Abstract：
:Telmisartan is known to block angiotensin (Ang) II type-1 receptors (AT(1)R), and also activate peroxisome proliferator-activated receptor gamma (PPARgamma) signaling. Recently, PPARgamma has been implicated as a regulator of cellular proliferation and inflammatory responses. In the present study, we investigated the anti-inflammatory effects of telmisartan on middle cerebral artery (MCA) occlusion in mice. Telmisartan was administered orally to mice at 2h before and 2h after MCA occlusion. Infarct size was determined at 24h after MCA occlusion. In addition, cerebral blood flow (CBF) was measured during MCA occlusion. The effect of telmisartan on inflammatory markers, including Iba1 (macrophage/microglia marker) immunoreactivity and plasma high-mobility group box1 (HMGB1), was also investigated at 24h after MCA. Telmisartan significantly decreased the infarct area in dose-dependent manner without affecting CBF. Furthermore, the cerebroprotective effect of telmisartan was inhibited by GW9662, PPARgamma antagonist. Telmisartan significantly decreased the number of Iba1-positive cells expressing HMGB1 and decreased plasma HMGB1 levels. These effects were partially inhibited by GW9662. These data suggest that telmisartan may be a potential treatment for post-ischemic injury by partially inhibiting the inflammatory reaction after cerebral ischemia via a PPARgamma-dependent HMGB1 inhibiting mechanism.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Haraguchi T,Takasaki K,Naito T,Hayakawa K,Katsurabayashi S,Mishima K,Iwasaki K,Fujiwara Mdoi
10.1016/j.neulet.2009.08.043subject
Has Abstractpub_date
2009-10-30 00:00:00pages
151-5issue
3eissn
0304-3940issn
1872-7972pii
S0304-3940(09)01082-9journal_volume
464pub_type
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