000			03012na a2200457 4500
999			_c728 _d728
003			PC728
005			20210625062754.0
008			130622s2013 xxx||||| |||| 00| 0 eng d
040			_cH12O
041			_aeng
100			_aGarcía Bueno, Borja _91897 _eInstituto de Investigación i+12
100			_aLeza, Juan Carlos _91995 _eInstituto de Investigación i+12
100			_aMacDowell, Karina S. _92610 _eInstituto de Investigación i+12
100			_92441 _aMuñoz Madrigal, José Luis _eInstituto de Investigación i+12
100			_aParellada, Mara _92611 _eInstituto de Investigación i+12
245	0	0	_aRisperidone normalizes increased inflammatory parameters and restores anti-inflammatory pathways in a model of neuroinflammation. _h[artículo]
260			_c2013 _bInternational Journal of Neuropsychopharmacology,
300			_a16(1):121-35.
500			_aFormato Vancouver: MacDowell KS, García-Bueno B, Madrigal JL, Parellada M, Arango C, Micó JA, et al. Risperidone normalizes increased inflammatory parameters and restores anti-inflammatory pathways in a model of neuroinflammation. Int J Neuropsychopharmacol. 2013 Feb;16(1):121-35.
501			_aPMID: 22176740
504			_aContiene 68 referencias
520			_aInflammation, caused by both external and endogenous factors, has been implicated as a main pathophysiological feature of chronic mental illnesses, including schizophrenia. An increase in pro-inflammatory cytokines has been described both in experimental models and in schizophrenia patients. However, not much is known about the effects that antipsychotic drugs have on intra-and intercellular mechanisms controlling inflammation. The aim of the present study was to investigate the possible anti-inflammatory effect of a standard schizophrenia treatment not only at the level of soluble mediators, but also at intra-and intercellular inflammatory pathways. The present study was conducted in a model of mild neuroinflammation using a lipopolysaccharide (LPS) challenge that was not an endotoxaemic dose (0.5 mg/kg i.p.) in young adult rats. Main results : single doses of risperidone (0.3-3.0 mg/kg i.p.) prevented increased inflammatory parameters induced by LPS in brain cortex [expression of inflammatory cytokines, interleukin (IL)-1 beta and tumour necrosis factor (TNF)-alpha, activity of the inducible inflammatory enzymes nitric oxide synthase and cyclooxygenase, p38 mitogen-activated protein kinase (MAPK) and inflammatory nuclear transcription factor kappa B] and restored anti-inflammatory pathways decreased by LPS challenge (deoxyprostaglandins and peroxisome proliferator activated receptor c). This is the first study demonstrating that risperidone elicits a preventive effect on the anti-inflammatory arm of the homeostatic mechanism controlling inflammation in a model of mild encephalitis in rats. Our findings suggest a possible protective effect of risperidone on brain cells.
710			_9625 _aInstituto de Investigación imas12
856			_uhttp://pc-h12o-es.m-hdoct.a17.csinet.es/pdf/pc/7/pc728.pdf _ySolicitar documento
942			_n0 _2ddc _cART