Neuroprotective effect of nicotine on dopaminergic neurons by anti‐inflammatory action
Identifieur interne : 001004 ( Main/Exploration ); précédent : 001003; suivant : 001005Neuroprotective effect of nicotine on dopaminergic neurons by anti‐inflammatory action
Auteurs : Hyun Jung Park [Corée du Sud] ; Phil Hyu Lee [Corée du Sud] ; Young Whan Ahn [Corée du Sud] ; Yun Jung Choi [Corée du Sud] ; Gwang Lee [Corée du Sud] ; Da-Yong Lee [Corée du Sud] ; Eun S. Chung [Corée du Sud] ; Byung Kwan Jin [Corée du Sud]Source :
- European Journal of Neuroscience [ 0953-816X ] ; 2007-07.
English descriptors
Abstract
Epidemiological studies have reported that smoking is associated with a lower incidence of Parkinson's disease (PD), leading to theories that smoking in general and nicotine in particular might be neuroprotective. Recent studies suggested cholinergic anti‐inflammatory pathway‐regulating microglial activation through α7 nicotinic receptors. In the present study, we used lipopolysaccharide (LPS)‐induced in vitro and in vivo inflammation models to investigate whether nicotine has a protective effect on the dopaminergic system through an anti‐inflammatory mechanism. Nicotine pretreatment considerably decreased microglial activation with significant reduction of tumour necrosis factor (TNF)‐α mRNA expression and TNF‐α release induced by LPS stimulation. In co‐cultures of microglia and mesencephalic neurons, nicotine pretreatment significantly decreased the loss of tyrosine hydroxylase‐immunopositive (TH‐ip) cells, approximately twice more than the LPS‐only treatment. α‐Bungarotoxin, an α7 nicotinic acetylcholine receptor subunit‐selective blocker, considerably blocked the inhibitory effects of nicotine on microglial activation and TH‐ip neuronal loss. Chronic nicotine pretreatment in rats showed that TH‐ip neuronal loss induced by LPS stimulation in the substantia nigra was dramatically decreased, which was clearly accompanied by a reduction in the formation of TNF‐α. The present study demonstrated that nicotine has a neuroprotective effect on dopaminergic neurons via an anti‐inflammatory mechanism mediated by the modulation of microglial activation. Along with various neuroprotective effects of nicotine, the anti‐inflammatory mechanism of nicotine could have a major therapeutic implication in the preventive treatment of PD.
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DOI: 10.1111/j.1460-9568.2007.05636.x
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Recent studies suggested cholinergic anti‐inflammatory pathway‐regulating microglial activation through α7 nicotinic receptors. In the present study, we used lipopolysaccharide (LPS)‐induced in vitro and in vivo inflammation models to investigate whether nicotine has a protective effect on the dopaminergic system through an anti‐inflammatory mechanism. Nicotine pretreatment considerably decreased microglial activation with significant reduction of tumour necrosis factor (TNF)‐α mRNA expression and TNF‐α release induced by LPS stimulation. In co‐cultures of microglia and mesencephalic neurons, nicotine pretreatment significantly decreased the loss of tyrosine hydroxylase‐immunopositive (TH‐ip) cells, approximately twice more than the LPS‐only treatment. α‐Bungarotoxin, an α7 nicotinic acetylcholine receptor subunit‐selective blocker, considerably blocked the inhibitory effects of nicotine on microglial activation and TH‐ip neuronal loss. Chronic nicotine pretreatment in rats showed that TH‐ip neuronal loss induced by LPS stimulation in the substantia nigra was dramatically decreased, which was clearly accompanied by a reduction in the formation of TNF‐α. The present study demonstrated that nicotine has a neuroprotective effect on dopaminergic neurons via an anti‐inflammatory mechanism mediated by the modulation of microglial activation. Along with various neuroprotective effects of nicotine, the anti‐inflammatory mechanism of nicotine could have a major therapeutic implication in the preventive treatment of PD.</div></front></TEI><affiliations><list><country><li>Corée du Sud</li></country></list><tree><country name="Corée du Sud"><noRegion><name sortKey="Park, Hyun Jung" sort="Park, Hyun Jung" uniqKey="Park H" first="Hyun Jung" last="Park">Hyun Jung Park</name></noRegion><name sortKey="Ahn, Young Whan" sort="Ahn, Young Whan" uniqKey="Ahn Y" first="Young Whan" last="Ahn">Young Whan Ahn</name><name sortKey="Choi, Yun Jung" sort="Choi, Yun Jung" uniqKey="Choi Y" first="Yun Jung" last="Choi">Yun Jung Choi</name><name sortKey="Chung, Eun S" sort="Chung, Eun S" uniqKey="Chung E" first="Eun S." last="Chung">Eun S. Chung</name><name sortKey="Jin, Byung Kwan" sort="Jin, Byung Kwan" uniqKey="Jin B" first="Byung Kwan" last="Jin">Byung Kwan Jin</name><name sortKey="Lee, Da Ong" sort="Lee, Da Ong" uniqKey="Lee D" first="Da-Yong" last="Lee">Da-Yong Lee</name><name sortKey="Lee, Gwang" sort="Lee, Gwang" uniqKey="Lee G" first="Gwang" last="Lee">Gwang Lee</name><name sortKey="Lee, Phil Hyu" sort="Lee, Phil Hyu" uniqKey="Lee P" first="Phil Hyu" last="Lee">Phil Hyu Lee</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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