{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,19]],"date-time":"2025-11-19T06:51:33Z","timestamp":1763535093704},"reference-count":44,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2011,10,27]],"date-time":"2011-10-27T00:00:00Z","timestamp":1319673600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Neuropathology Appl Neurobio"],"published-print":{"date-parts":[[2011,12]]},"abstract":"<jats:p>M. Zuhayra, Y. Zhao, C. von Forstner, E. Henze, P. Gohlke, J. Culman and U. L\u00fctzen (2011) <jats:italic>Neuropathology and Applied Neurobiology<\/jats:italic><jats:bold>37,<\/jats:bold> 738\u2013752<\/jats:p><jats:p><jats:bold>Activation of cerebral peroxisome proliferator\u2010activated receptors \u03b3 (PPAR\u03b3) reduces neuronal damage in the substantia nigra after transient focal cerebral ischaemia in the rat<\/jats:bold><\/jats:p><jats:p><jats:bold>Aim:<\/jats:bold> The function of brain (neuronal) peroxisome proliferator\u2010activated receptor(s) \u03b3 (PPAR\u03b3) in the delayed degeneration and loss of neurones in the substantia nigra (SN) was studied in rats after transient occlusion of the middle cerebral artery (MCAO). <jats:bold>Methods:<\/jats:bold> The PPAR\u03b3 agonist, pioglitazone, or vehicle was infused intracerebroventricularly over a 5\u2010day period before, during and 5 days after MCAO (90\u2003min). The neuronal degeneration in the SN pars reticularis (SNr) and pars compacta (SNc), the analysis of the number of tyrosine hydroxylase\u2010immunoreactive (TH\u2010IR) neurones and the expression of the PPAR\u03b3 in these neurones were studied by immunohistochemistry and immunofluorescence staining. The effects of PPAR\u03b3 activation on excitotoxic and oxidative neuronal damage induced by glutamate and 6\u2010hydroxydopamine were investigated in primary cortical neurones expressing PPAR\u03b3. <jats:bold>Results:<\/jats:bold> Pioglitazone reduced the total and striatal infarct size, neuronal degeneration in both parts of the ipsilateral SN, the loss of TH\u2010IR neurones in the SNc and increased the number of PPAR\u03b3\u2010positive TH\u2010IR neurones. Pioglitazone protected primary cortical neurones against oxidative and excitotoxic damage, prevented the loss of neurites and supported the formation of synaptic networks in neurones exposed to glutamate or 6\u2010hydroxydopamine by a PPAR\u03b3\u2010dependent mechanism. <jats:bold>Conclusions:<\/jats:bold> Activation of cerebral PPAR\u03b3 confers neuroprotection after ischaemic stroke by preventing both, neuronal damage within the peri\u2010infarct zone and delayed degeneration of neurones and neuronal death in areas remote from the site of ischaemic injury. Pioglitazone and other PPAR\u03b3 agonists may be useful therapeutic agents to prevent progression of brain damage after cerebral ischaemia.<\/jats:p>","DOI":"10.1111\/j.1365-2990.2011.01169.x","type":"journal-article","created":{"date-parts":[[2011,3,2]],"date-time":"2011-03-02T15:20:04Z","timestamp":1299079204000},"page":"738-752","source":"Crossref","is-referenced-by-count":22,"title":["Activation of cerebral peroxisome proliferator\u2010activated receptors \u03b3 (PPAR\u03b3) reduces neuronal damage in the substantia nigra after transient focal cerebral ischaemia in the rat"],"prefix":"10.1111","volume":"37","author":[{"given":"M.","family":"Zuhayra","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Y.","family":"Zhao","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"C.","family":"von 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