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Neuroprotective mechanisms of curcumin against cerebral ischemia-induced neuronal apoptosis and behavioral deficits.
J Neurosci Res. 2005 Oct 01; 82(1):138-48.JN

Abstract

Increased oxidative stress has been regarded as an important underlying cause for neuronal damage induced by cerebral ischemia/reperfusion (I/R) injury. In recent years, there has been increasing interest in investigating polyphenols from botanical source for possible neuroprotective effects against neurodegenerative diseases. In this study, we investigated the mechanisms underlying the neuroprotective effects of curcumin, a potent polyphenol antioxidant enriched in tumeric. Global cerebral ischemia was induced in Mongolian gerbils by transient occlusion of the common carotid arteries. Histochemical analysis indicated extensive neuronal death together with increased reactive astrocytes and microglial cells in the hippocampal CA1 area at 4 days after I/R. These ischemic changes were preceded by a rapid increase in lipid peroxidation and followed by decrease in mitochondrial membrane potential, increased cytochrome c release, and subsequently caspase-3 activation and apoptosis. Administration of curcumin by i.p. injections (30 mg/kg body wt) or by supplementation to the AIN76 diet (2.0 g/kg diet) for 2 months significantly attenuated ischemia-induced neuronal death as well as glial activation. Curcumin administration also decreased lipid peroxidation, mitochondrial dysfunction, and the apoptotic indices. The biochemical changes resulting from curcumin also correlated well with its ability to ameliorate the changes in locomotor activity induced by I/R. Bioavailability study indicated a rapid increase in curcumin in plasma and brain within 1 hr after treatment. Together, these findings attribute the neuroprotective effect of curcumin against I/R-induced neuronal damage to its antioxidant capacity in reducing oxidative stress and the signaling cascade leading to apoptotic cell death.

Authors+Show Affiliations

Department of Biochemistry, University of Missouri, Columbia, Missouri 65212, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

16075466

Citation

Wang, Qun, et al. "Neuroprotective Mechanisms of Curcumin Against Cerebral Ischemia-induced Neuronal Apoptosis and Behavioral Deficits." Journal of Neuroscience Research, vol. 82, no. 1, 2005, pp. 138-48.
Wang Q, Sun AY, Simonyi A, et al. Neuroprotective mechanisms of curcumin against cerebral ischemia-induced neuronal apoptosis and behavioral deficits. J Neurosci Res. 2005;82(1):138-48.
Wang, Q., Sun, A. Y., Simonyi, A., Jensen, M. D., Shelat, P. B., Rottinghaus, G. E., MacDonald, R. S., Miller, D. K., Lubahn, D. E., Weisman, G. A., & Sun, G. Y. (2005). Neuroprotective mechanisms of curcumin against cerebral ischemia-induced neuronal apoptosis and behavioral deficits. Journal of Neuroscience Research, 82(1), 138-48.
Wang Q, et al. Neuroprotective Mechanisms of Curcumin Against Cerebral Ischemia-induced Neuronal Apoptosis and Behavioral Deficits. J Neurosci Res. 2005 Oct 1;82(1):138-48. PubMed PMID: 16075466.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Neuroprotective mechanisms of curcumin against cerebral ischemia-induced neuronal apoptosis and behavioral deficits. AU - Wang,Qun, AU - Sun,Albert Y, AU - Simonyi,Agnes, AU - Jensen,Michael D, AU - Shelat,Phullara B, AU - Rottinghaus,George E, AU - MacDonald,Ruth S, AU - Miller,Dennis K, AU - Lubahn,Dennis E, AU - Weisman,Gary A, AU - Sun,Grace Y, PY - 2005/8/3/pubmed PY - 2006/2/8/medline PY - 2005/8/3/entrez SP - 138 EP - 48 JF - Journal of neuroscience research JO - J Neurosci Res VL - 82 IS - 1 N2 - Increased oxidative stress has been regarded as an important underlying cause for neuronal damage induced by cerebral ischemia/reperfusion (I/R) injury. In recent years, there has been increasing interest in investigating polyphenols from botanical source for possible neuroprotective effects against neurodegenerative diseases. In this study, we investigated the mechanisms underlying the neuroprotective effects of curcumin, a potent polyphenol antioxidant enriched in tumeric. Global cerebral ischemia was induced in Mongolian gerbils by transient occlusion of the common carotid arteries. Histochemical analysis indicated extensive neuronal death together with increased reactive astrocytes and microglial cells in the hippocampal CA1 area at 4 days after I/R. These ischemic changes were preceded by a rapid increase in lipid peroxidation and followed by decrease in mitochondrial membrane potential, increased cytochrome c release, and subsequently caspase-3 activation and apoptosis. Administration of curcumin by i.p. injections (30 mg/kg body wt) or by supplementation to the AIN76 diet (2.0 g/kg diet) for 2 months significantly attenuated ischemia-induced neuronal death as well as glial activation. Curcumin administration also decreased lipid peroxidation, mitochondrial dysfunction, and the apoptotic indices. The biochemical changes resulting from curcumin also correlated well with its ability to ameliorate the changes in locomotor activity induced by I/R. Bioavailability study indicated a rapid increase in curcumin in plasma and brain within 1 hr after treatment. Together, these findings attribute the neuroprotective effect of curcumin against I/R-induced neuronal damage to its antioxidant capacity in reducing oxidative stress and the signaling cascade leading to apoptotic cell death. SN - 0360-4012 UR - https://www.unboundmedicine.com/medline/citation/16075466/Neuroprotective_mechanisms_of_curcumin_against_cerebral_ischemia_induced_neuronal_apoptosis_and_behavioral_deficits_ L2 - https://doi.org/10.1002/jnr.20610 DB - PRIME DP - Unbound Medicine ER -