Lab Anim Res.  2017 Jun;33(2):98-104. 10.5625/lar.2017.33.2.98.

Hyperglycemia decreases preoxiredoxin-2 expression in a middle cerebral artery occlusion model

Affiliations
  • 1Department of Anatomy, College of Veterinary Medicine, Research Institute of Life Science, Gyeongsang National University, 501 Jinjudaero, Jinju 660-701, Korea. pokoh@gnu.ac.kr

Abstract

Diabetes is a major risk factor for stroke and is also associated with worsened outcomes following a stroke. Peroxiredoxin-2 exerts potent neuroprotective effects against oxidative stress. In the present study, we identified altered peroxiredoxin-2 expression in an ischemic stroke model under hyperglycemic conditions. Adult male rats were administrated streptozotocin (40 mg/kg) via intraperitoneal injection to induce diabetes. Middle cerebral artery occlusion (MCAO) was induced surgically 4 weeks after streptozotocin treatment and cerebral cortex tissues were isolated 24 hours after MCAO. Peroxiredoxin-2 expression was evaluated in the cerebral cortex of MCAO-operated animals using a proteomics approach, and was found to be decreased. In addition, the reduction in peroxiredoxin-2 levels was more severe in cerebral ischemia with diabetes compared to animals without diabetes. Reverse-transcriptase PCR and Western blot analyses confirmed the significantly reduced peroxiredoxin-2 expression in MCAO-operated animals under hyperglycemic conditions. It is an accepted fact that peroxiredoxin-2 has antioxidative activity against ischemic injury. Thus, the findings of this study suggest that a more severe reduction in peroxiredoxin-2 under hyperglycemic conditions leads to worsened brain damage during cerebral ischemia with diabetes.

Keyword

Brain ischemia; diabetes; peroxiredoxin-2; MCAO

MeSH Terms

Adult
Animals
Blotting, Western
Brain
Brain Ischemia
Cerebral Cortex
Humans
Hyperglycemia*
Infarction, Middle Cerebral Artery*
Injections, Intraperitoneal
Male
Middle Cerebral Artery*
Neuroprotective Agents
Oxidative Stress
Polymerase Chain Reaction
Proteomics
Rats
Risk Factors
Streptozocin
Stroke
Neuroprotective Agents
Streptozocin

Figure

  • Figure 1 Proteomic analysis of peroxiredoxin 2 in the cerebral cortex of non-diabetic+sham, diabetic+sham, non-diabetic+middle cerebral artery occlusion (MCAO), and diabetic+MCAO animals. Circles indicate peroxiredoxin 2 protein spots. Mw and pI indicate molecular weight and isoelectrical point, respectively. Spot intensities were measured by PDQuest software. Spot intensities are represented as a ratio relative to non-diabetic+sham control animals. Data (n=5) are shown as the mean±SEM. *P<0.05.

  • Figure 2 Reverse transcriptase-PCR of peroxiredoxin 2 in the cerebral cortex of non-diabetic+sham, diabetic+sham, non-diabetic+middle cerebral artery occlusion (MCAO), and diabetic+MCAO animals. Each lane represents an individual experimental animal. The band intensity of RT-PCR product was normalized to that of the actin product. Data (n=5) are shown as the mean±SEM. *P<0.05.

  • Figure 3 Western blot analysis of peroxiredoxin 2 in the cerebral cortex from non-diabetic+sham, diabetic+sham, non-diabetic+middle cerebral artery occlusion (MCAO), and diabetic+MCAO animals. Each lane represents an individual animal. Densitometric analysis is represented as a ratio of protein intensity to actin intensity. Data (n=5) are shown as the mean±SEM. *P<0.05.


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