Telmisartan suppresses cerebral injury in a murine model of transient focal ischemia

Kasahara, Yukiko; Taguchi, Akihiko; Uno, Hisakazu; Nakano, Akiko; Nakagomi, Takayuki; Hirose, Haruka; Stern, David M.; Matsuyama, Tomohiro

doi:10.1016/j.brainres.2010.03.101

Cited by 45 publications

(40 citation statements)

References 42 publications

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“…Telmisartan is an ARB with a high degree of lipophilicity and is able to cross the blood-brain barrier (BBB). Recently it has been reported that telmisartan shows cerebroprotective effects, improves cognitive decline in AD, and provides neuroprotection (20,42,43); and these actions of telmisartan are attributed to its potential anti-oxidative (13), antiinflammatory (12), and anti-Ab (20) effects. In the study, telmisartan at either 0.7 or 0.35 mg/kg body weight did not produce a hypotensive effect confirmed by blood pressure recording.…”

Section: Discussionmentioning

confidence: 99%

“…Recently, the focus on ARBs has been intensified because their novel biological roles have emerged, particularly for their therapeutic potential in brain disorders (10,11). It has been reported that telmisartan has a beneficial effect in a murine model of ischemia/reperfusion injury through blockade of AT 1 R and exhibited neural protection, including anti-apoptosis, anti-inflammatory, and antioxidant benefits in the intracerebral hemorrhage rat model (12,13). Recent studies showed that telmisartan protects mouse dopaminergic neurons and inhibits the microglial response in a mouse MPTP model of Parkinson's disease (14).…”

Section: Introductionmentioning

confidence: 99%

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Telmisartan Treatment Ameliorates Memory Deficits in Streptozotocin-Induced Diabetic Mice via Attenuating Cerebral Amyloidosis

Du¹,

Meng²,

Mei³

et al. 2014

J Pharmacol Sci

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Abstract. Telmisartan, an angiotensin II type 1-receptor blocker (ARBs), has been reported to exert beneficial effects on the central nervous system (CNS). However, the effect of telmisartan on cognitive impairment associated with type 1 diabetes is not well known. Here, we examined the possibility that telmisartan could improve memory function in a type 1 diabetic mouse model, streptozotocin (STZ)-induced diabetic mice. STZ-induced diabetic mice subjected to the Morris Water Maze (MWM) task exhibited a significant decline of spatial learning and memory. Oral administration of telmisartan at two nonhypotensive doses (0.7 or 0.35 mg/kg) significantly improved memory deficits in STZ-induced diabetic mice. Telmisartan treatment markedly reduced Ab 42 , APP, BACE1, RAGE, and NF-kB p65 of the hippocampus and cortex, but did not beneficially affect hyperglycemia and hypoinsulinemia in the STZ-induced diabetic mice compared with untreated diabetic mice. Taken together, our findings suggest that telmisartan ameliorates memory deficits in type 1 diabetic mice, at least partly because of attenuation of amyloidosis in the brain.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Telmisartan Treatment Ameliorates Memory Deficits in Streptozotocin-Induced Diabetic Mice via Attenuating Cerebral Amyloidosis

Du¹,

Meng²,

Mei³

et al. 2014

J Pharmacol Sci

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“…63,64 ACEIs like lisinopril and ARBs like telmisartan have been reported in recent studies to possess anti-inflammatory actions. [65][66][67][68] Clinical exposure to ACEIs that do cross the blood brain barrier (BBB) have been found to be associated with a significant reduction in cognitive decline as compared to those ACEIs which do not cross the BBB. 60,69 Lisinopril has been reported for its easy entry in the brain through the BBB and it can cause marked inhibition of brain ACE by its central action.…”

Section: Discussionmentioning

confidence: 99%

Attenuating effect of lisinopril and telmisartan in intracerebroventricular streptozotocin induced experimental dementia of Alzheimer’s disease type: possible involvement of PPAR-γ agonistic property

Singh

Sharma

Jaggi

et al. 2012

J Renin Angiotensin Aldosterone Syst

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This study investigates the beneficial role of lisinopril, an angiotensin converting enzyme inhibitor (ACEI) and telmisartan, an angiotensin receptor blocker (ARB), in intracerebroventricular (i.c.v.) streptozotocin (STZ) induced dementia of Alzheimer's disease (AD) type in mice. This study also aimed to explore the role of PPAR-γ in lisinopril and telmisartan mediated effects in i.c.v. STZ mice. Donepezil served as the positive control in the study. Mice underwent i.c.v. injection of STZ. The Morris water maze (MWM) test was employed for assessment of learning and memory. Various biochemical estimations, namely brain acetylcholinesterase (AChE) activity, myeloperoxidase (MPO) activity, nitrite/nitrate and thiobarbituric acid reactive species (TBARS) levels and reduced glutathione (GSH) levels, were also performed. The study showed that i.c.v. STZ significantly impaired learning and memory of the animals along with a significant enhancement in brain AChE, MPO, TBARS, nitrite/nitrate levels and reduction in brain GSH levels. Treatments of lisinopril/telmisartan/ donepezil significantly attenuated STZ induced behavioral and biochemical changes. Pre-treatment with bisphenol-Adiglycidyl ether (BADGE), a selective PPAR-γ antagonist, significantly abolished the beneficial effect of lisinopril/telmisartan in i.c.v. STZ treated animals. The results of this investigation document a potential role of PPAR-γ in the beneficial effects of lisinopril and telmisartan in i.c.v. STZ dementia of AD type.

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“…18 In brief, the left middle cerebral artery (MCA) was isolated in male 7-week-old CB17/Icr mice (Clea, Tokyo, Japan) under halothane inhalation (3%) anesthesia and transient focal cerebral ischemia was induced under direct vision by transiently occluding the distal portion of the left MCA with a monofilament nylon suture (7-0 in size; Tyco) for 90, 120, 180, or 240 minutes. During surgical procedures, rectal temperature was monitored and controlled at 37.0Ϯ0.2°C by a feedback-regulated heating pad.…”

Section: Induction Of Focal Cerebral Ischemiamentioning

confidence: 99%

Cilostazol Reduces the Risk of Hemorrhagic Infarction After Administration of Tissue-Type Plasminogen Activator in a Murine Stroke Model

Kasahara

Nakagomi

Matsuyama

et al. 2012

Stroke

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Background and Purpose-Prior use of antiplatelet agents improves stroke outcome in patients undergoing thrombolytic therapy as shown by reduced arterial reocclusion, although the risk of cerebral hemorrhage can be increased. Methods-The effect of cilostazol, an antiplatelet drug that improves endothelial function through upregulation of intracellular cAMP, on cerebral hemorrhage after thrombolytic therapy was investigated using a highly reproducible transient ischemia model. Results-Treatment with cilostazol for 7 days before ischemia significantly suppressed the risk and severity of cerebral hemorrhage after injection of tissue-type plasminogen activator, although treatment with aspirin had no such protective effect compared with nontreated mice. Immunohistological analysis revealed that treatment with cilostazol suppressed disruption of the microvasculature in the ischemic area associated with reduced matrix metalloproteinase-9 activity. Conclusions-Our results suggest that patients treated with cilostazol before onset of stroke could have a lower risk of cerebral hemorrhage after thrombolytic therapy and might also have a longer therapeutic time window for thrombolysis. Furthermore, the risk of cerebral hemorrhage can be significantly altered by prestroke therapies, and analysis of the effects of multiple drugs on tissue-type plasminogen activator-induced cerebral hemorrhage in animal models is essential for the extending safe and effective thrombolytic therapy to a wider group of patients.

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Telmisartan suppresses cerebral injury in a murine model of transient focal ischemia

Cited by 45 publications

References 42 publications

Telmisartan Treatment Ameliorates Memory Deficits in Streptozotocin-Induced Diabetic Mice via Attenuating Cerebral Amyloidosis

Telmisartan Treatment Ameliorates Memory Deficits in Streptozotocin-Induced Diabetic Mice via Attenuating Cerebral Amyloidosis

Attenuating effect of lisinopril and telmisartan in intracerebroventricular streptozotocin induced experimental dementia of Alzheimer’s disease type: possible involvement of PPAR-γ agonistic property

Cilostazol Reduces the Risk of Hemorrhagic Infarction After Administration of Tissue-Type Plasminogen Activator in a Murine Stroke Model

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