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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

Vanillin stabilizes MMP as stained by Rh-123. Rotenone (100 nM) significantly decreased mitochondria membrane potential, while cells that were pretreated with vanillin (100 nM) significantly increased MMP. Values are given as mean ± SD of four independent experiments in each group. ∗p < 0.05 compared to control; #p < 0.05 compared to rotenone groups (DMRT).
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fig5: Vanillin stabilizes MMP as stained by Rh-123. Rotenone (100 nM) significantly decreased mitochondria membrane potential, while cells that were pretreated with vanillin (100 nM) significantly increased MMP. Values are given as mean ± SD of four independent experiments in each group. ∗p < 0.05 compared to control; #p < 0.05 compared to rotenone groups (DMRT).

Mentions: Alteration in the MMP is considered to be one of the important events related to apoptosis. The effect of vanillin on MMP in rotenone induced toxicity was analyzed by measuring the uptake of Rh-123. In normal cells, Rh-123 steadily penetrates the cells, stains mitochondria, and exhibits high fluorescent intensity. The depolarization of MMP due to rotenone treatment results in the loss of Rh-123 from the mitochondria and a decrease in intracellular green fluorescence. Cell cultures pretreated with vanillin before rotenone treatment partially reduced this decline in fluorescence and approached control levels (Figure 5).


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)

Vanillin stabilizes MMP as stained by Rh-123. Rotenone (100 nM) significantly decreased mitochondria membrane potential, while cells that were pretreated with vanillin (100 nM) significantly increased MMP. Values are given as mean ± SD of four independent experiments in each group. ∗p < 0.05 compared to control; #p < 0.05 compared to rotenone groups (DMRT).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig5: Vanillin stabilizes MMP as stained by Rh-123. Rotenone (100 nM) significantly decreased mitochondria membrane potential, while cells that were pretreated with vanillin (100 nM) significantly increased MMP. Values are given as mean ± SD of four independent experiments in each group. ∗p < 0.05 compared to control; #p < 0.05 compared to rotenone groups (DMRT).
Mentions: Alteration in the MMP is considered to be one of the important events related to apoptosis. The effect of vanillin on MMP in rotenone induced toxicity was analyzed by measuring the uptake of Rh-123. In normal cells, Rh-123 steadily penetrates the cells, stains mitochondria, and exhibits high fluorescent intensity. The depolarization of MMP due to rotenone treatment results in the loss of Rh-123 from the mitochondria and a decrease in intracellular green fluorescence. Cell cultures pretreated with vanillin before rotenone treatment partially reduced this decline in fluorescence and approached control levels (Figure 5).

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