Long-term amelioration of telmisartan on metabolic syndrome-related molecules in stroke-resistant spontaneously hypertensive rat after transient middle cerebral artery occlusion

Kentaro Deguchi, Tomoko Kurata, Yusuke Fukui, Wentao Liu, Zhai Yun, Yoshio Omote, Kota Sato, Syoichiro Kono, Nozomi Hishikawa, Toru Yamashita, Koji Abe

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Telmisartan is expected to ameliorate not only hypertension, but also metabolic syndrome as a metabosartan. We examined the effects of telmisartan on metabolic syndrome-related molecules such as insulin receptor (IR), peroxisome proliferatoractivated receptor gamma (PPAR-g), and angiotensin 2 type 1 receptor (AT1R) in stroke-resistant spontaneously hypertensive rat (SHR-SR) after transient middle cerebral artery occlusion (tMCAO), by administering telmisartan at either 0 (vehicle), .3 mg/kg/day (low dose), or 3 mg/kg/day (high dose), postoperatively, from 3 months of age and performed immunohistologic analysis at 6, 12, and 18 months of age. Compared with the vehicle group, the 2 telmisartan groups dose dependently decreased the number of IR- and AT1R-positive neurons in the cerebral cortex in the ipsilateral cerebral cortex from 6 to 18 months after tMCAO. On the other hand, the number of PPAR-g-positive neurons increased in a dose-dependent manner in the 2 telmisartan groups from 6 to 18 months. The present study suggests that telmisartan dose-dependently ameliorated metabolic syndrome-related changes in the poststroke brain of SHR-SR with a direct protective effect (low dose) and an additive benefit, an antihypertensive effect at a high dose, for long-term protection after tMCAO.

Original languageEnglish
Pages (from-to)2646-2653
Number of pages8
JournalJournal of Stroke and Cerebrovascular Diseases
Volume23
Issue number10
DOIs
Publication statusPublished - 2014

Fingerprint

Middle Cerebral Artery Infarction
Inbred SHR Rats
Stroke
Angiotensin Type 1 Receptor
Peroxisomes
Insulin Receptor
Cerebral Cortex
Neurons
Antihypertensive Agents
telmisartan
Hypertension
Brain

Keywords

  • Activated receptor gamma
  • Angiotensin 2 type 1 receptor
  • Ischemic stroke
  • Metabolic syndrome
  • Peroxisome proliferators
  • Spontaneously hypertensive rat
  • Transient middle cerebral artery occlusion

ASJC Scopus subject areas

  • Clinical Neurology
  • Surgery
  • Rehabilitation
  • Cardiology and Cardiovascular Medicine
  • Medicine(all)

Cite this

Long-term amelioration of telmisartan on metabolic syndrome-related molecules in stroke-resistant spontaneously hypertensive rat after transient middle cerebral artery occlusion. / Deguchi, Kentaro; Kurata, Tomoko; Fukui, Yusuke; Liu, Wentao; Yun, Zhai; Omote, Yoshio; Sato, Kota; Kono, Syoichiro; Hishikawa, Nozomi; Yamashita, Toru; Abe, Koji.

In: Journal of Stroke and Cerebrovascular Diseases, Vol. 23, No. 10, 2014, p. 2646-2653.

Research output: Contribution to journalArticle

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T1 - Long-term amelioration of telmisartan on metabolic syndrome-related molecules in stroke-resistant spontaneously hypertensive rat after transient middle cerebral artery occlusion

AU - Deguchi, Kentaro

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AU - Fukui, Yusuke

AU - Liu, Wentao

AU - Yun, Zhai

AU - Omote, Yoshio

AU - Sato, Kota

AU - Kono, Syoichiro

AU - Hishikawa, Nozomi

AU - Yamashita, Toru

AU - Abe, Koji

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AB - Telmisartan is expected to ameliorate not only hypertension, but also metabolic syndrome as a metabosartan. We examined the effects of telmisartan on metabolic syndrome-related molecules such as insulin receptor (IR), peroxisome proliferatoractivated receptor gamma (PPAR-g), and angiotensin 2 type 1 receptor (AT1R) in stroke-resistant spontaneously hypertensive rat (SHR-SR) after transient middle cerebral artery occlusion (tMCAO), by administering telmisartan at either 0 (vehicle), .3 mg/kg/day (low dose), or 3 mg/kg/day (high dose), postoperatively, from 3 months of age and performed immunohistologic analysis at 6, 12, and 18 months of age. Compared with the vehicle group, the 2 telmisartan groups dose dependently decreased the number of IR- and AT1R-positive neurons in the cerebral cortex in the ipsilateral cerebral cortex from 6 to 18 months after tMCAO. On the other hand, the number of PPAR-g-positive neurons increased in a dose-dependent manner in the 2 telmisartan groups from 6 to 18 months. The present study suggests that telmisartan dose-dependently ameliorated metabolic syndrome-related changes in the poststroke brain of SHR-SR with a direct protective effect (low dose) and an additive benefit, an antihypertensive effect at a high dose, for long-term protection after tMCAO.

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