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

Dhanalakshmi C, Manivasagam T, Nataraj J, Justin Thenmozhi A, Essa MM - Evid Based Complement Alternat Med (2015)

Bottom Line: 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.Our results indicated that the pretreatment of vanillin attenuated rotenone induced mitochondrial dysfunction, oxidative stress, and apoptosis.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry and Biotechnology, Annamalai University, Annamalainagar, Tamil Nadu 608002, India.

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.

No MeSH data available.


Related in: MedlinePlus

The protective effect of vanillin (5, 10, 20, 50, and 100 nM) against rotenone induced cell death was determined by MTT assay. Values are expressed as the percentage of the untreated control and represented as mean ± SD of four independent experiments in each group.
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fig3: The protective effect of vanillin (5, 10, 20, 50, and 100 nM) against rotenone induced cell death was determined by MTT assay. Values are expressed as the percentage of the untreated control and represented as mean ± SD of four independent experiments in each group.

Mentions: Figure 3 shows the protective effect of vanillin against rotenone induced injury (100 nM) with cell viability increasing to 84 ± 6.7% of control in the presence of 100 nM vanillin. So based on the dose-response data, the treatments of 100 nM vanillin and 100 nM rotenone were chosen for further experiments (Figure 3).


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

Dhanalakshmi C, Manivasagam T, Nataraj J, Justin Thenmozhi A, Essa MM - Evid Based Complement Alternat Med (2015)

The protective effect of vanillin (5, 10, 20, 50, and 100 nM) against rotenone induced cell death was determined by MTT assay. Values are expressed as the percentage of the untreated control and represented as mean ± SD of four independent experiments in each group.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4664805&req=5

fig3: The protective effect of vanillin (5, 10, 20, 50, and 100 nM) against rotenone induced cell death was determined by MTT assay. Values are expressed as the percentage of the untreated control and represented as mean ± SD of four independent experiments in each group.
Mentions: Figure 3 shows the protective effect of vanillin against rotenone induced injury (100 nM) with cell viability increasing to 84 ± 6.7% of control in the presence of 100 nM vanillin. So based on the dose-response data, the treatments of 100 nM vanillin and 100 nM rotenone were chosen for further experiments (Figure 3).

Bottom Line: 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.Our results indicated that the pretreatment of vanillin attenuated rotenone induced mitochondrial dysfunction, oxidative stress, and apoptosis.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry and Biotechnology, Annamalai University, Annamalainagar, Tamil Nadu 608002, India.

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.

No MeSH data available.


Related in: MedlinePlus