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Hyperbaric oxygen preconditioning attenuates hyperglycemia enhanced hemorrhagic transformation after transient MCAO in rats.

Soejima Y, Ostrowski RP, Manaenko A, Fujii M, Tang J, Zhang JH - Med Gas Res (2012)

Bottom Line: HBO-PC improved neurological behavior test, and reduced infarction volume, HT and Evans blue extravasation in the ipsilateral hemisphere at 24 h after MCAO.Western blot analysis failed to demonstrate up-regulation of Nrf2 in HBO-PC group before and after MCAO.Paradoxically, HBO-PC decreased HO-1 expression at 24 h after MCAO, as compared with htMCAO group.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Physiology and Pharmacology, Loma Linda University School of Medicine, Loma Linda, CA, USA. johnzhang3910@yahoo.com.

ABSTRACT

Background: Hemorrhagic transformation (HT) can be a devastating complication of ischemic stroke. Hyperbaric oxygen preconditioning (HBO-PC) has been shown to improve blood-brain barrier (BBB) permeability in stroke models. The purpose of this study is to examine whether HBO-PC attenuates HT after focal cerebral ischemia, and to investigate whether the mechanism of HBO-PC against HT includes up-regulation of antioxidants in hyperglycemic rats.

Methods: Male Sprague-Dawley rats (280-320 g) were divided into the following groups: sham, middle cerebral artery occlusion (MCAO) for 2 h, and MCAO treated with HBO-PC. HBO-PC was conducted giving 100% oxygen at 2.5 atm absolute (ATA), for 1 h at every 24 h interval for 5 days. At 24 h after the last session of HBO-PC, rats received an injection of 50% glucose (6 ml/kg intraperitoneally) and were subjected to MCAO 15 min later. At 24 h after MCAO, neurological behavior tests, infarct volume, blood-brain barrier permeability, and hemoglobin content were measured to evaluate the effect of HBO-PC. Western blot analysis of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) was evaluated at multiple time-points before and after MCAO.

Results: HBO-PC improved neurological behavior test, and reduced infarction volume, HT and Evans blue extravasation in the ipsilateral hemisphere at 24 h after MCAO. Western blot analysis failed to demonstrate up-regulation of Nrf2 in HBO-PC group before and after MCAO. Paradoxically, HBO-PC decreased HO-1 expression at 24 h after MCAO, as compared with htMCAO group.

Conclusions: HBO-PC improved neurological deficits, infarction volume, BBB disruption, and HT after focal cerebral ischemia. However, its mechanism against focal cerebral ischemia and HT may not include activation of Nrf2 and subsequent HO-1 expression.

No MeSH data available.


Related in: MedlinePlus

HBO preconditioning had no effect on Nrf2 regulation, and significantly reduced HO-1 expression. Representative immunoblots and densitometric analysis of Nrf2 in nuclear fraction (A), Nrf2 in cytosolic fraction (B), and HO-1 in cytosolic fraction (C) at 24 h after MCAO. HBO-PC had no effect on Nrf2 regulation. Furthermore, HO-1 was downregulated by HBO-PC. *P > 0.05 vs. htMCAO, #P > 0.05 vs. sham.
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Figure 6: HBO preconditioning had no effect on Nrf2 regulation, and significantly reduced HO-1 expression. Representative immunoblots and densitometric analysis of Nrf2 in nuclear fraction (A), Nrf2 in cytosolic fraction (B), and HO-1 in cytosolic fraction (C) at 24 h after MCAO. HBO-PC had no effect on Nrf2 regulation. Furthermore, HO-1 was downregulated by HBO-PC. *P > 0.05 vs. htMCAO, #P > 0.05 vs. sham.

Mentions: Western blot analysis showed that HBO-PC had no effect on Nrf2 regulation. No change was found in the protein expression of Nrf2 in both fractions at 2 or 24 h after the last session of HBO, without subsequent MCAO (Figure 5). Furthermore, there was no significant difference in Nrf2 expression of both fractions at 24 h after MCAO as compared with htMCAO group (Figure 6). Result also shows that no change was found in time-course of HO-1 expression (Figure 5C). However, It is notable that HBO-PC decreased HO-1 at 24 h after MCAO as compared with htMCAO group (Figure 6C).


Hyperbaric oxygen preconditioning attenuates hyperglycemia enhanced hemorrhagic transformation after transient MCAO in rats.

Soejima Y, Ostrowski RP, Manaenko A, Fujii M, Tang J, Zhang JH - Med Gas Res (2012)

HBO preconditioning had no effect on Nrf2 regulation, and significantly reduced HO-1 expression. Representative immunoblots and densitometric analysis of Nrf2 in nuclear fraction (A), Nrf2 in cytosolic fraction (B), and HO-1 in cytosolic fraction (C) at 24 h after MCAO. HBO-PC had no effect on Nrf2 regulation. Furthermore, HO-1 was downregulated by HBO-PC. *P > 0.05 vs. htMCAO, #P > 0.05 vs. sham.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3351373&req=5

Figure 6: HBO preconditioning had no effect on Nrf2 regulation, and significantly reduced HO-1 expression. Representative immunoblots and densitometric analysis of Nrf2 in nuclear fraction (A), Nrf2 in cytosolic fraction (B), and HO-1 in cytosolic fraction (C) at 24 h after MCAO. HBO-PC had no effect on Nrf2 regulation. Furthermore, HO-1 was downregulated by HBO-PC. *P > 0.05 vs. htMCAO, #P > 0.05 vs. sham.
Mentions: Western blot analysis showed that HBO-PC had no effect on Nrf2 regulation. No change was found in the protein expression of Nrf2 in both fractions at 2 or 24 h after the last session of HBO, without subsequent MCAO (Figure 5). Furthermore, there was no significant difference in Nrf2 expression of both fractions at 24 h after MCAO as compared with htMCAO group (Figure 6). Result also shows that no change was found in time-course of HO-1 expression (Figure 5C). However, It is notable that HBO-PC decreased HO-1 at 24 h after MCAO as compared with htMCAO group (Figure 6C).

Bottom Line: HBO-PC improved neurological behavior test, and reduced infarction volume, HT and Evans blue extravasation in the ipsilateral hemisphere at 24 h after MCAO.Western blot analysis failed to demonstrate up-regulation of Nrf2 in HBO-PC group before and after MCAO.Paradoxically, HBO-PC decreased HO-1 expression at 24 h after MCAO, as compared with htMCAO group.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Physiology and Pharmacology, Loma Linda University School of Medicine, Loma Linda, CA, USA. johnzhang3910@yahoo.com.

ABSTRACT

Background: Hemorrhagic transformation (HT) can be a devastating complication of ischemic stroke. Hyperbaric oxygen preconditioning (HBO-PC) has been shown to improve blood-brain barrier (BBB) permeability in stroke models. The purpose of this study is to examine whether HBO-PC attenuates HT after focal cerebral ischemia, and to investigate whether the mechanism of HBO-PC against HT includes up-regulation of antioxidants in hyperglycemic rats.

Methods: Male Sprague-Dawley rats (280-320 g) were divided into the following groups: sham, middle cerebral artery occlusion (MCAO) for 2 h, and MCAO treated with HBO-PC. HBO-PC was conducted giving 100% oxygen at 2.5 atm absolute (ATA), for 1 h at every 24 h interval for 5 days. At 24 h after the last session of HBO-PC, rats received an injection of 50% glucose (6 ml/kg intraperitoneally) and were subjected to MCAO 15 min later. At 24 h after MCAO, neurological behavior tests, infarct volume, blood-brain barrier permeability, and hemoglobin content were measured to evaluate the effect of HBO-PC. Western blot analysis of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) was evaluated at multiple time-points before and after MCAO.

Results: HBO-PC improved neurological behavior test, and reduced infarction volume, HT and Evans blue extravasation in the ipsilateral hemisphere at 24 h after MCAO. Western blot analysis failed to demonstrate up-regulation of Nrf2 in HBO-PC group before and after MCAO. Paradoxically, HBO-PC decreased HO-1 expression at 24 h after MCAO, as compared with htMCAO group.

Conclusions: HBO-PC improved neurological deficits, infarction volume, BBB disruption, and HT after focal cerebral ischemia. However, its mechanism against focal cerebral ischemia and HT may not include activation of Nrf2 and subsequent HO-1 expression.

No MeSH data available.


Related in: MedlinePlus