Volume 29, Issue 9 (Monthly_Dec 2018)
Studies in Medical Sciences 2018, 29(9): 631-641 |
Back to browse issues page
Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
Ghoshooni H, Shahyad S, Noroozzadeh A, Mohammadi M T. EVALUATION OF THE INHIBITION OF NITRIC OXIDE PRODUCTION BY L-NAME ON BLOOD-BRAIN BARRIER PERMEABILITY AND TRANSCRIPTION OF CLAUDIN-3 AND 12 GENES AT THE SUBCORTICAL AREAS FOLLOWING CEREBRAL ISCHEMIA-REPERFUSION IN MALE RAT. Studies in Medical Sciences 2018; 29 (9) :631-641
URL: http://umj.umsu.ac.ir/article-1-4544-en.html
URL: http://umj.umsu.ac.ir/article-1-4544-en.html
Baqiyatallah University of Medical Sciences , Mohammadi.mohammadt@yahoo.com
Abstract: (3772 Views)
Background & Aims: Blood-brain barrier (BBB) breakdown and nitric oxide (NO) overproduction following cerebral ischemia-reperfusion extensively happens in the subcortical regions (core areas). Hence, we assessed the effects of NO inhibition by L-NAME on transcription of the transmembrane proteins claudin-3 and 12, with key role in BBB structure, at subcortical areas following cerebral ischemia-reperfusion in rat.
Materials & Methods: Eighteen male Wistar rats (270-320 g) were randomly divided into three groups; sham, control ischemia and treated ischemic groups. Brain ischemia was induced by 90 min right middle cerebral artery occlusion (MCAO) followed by 24 hours reperfusion. Rats received L-NAME intraperitoneally at dose of 1 mg/kg 30 min before MCAO. Neurological deficit score (NDS), BBB permeability and transcription of the claudin-3 and 12 genes at subcortical areas were assessed 24 hours after termination of MCAO.
Results: MCAO induced neurological dysfunction (2.83±0.30) and BBB interruption in the ischemic hemispheres of control ischemic group, whereas L-NAME administration in ischemic treated rats significantly declined neurological dysfunction (1.50±0.22) and also BBB permeability. L-NAME administration in treated ischemic group also enhanced the transcription levels of caudin-3 and 12 by 76% and 71%, respectively, which declined in control ischemic group.
Conclusion: Our findings indicate that NO inhibition in cerebral ischemia-reperfusion declines the BBB interruption and stroke outcomes through preventing from reduction of the transcription levels of caudin-3 and 12 in subcortical areas.
Materials & Methods: Eighteen male Wistar rats (270-320 g) were randomly divided into three groups; sham, control ischemia and treated ischemic groups. Brain ischemia was induced by 90 min right middle cerebral artery occlusion (MCAO) followed by 24 hours reperfusion. Rats received L-NAME intraperitoneally at dose of 1 mg/kg 30 min before MCAO. Neurological deficit score (NDS), BBB permeability and transcription of the claudin-3 and 12 genes at subcortical areas were assessed 24 hours after termination of MCAO.
Results: MCAO induced neurological dysfunction (2.83±0.30) and BBB interruption in the ischemic hemispheres of control ischemic group, whereas L-NAME administration in ischemic treated rats significantly declined neurological dysfunction (1.50±0.22) and also BBB permeability. L-NAME administration in treated ischemic group also enhanced the transcription levels of caudin-3 and 12 by 76% and 71%, respectively, which declined in control ischemic group.
Conclusion: Our findings indicate that NO inhibition in cerebral ischemia-reperfusion declines the BBB interruption and stroke outcomes through preventing from reduction of the transcription levels of caudin-3 and 12 in subcortical areas.
Type of Study: Research |
Subject:
داخلی مغز و اعصاب
Send email to the article author
| Rights and permissions | |
 |
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License. |
