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Flavonoid baicalein modulates H2O2-induced mitogen-activated protein kinases activation and cell death in SK-N-MC cells.
Cell Mol Neurobiol. 2012 May; 32(4):549-60.CM

Abstract

It is believed that ROS-induced oxidative stress triggers numerous signaling pathways which are involved in neurodegenerative diseases, including Alzheimer's disease. To find the effective drugs for neurodegenerative diseases, the deep delve into molecular mechanisms underlie these diseases is necessary. In the current study, we investigated the effects of flavonoid baicalein on H(2)O(2)-induced oxidative stress and cell death in SK-N-MC cells. Our results revealed that the treatment of SK-N-MC cells with H(2)O(2) led to a decrease in cell viability through phosphorylation and activation of extracellular signal-regulated kinases (ERKs) and c-Jun N-terminal kinases (JNKs) pathways followed by increase in Bax/Bcl2 ratio and initiation of caspase-dependent apoptotic pathways. In addition, our results showed that the exposure of SK-N-MC cells to H(2)O(2) ended up in reduction of glutathione (GSH) levels of SK-N-MC cells via JNK/ERK-mediated down-regulation of γ-glutamyl-cysteine synthetase (γ-GCS) expression. Our results demonstrated that flavonoid baicalein protected against H(2)O(2)-induced cell death by inhibition of JNK/ERK pathways activation and other key molecules in apoptotic pathways, including blockage of Bax and caspase-9 activation, induction of Bcl-2 expression and prevention of cell death. Baicalein supported intracellular defense mechanisms through maintaining GSH levels in SK-N-MC cells by the removal of inhibition effects of JNK/ERK pathways from γ-GCS expression. In addition, baicalein attenuated lipid and protein peroxidation and intracellular reactive oxygen species in SK-N-MC cells. In accordance with these observations, baicalein can be a promising candidate in antioxidant therapy and designing of natural-based drug for ROS-induced neurodegenerative disorders.

Authors+Show Affiliations

Institute of Biochemistry and Biophysics, University of Tehran, Tehran, Iran.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22246135

Citation

Moslehi, Maryam, et al. "Flavonoid Baicalein Modulates H2O2-induced Mitogen-activated Protein Kinases Activation and Cell Death in SK-N-MC Cells." Cellular and Molecular Neurobiology, vol. 32, no. 4, 2012, pp. 549-60.
Moslehi M, Meshkini A, Yazdanparast R. Flavonoid baicalein modulates H2O2-induced mitogen-activated protein kinases activation and cell death in SK-N-MC cells. Cell Mol Neurobiol. 2012;32(4):549-60.
Moslehi, M., Meshkini, A., & Yazdanparast, R. (2012). Flavonoid baicalein modulates H2O2-induced mitogen-activated protein kinases activation and cell death in SK-N-MC cells. Cellular and Molecular Neurobiology, 32(4), 549-60. https://doi.org/10.1007/s10571-011-9795-x
Moslehi M, Meshkini A, Yazdanparast R. Flavonoid Baicalein Modulates H2O2-induced Mitogen-activated Protein Kinases Activation and Cell Death in SK-N-MC Cells. Cell Mol Neurobiol. 2012;32(4):549-60. PubMed PMID: 22246135.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Flavonoid baicalein modulates H2O2-induced mitogen-activated protein kinases activation and cell death in SK-N-MC cells. AU - Moslehi,Maryam, AU - Meshkini,Azadeh, AU - Yazdanparast,Razieh, Y1 - 2012/01/14/ PY - 2011/11/16/received PY - 2011/12/26/accepted PY - 2012/1/17/entrez PY - 2012/1/17/pubmed PY - 2013/2/1/medline SP - 549 EP - 60 JF - Cellular and molecular neurobiology JO - Cell Mol Neurobiol VL - 32 IS - 4 N2 - It is believed that ROS-induced oxidative stress triggers numerous signaling pathways which are involved in neurodegenerative diseases, including Alzheimer's disease. To find the effective drugs for neurodegenerative diseases, the deep delve into molecular mechanisms underlie these diseases is necessary. In the current study, we investigated the effects of flavonoid baicalein on H(2)O(2)-induced oxidative stress and cell death in SK-N-MC cells. Our results revealed that the treatment of SK-N-MC cells with H(2)O(2) led to a decrease in cell viability through phosphorylation and activation of extracellular signal-regulated kinases (ERKs) and c-Jun N-terminal kinases (JNKs) pathways followed by increase in Bax/Bcl2 ratio and initiation of caspase-dependent apoptotic pathways. In addition, our results showed that the exposure of SK-N-MC cells to H(2)O(2) ended up in reduction of glutathione (GSH) levels of SK-N-MC cells via JNK/ERK-mediated down-regulation of γ-glutamyl-cysteine synthetase (γ-GCS) expression. Our results demonstrated that flavonoid baicalein protected against H(2)O(2)-induced cell death by inhibition of JNK/ERK pathways activation and other key molecules in apoptotic pathways, including blockage of Bax and caspase-9 activation, induction of Bcl-2 expression and prevention of cell death. Baicalein supported intracellular defense mechanisms through maintaining GSH levels in SK-N-MC cells by the removal of inhibition effects of JNK/ERK pathways from γ-GCS expression. In addition, baicalein attenuated lipid and protein peroxidation and intracellular reactive oxygen species in SK-N-MC cells. In accordance with these observations, baicalein can be a promising candidate in antioxidant therapy and designing of natural-based drug for ROS-induced neurodegenerative disorders. SN - 1573-6830 UR - https://www.unboundmedicine.com/medline/citation/22246135/Flavonoid_baicalein_modulates_H2O2_induced_mitogen_activated_protein_kinases_activation_and_cell_death_in_SK_N_MC_cells_ L2 - https://doi.org/10.1007/s10571-011-9795-x DB - PRIME DP - Unbound Medicine ER -