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Curcumin ameliorates dopaminergic neuronal oxidative damage via activation of the Akt/Nrf2 pathway.
Mol Med Rep. 2016 Feb; 13(2):1381-8.MM

Abstract

Parkinson's disease (PD) is an age-related complex neurodegenerative disease that affects ≤ 80% of dopaminergic neurons in the substantia nigra pars compacta (SNpc). It has previously been suggested that mitochondrial dysfunction, oxidative stress and oxidative damage underlie the pathogenesis of PD. Curcumin, which is a major active polyphenol component extracted from the rhizomes of Curcuma longa (Zingiberaceae), has been reported to exert neuroprotective effects on an experimental model of PD. The present study conducted a series of in vivo experiments, in order to investigate the effects of curcumin on behavioral deficits, oxidative damage and related mechanisms. The results demonstrated that curcumin was able to significantly alleviate motor dysfunction and increase suppressed tyrosine hydroxylase (TH) activity in the SNpc of rotenone (ROT)-injured rats. Biochemical measurements indicated that rats pretreated with curcumin exhibited increased glutathione (GSH) levels, and reduced reactive oxygen species activity and malondialdehyde content. Mechanistic studies demonstrated that curcumin significantly restored the expression levels of heme oxygenase-1 and

NAD(P)H

quinone oxidoreductase 1, thus ameliorating ROT-induced damage in vivo, via the phosphorylation of Akt and nuclear factor erythroid 2-related factor 2 (Nrf2). Further studies indicated that the Akt/Nrf2 signaling pathway was associated with the protective role of curcumin in ROT-treated rats. Inhibiting the Akt/Nrf2 pathway using a lentiviral vector containing Nrf2-specific short hairpin RNA, or the phosphoinositide 3-kinase inhibitor LY294002, markedly reduced the expression levels of TH and GSH, ultimately attenuating the neuroprotective effects of curcumin against oxidative damage. These results indicated that curcumin was able to significantly ameliorate ROT-induced dopaminergic neuronal oxidative damage in the SNpc of rats via activation of the Akt/Nrf2 signaling pathway.

Authors+Show Affiliations

Department of Neurology, The Second Teaching Hospital of Zhengzhou University, Zhengzhou, Henan 450014, P.R. China.Department of Neurology, The Second Teaching Hospital of Zhengzhou University, Zhengzhou, Henan 450014, P.R. China.Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, P.R. China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

26648392

Citation

Cui, Qunli, et al. "Curcumin Ameliorates Dopaminergic Neuronal Oxidative Damage Via Activation of the Akt/Nrf2 Pathway." Molecular Medicine Reports, vol. 13, no. 2, 2016, pp. 1381-8.
Cui Q, Li X, Zhu H. Curcumin ameliorates dopaminergic neuronal oxidative damage via activation of the Akt/Nrf2 pathway. Mol Med Rep. 2016;13(2):1381-8.
Cui, Q., Li, X., & Zhu, H. (2016). Curcumin ameliorates dopaminergic neuronal oxidative damage via activation of the Akt/Nrf2 pathway. Molecular Medicine Reports, 13(2), 1381-8. https://doi.org/10.3892/mmr.2015.4657
Cui Q, Li X, Zhu H. Curcumin Ameliorates Dopaminergic Neuronal Oxidative Damage Via Activation of the Akt/Nrf2 Pathway. Mol Med Rep. 2016;13(2):1381-8. PubMed PMID: 26648392.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Curcumin ameliorates dopaminergic neuronal oxidative damage via activation of the Akt/Nrf2 pathway. AU - Cui,Qunli, AU - Li,Xin, AU - Zhu,Hongcan, Y1 - 2015/12/08/ PY - 2015/01/19/received PY - 2015/11/06/accepted PY - 2015/12/10/entrez PY - 2015/12/10/pubmed PY - 2016/11/1/medline SP - 1381 EP - 8 JF - Molecular medicine reports JO - Mol Med Rep VL - 13 IS - 2 N2 - UNLABELLED: Parkinson's disease (PD) is an age-related complex neurodegenerative disease that affects ≤ 80% of dopaminergic neurons in the substantia nigra pars compacta (SNpc). It has previously been suggested that mitochondrial dysfunction, oxidative stress and oxidative damage underlie the pathogenesis of PD. Curcumin, which is a major active polyphenol component extracted from the rhizomes of Curcuma longa (Zingiberaceae), has been reported to exert neuroprotective effects on an experimental model of PD. The present study conducted a series of in vivo experiments, in order to investigate the effects of curcumin on behavioral deficits, oxidative damage and related mechanisms. The results demonstrated that curcumin was able to significantly alleviate motor dysfunction and increase suppressed tyrosine hydroxylase (TH) activity in the SNpc of rotenone (ROT)-injured rats. Biochemical measurements indicated that rats pretreated with curcumin exhibited increased glutathione (GSH) levels, and reduced reactive oxygen species activity and malondialdehyde content. Mechanistic studies demonstrated that curcumin significantly restored the expression levels of heme oxygenase-1 and NAD(P)H: quinone oxidoreductase 1, thus ameliorating ROT-induced damage in vivo, via the phosphorylation of Akt and nuclear factor erythroid 2-related factor 2 (Nrf2). Further studies indicated that the Akt/Nrf2 signaling pathway was associated with the protective role of curcumin in ROT-treated rats. Inhibiting the Akt/Nrf2 pathway using a lentiviral vector containing Nrf2-specific short hairpin RNA, or the phosphoinositide 3-kinase inhibitor LY294002, markedly reduced the expression levels of TH and GSH, ultimately attenuating the neuroprotective effects of curcumin against oxidative damage. These results indicated that curcumin was able to significantly ameliorate ROT-induced dopaminergic neuronal oxidative damage in the SNpc of rats via activation of the Akt/Nrf2 signaling pathway. SN - 1791-3004 UR - https://www.unboundmedicine.com/medline/citation/26648392/Curcumin_ameliorates_dopaminergic_neuronal_oxidative_damage_via_activation_of_the_Akt/Nrf2_pathway_ L2 - http://www.spandidos-publications.com/mmr/13/2/1381 DB - PRIME DP - Unbound Medicine ER -