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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 protects SH-SY5Y cells against rotenone induced apoptosis. (a) Photomicrograph showing the antiapoptotic effect of vanillin (100 nM) against rotenone at a concentration of 100 nM effective dose. (A) Control, (B) rotenone, (C) vanillin + rotenone, and (D) vanillin. (b) Rotenone (100 nM) treatment induced cell apoptosis compared to control cells; pretreatment with vanillin (100 nM) suppresses these apoptotic features. Values are given as mean ± SD of four independent experiments in each group. ∗p < 0.05 compared to control and #p < 0.05 compared to rotenone group (DMRT).
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fig6: Vanillin protects SH-SY5Y cells against rotenone induced apoptosis. (a) Photomicrograph showing the antiapoptotic effect of vanillin (100 nM) against rotenone at a concentration of 100 nM effective dose. (A) Control, (B) rotenone, (C) vanillin + rotenone, and (D) vanillin. (b) Rotenone (100 nM) treatment induced cell apoptosis compared to control cells; pretreatment with vanillin (100 nM) suppresses these apoptotic features. Values are given as mean ± SD of four independent experiments in each group. ∗p < 0.05 compared to control and #p < 0.05 compared to rotenone group (DMRT).

Mentions: Double staining of rotenone and vanillin treated SH-SY5Y cells, with AO and EB, was used to determine the rate of apoptosis. Control cells which fluoresced brightly with green nuclei and normal morphology were showed in Figure 6(a). In contrast, at 100 nM rotenone exposure, cells revealed orange luminescent apoptotic body formation, when compared to control (p < 0.05), and treatment with vanillin increased cell viability and decreased apoptotic cell death when compared to cells exposed merely to rotenone (Figure 6(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)

Vanillin protects SH-SY5Y cells against rotenone induced apoptosis. (a) Photomicrograph showing the antiapoptotic effect of vanillin (100 nM) against rotenone at a concentration of 100 nM effective dose. (A) Control, (B) rotenone, (C) vanillin + rotenone, and (D) vanillin. (b) Rotenone (100 nM) treatment induced cell apoptosis compared to control cells; pretreatment with vanillin (100 nM) suppresses these apoptotic features. Values are given as mean ± SD of four independent experiments in each group. ∗p < 0.05 compared to control and #p < 0.05 compared to rotenone group (DMRT).
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4664805&req=5

fig6: Vanillin protects SH-SY5Y cells against rotenone induced apoptosis. (a) Photomicrograph showing the antiapoptotic effect of vanillin (100 nM) against rotenone at a concentration of 100 nM effective dose. (A) Control, (B) rotenone, (C) vanillin + rotenone, and (D) vanillin. (b) Rotenone (100 nM) treatment induced cell apoptosis compared to control cells; pretreatment with vanillin (100 nM) suppresses these apoptotic features. Values are given as mean ± SD of four independent experiments in each group. ∗p < 0.05 compared to control and #p < 0.05 compared to rotenone group (DMRT).
Mentions: Double staining of rotenone and vanillin treated SH-SY5Y cells, with AO and EB, was used to determine the rate of apoptosis. Control cells which fluoresced brightly with green nuclei and normal morphology were showed in Figure 6(a). In contrast, at 100 nM rotenone exposure, cells revealed orange luminescent apoptotic body formation, when compared to control (p < 0.05), and treatment with vanillin increased cell viability and decreased apoptotic cell death when compared to cells exposed merely to rotenone (Figure 6(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