Limits...
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

Effect of vanillin on rotenone induced cytotoxicity (MTT assay) in SH-SY5Y neuroblastoma cells. Cell viability was determined by measuring MTT method. (a) shows the dose-dependent effect of rotenone (5, 10, 50, 100, and 200 nM) induced cell toxicity after 24 h. An approximately half-maximal inhibition of cell viability was obtained at 100 nM rotenone concentration. (b) shows the dose-dependent effect of vanillin at various concentrations. Low concentrations (5, 10, 20, 50, 100, and 200 nM) did not induce any toxicity after 24 h treatment, whereas slight toxicity was induced at 500 μM concentration. 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


getmorefigures.php?uid=PMC4664805&req=5

fig2: Effect of vanillin on rotenone induced cytotoxicity (MTT assay) in SH-SY5Y neuroblastoma cells. Cell viability was determined by measuring MTT method. (a) shows the dose-dependent effect of rotenone (5, 10, 50, 100, and 200 nM) induced cell toxicity after 24 h. An approximately half-maximal inhibition of cell viability was obtained at 100 nM rotenone concentration. (b) shows the dose-dependent effect of vanillin at various concentrations. Low concentrations (5, 10, 20, 50, 100, and 200 nM) did not induce any toxicity after 24 h treatment, whereas slight toxicity was induced at 500 μM concentration. Values are expressed as the percentage of the untreated control and represented as mean ± SD of four independent experiments in each group.

Mentions: A dose-dependent cytotoxic effect of rotenone was evaluated by MTT assay in SH-SY5Y human neuroblastoma cells, which measures mitochondrial function or integrity with a dose of 100 nM which caused ~50% of cell death as compared with controls and was taken as inhibitory dose (Figures 2(a) and 2(b)).


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)

Effect of vanillin on rotenone induced cytotoxicity (MTT assay) in SH-SY5Y neuroblastoma cells. Cell viability was determined by measuring MTT method. (a) shows the dose-dependent effect of rotenone (5, 10, 50, 100, and 200 nM) induced cell toxicity after 24 h. An approximately half-maximal inhibition of cell viability was obtained at 100 nM rotenone concentration. (b) shows the dose-dependent effect of vanillin at various concentrations. Low concentrations (5, 10, 20, 50, 100, and 200 nM) did not induce any toxicity after 24 h treatment, whereas slight toxicity was induced at 500 μM concentration. 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

fig2: Effect of vanillin on rotenone induced cytotoxicity (MTT assay) in SH-SY5Y neuroblastoma cells. Cell viability was determined by measuring MTT method. (a) shows the dose-dependent effect of rotenone (5, 10, 50, 100, and 200 nM) induced cell toxicity after 24 h. An approximately half-maximal inhibition of cell viability was obtained at 100 nM rotenone concentration. (b) shows the dose-dependent effect of vanillin at various concentrations. Low concentrations (5, 10, 20, 50, 100, and 200 nM) did not induce any toxicity after 24 h treatment, whereas slight toxicity was induced at 500 μM concentration. Values are expressed as the percentage of the untreated control and represented as mean ± SD of four independent experiments in each group.
Mentions: A dose-dependent cytotoxic effect of rotenone was evaluated by MTT assay in SH-SY5Y human neuroblastoma cells, which measures mitochondrial function or integrity with a dose of 100 nM which caused ~50% of cell death as compared with controls and was taken as inhibitory dose (Figures 2(a) and 2(b)).

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