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Neuroprotective effect of vasoactive intestinal peptide (VIP) in a mouse model of Parkinson's disease by blocking microglial activation.
FASEB J. 2003 May; 17(8):944-6.FJ

Abstract

Parkinson's disease (PD) is a common neurodegenerative disorder with no effective protective treatment, characterized by a massive degeneration of dopaminergic neurons in the substantia nigra (SNpc) and the subsequent loss of their projecting nerve fibers in the striatum. To elucidate PD pathogenic factors, and thus to develop therapeutic strategies, a murine PD model based on the administration of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) has been used extensively. It has been demonstrated that activated microglia cells actively participate in the pathogenesis of MPTP-induced PD through the release of cytotoxic factors. Because current treatments for PD are not effective, considerable research focused lately on a number of regulatory molecules termed microglia-deactivating factors. Vasoactive intestinal peptide (VIP), a neuropeptide with a potent anti-inflammatory effect, has been found to be protective in several inflammatory disorders. This study investigates the putative protective effect of VIP in the MPTP model for PD. VIP treatment significantly decreases MPTP-induced dopaminergic neuronal loss in SNpc and nigrostriatal nerve-fiber loss. VIP prevents MPTP-induced activation of microglia in SNpc and striatum and the expression of the cytotoxic mediators, iNOS, interleukin 1beta, and numor necrosis factor alpha. VIP emerges as a potential valuable neuroprotective agent for the treatment of pathologic conditions in the central nervous system, such as PD, where inflammation-induced neurodegeneration occurs.

Authors+Show Affiliations

Delgado M
Department of Biological Sciences, Rutgers University, Newark, New Jersey, USA. mariodm@bio.ucm.es
Ganea D
No affiliation info available

MeSH

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine1-Methyl-4-phenylpyridiniumAnimalsCell DeathCells, CulturedDisease Models, AnimalDopamineDopamine AgentsGene Expression RegulationInterleukin-1MPTP PoisoningMesencephalonMiceNeurogliaNeuronsNeuroprotective AgentsNitric Oxide SynthaseNitric Oxide Synthase Type IIRNA, MessengerTumor Necrosis Factor-alphaVasoactive Intestinal Peptide

Pub Type(s)

Journal Article

Language

eng

PubMed ID

12626429

Citation

Delgado, Mario, and Doina Ganea. "Neuroprotective Effect of Vasoactive Intestinal Peptide (VIP) in a Mouse Model of Parkinson's Disease By Blocking Microglial Activation." FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology, vol. 17, no. 8, 2003, pp. 944-6.
Delgado M, Ganea D. Neuroprotective effect of vasoactive intestinal peptide (VIP) in a mouse model of Parkinson's disease by blocking microglial activation. FASEB J. 2003;17(8):944-6.
Delgado, M., & Ganea, D. (2003). Neuroprotective effect of vasoactive intestinal peptide (VIP) in a mouse model of Parkinson's disease by blocking microglial activation. FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology, 17(8), 944-6.
Delgado M, Ganea D. Neuroprotective Effect of Vasoactive Intestinal Peptide (VIP) in a Mouse Model of Parkinson's Disease By Blocking Microglial Activation. FASEB J. 2003;17(8):944-6. PubMed PMID: 12626429.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Neuroprotective effect of vasoactive intestinal peptide (VIP) in a mouse model of Parkinson's disease by blocking microglial activation. AU - Delgado,Mario, AU - Ganea,Doina, Y1 - 2003/03/05/ PY - 2003/3/11/pubmed PY - 2003/6/5/medline PY - 2003/3/11/entrez SP - 944 EP - 6 JF - FASEB journal : official publication of the Federation of American Societies for Experimental Biology JO - FASEB J VL - 17 IS - 8 N2 - Parkinson's disease (PD) is a common neurodegenerative disorder with no effective protective treatment, characterized by a massive degeneration of dopaminergic neurons in the substantia nigra (SNpc) and the subsequent loss of their projecting nerve fibers in the striatum. To elucidate PD pathogenic factors, and thus to develop therapeutic strategies, a murine PD model based on the administration of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) has been used extensively. It has been demonstrated that activated microglia cells actively participate in the pathogenesis of MPTP-induced PD through the release of cytotoxic factors. Because current treatments for PD are not effective, considerable research focused lately on a number of regulatory molecules termed microglia-deactivating factors. Vasoactive intestinal peptide (VIP), a neuropeptide with a potent anti-inflammatory effect, has been found to be protective in several inflammatory disorders. This study investigates the putative protective effect of VIP in the MPTP model for PD. VIP treatment significantly decreases MPTP-induced dopaminergic neuronal loss in SNpc and nigrostriatal nerve-fiber loss. VIP prevents MPTP-induced activation of microglia in SNpc and striatum and the expression of the cytotoxic mediators, iNOS, interleukin 1beta, and numor necrosis factor alpha. VIP emerges as a potential valuable neuroprotective agent for the treatment of pathologic conditions in the central nervous system, such as PD, where inflammation-induced neurodegeneration occurs. SN - 1530-6860 UR - https://www.unboundmedicine.com/medline/citation/12626429/Neuroprotective_effect_of_vasoactive_intestinal_peptide__VIP__in_a_mouse_model_of_Parkinson's_disease_by_blocking_microglial_activation_ DB - PRIME DP - Unbound Medicine ER -