. Cell viability was assessed by exposing SH-SY5Y cells to various concentrations of rotenone (5-200 nM) for 24 h. The therapeutic effectiveness of vanillin against rotenone was measured by pretreatment of vanillin at various concentrations (5-200 nM) and then incubation with rotenone (100 nM). Using effective dose of vanillin (100 nM), mitochondrial membrane potential, levels of reactive oxygen species (ROS), and expression patterns of apoptotic markers were assessed. Toxicity of rotenone was accompanied by the loss of mitochondrial membrane potential, increased ROS generation, release of cyt-c, and enhanced expressions of proapoptotic and downregulation of antiapoptotic indices via the upregulation of p38 and JNK-MAPK pathway proteins. Our results indicated that the pretreatment of vanillin attenuated rotenone induced mitochondrial dysfunction, oxidative stress, and apoptosis. Thus, vanillin may serve as a potent therapeutic agent in the future by virtue of its multiple pharmacological properties in the treatment of neurodegenerative diseases including PD.

Original languageEnglish
Article number626028
JournalEvidence-based Complementary and Alternative Medicine
Volume2015
DOIs
Publication statusPublished - 2015

Fingerprint

Rotenone
Neuroblastoma
Mitochondrial Membrane Potential
Reactive Oxygen Species
MAP Kinase Signaling System
Huntington Disease
p38 Mitogen-Activated Protein Kinases
vanillin
Neurodegenerative Diseases
Cell Survival
Oxidative Stress
Anti-Inflammatory Agents
Up-Regulation
Down-Regulation
Ischemia
Antioxidants
Pharmacology
Apoptosis
Therapeutics

ASJC Scopus subject areas

  • Complementary and alternative medicine

Cite this

Neurosupportive Role of Vanillin, a Natural Phenolic Compound, on Rotenone Induced Neurotoxicity in SH-SY5Y Neuroblastoma Cells. / Dhanalakshmi, Chinnasamy; Manivasagam, Thamilarasan; Nataraj, Jagatheesan; Justin Thenmozhi, Arokiasamy; Essa, Musthafa Mohamed.

In: Evidence-based Complementary and Alternative Medicine, Vol. 2015, 626028, 2015.

Research output: Contribution to journalArticle

@article{c86acc07f07a498b913aa28d5f62765e,
title = "Neurosupportive Role of Vanillin, a Natural Phenolic Compound, on Rotenone Induced Neurotoxicity in SH-SY5Y Neuroblastoma Cells",
abstract = "Vanillin, a phenolic compound, has been reported to offer neuroprotection against experimental Huntington's disease and global ischemia by virtue of its antioxidant, anti-inflammatory, and antiapoptotic properties. The present study aims to elucidate the underlying neuroprotective mechanism of vanillin in rotenone induced neurotoxicity. Cell viability was assessed by exposing SH-SY5Y cells to various concentrations of rotenone (5-200 nM) for 24 h. The therapeutic effectiveness of vanillin against rotenone was measured by pretreatment of vanillin at various concentrations (5-200 nM) and then incubation with rotenone (100 nM). Using effective dose of vanillin (100 nM), mitochondrial membrane potential, levels of reactive oxygen species (ROS), and expression patterns of apoptotic markers were assessed. Toxicity of rotenone was accompanied by the loss of mitochondrial membrane potential, increased ROS generation, release of cyt-c, and enhanced expressions of proapoptotic and downregulation of antiapoptotic indices via the upregulation of p38 and JNK-MAPK pathway proteins. Our results indicated that the pretreatment of vanillin attenuated rotenone induced mitochondrial dysfunction, oxidative stress, and apoptosis. Thus, vanillin may serve as a potent therapeutic agent in the future by virtue of its multiple pharmacological properties in the treatment of neurodegenerative diseases including PD.",
author = "Chinnasamy Dhanalakshmi and Thamilarasan Manivasagam and Jagatheesan Nataraj and {Justin Thenmozhi}, Arokiasamy and Essa, {Musthafa Mohamed}",
year = "2015",
doi = "10.1155/2015/626028",
language = "English",
volume = "2015",
journal = "Evidence-based Complementary and Alternative Medicine",
issn = "1741-427X",
publisher = "Hindawi Publishing Corporation",

}

TY - JOUR

T1 - Neurosupportive Role of Vanillin, a Natural Phenolic Compound, on Rotenone Induced Neurotoxicity in SH-SY5Y Neuroblastoma Cells

AU - Dhanalakshmi, Chinnasamy

AU - Manivasagam, Thamilarasan

AU - Nataraj, Jagatheesan

AU - Justin Thenmozhi, Arokiasamy

AU - Essa, Musthafa Mohamed

PY - 2015

Y1 - 2015

N2 - Vanillin, a phenolic compound, has been reported to offer neuroprotection against experimental Huntington's disease and global ischemia by virtue of its antioxidant, anti-inflammatory, and antiapoptotic properties. The present study aims to elucidate the underlying neuroprotective mechanism of vanillin in rotenone induced neurotoxicity. Cell viability was assessed by exposing SH-SY5Y cells to various concentrations of rotenone (5-200 nM) for 24 h. The therapeutic effectiveness of vanillin against rotenone was measured by pretreatment of vanillin at various concentrations (5-200 nM) and then incubation with rotenone (100 nM). Using effective dose of vanillin (100 nM), mitochondrial membrane potential, levels of reactive oxygen species (ROS), and expression patterns of apoptotic markers were assessed. Toxicity of rotenone was accompanied by the loss of mitochondrial membrane potential, increased ROS generation, release of cyt-c, and enhanced expressions of proapoptotic and downregulation of antiapoptotic indices via the upregulation of p38 and JNK-MAPK pathway proteins. Our results indicated that the pretreatment of vanillin attenuated rotenone induced mitochondrial dysfunction, oxidative stress, and apoptosis. Thus, vanillin may serve as a potent therapeutic agent in the future by virtue of its multiple pharmacological properties in the treatment of neurodegenerative diseases including PD.

AB - Vanillin, a phenolic compound, has been reported to offer neuroprotection against experimental Huntington's disease and global ischemia by virtue of its antioxidant, anti-inflammatory, and antiapoptotic properties. The present study aims to elucidate the underlying neuroprotective mechanism of vanillin in rotenone induced neurotoxicity. Cell viability was assessed by exposing SH-SY5Y cells to various concentrations of rotenone (5-200 nM) for 24 h. The therapeutic effectiveness of vanillin against rotenone was measured by pretreatment of vanillin at various concentrations (5-200 nM) and then incubation with rotenone (100 nM). Using effective dose of vanillin (100 nM), mitochondrial membrane potential, levels of reactive oxygen species (ROS), and expression patterns of apoptotic markers were assessed. Toxicity of rotenone was accompanied by the loss of mitochondrial membrane potential, increased ROS generation, release of cyt-c, and enhanced expressions of proapoptotic and downregulation of antiapoptotic indices via the upregulation of p38 and JNK-MAPK pathway proteins. Our results indicated that the pretreatment of vanillin attenuated rotenone induced mitochondrial dysfunction, oxidative stress, and apoptosis. Thus, vanillin may serve as a potent therapeutic agent in the future by virtue of its multiple pharmacological properties in the treatment of neurodegenerative diseases including PD.

UR - http://www.scopus.com/inward/record.url?scp=84948823201&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84948823201&partnerID=8YFLogxK

U2 - 10.1155/2015/626028

DO - 10.1155/2015/626028

M3 - Article

VL - 2015

JO - Evidence-based Complementary and Alternative Medicine

JF - Evidence-based Complementary and Alternative Medicine

SN - 1741-427X

M1 - 626028

ER -