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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

Structure of vanillin.
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fig1: Structure of vanillin.

Mentions: Since current therapies are ineffective in preventing degeneration of dopaminergic neurons, it is imperative to identify novel drugs that delay the progression of PD. Phytoconstituents, those of a dietary origin especially present in fruits, vegetables, and spices, have been a subject of intense investigation in recent years for their therapeutic potential in a multitude of age-related chronic ailments such as cardiovascular, endocrine, neoplastic, and neurodegenerative diseases [10–13]. Vanillin (4-hydroxy-3-methoxybenzaldehyde), whose chemical structure is shown in Figure 1, is the principal component of the bean and pod of tropical vanilla orchids (Vanilla planifolia, Vanilla tahitensis, and Vanilla pompona). It is one of the most widely used flavor components in beverage, food preservatives, cosmetics, and drugs industry, with an estimated annual worldwide consumption of more than 2000 tons [14]. Besides its industrial and food application, vanillin exhibits antimicrobial activity [15] as well as antimutagenic [16] and anticarcinogenic actions [17].


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)

Structure of vanillin.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig1: Structure of vanillin.
Mentions: Since current therapies are ineffective in preventing degeneration of dopaminergic neurons, it is imperative to identify novel drugs that delay the progression of PD. Phytoconstituents, those of a dietary origin especially present in fruits, vegetables, and spices, have been a subject of intense investigation in recent years for their therapeutic potential in a multitude of age-related chronic ailments such as cardiovascular, endocrine, neoplastic, and neurodegenerative diseases [10–13]. Vanillin (4-hydroxy-3-methoxybenzaldehyde), whose chemical structure is shown in Figure 1, is the principal component of the bean and pod of tropical vanilla orchids (Vanilla planifolia, Vanilla tahitensis, and Vanilla pompona). It is one of the most widely used flavor components in beverage, food preservatives, cosmetics, and drugs industry, with an estimated annual worldwide consumption of more than 2000 tons [14]. Besides its industrial and food application, vanillin exhibits antimicrobial activity [15] as well as antimutagenic [16] and anticarcinogenic actions [17].

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