Metabotropic glutamate receptors group II (mGLuR2/3) agonist exert neuroprotection by reducing apoptosis after hypoxic-ischemic preconditioning

• Autorzy: Bratek E. , Ziembowicz A. , Salinska E.
• Języki publikacji: EN

Abstrakty

EN

BACKGROUND AND AIMS: Perinatal asphyxia is characterized by clinical and laboratory evidence of acute brain injury due to asphyxia. It was shown that mGluR2/3 activation before or after ischemic insult results in neuroprotection but the exact mechanism of this effect is not clear. The aim of present study was to investigate whether mGluR2/3 activation after hypoxia-ischemia (HI) reduces brain damage and if the activation of antioxidant enzymes and decrease of oxidative stress. METHODS: We used an animal model of HI on 7-day old rat pups. Animals were anesthetized and the left common carotid artery was isolated and double-ligated and then cut between the ligatures. After completion of the surgical procedure the pups were subjected to hypoxia (7.4% oxygen in nitrogen for 75 min at 35°C). Animals were injected intraperitoneal with specific mGluR2 (LY379268) and mGluR3 (NAAG) agonists 24 h or 1 h after HI. First weight deficit of HI brain hemisphere were measured and examined the expression of Bax. Next in our investigation we were used TUNEL assay and TTC1% staining. RESULTS: Our results show a neuroprotective effect  of mGluR2/3 agonists.Both agonists applied decreased brain tissue weight loss in ischemic hemisphere independently on the time of application (from 40% in HI to 15–20% in treated). In our study we show the relative changes in the expression of Bax protein in ipsilateral and contralateral hemisphere. Our results show that both mGluR2/3 antagonists applied 24 h and 1 h after HI reduced number of TUNELpositive cells in ipsilateral hemispheres. We observed more number of TUNEL- positive cells in HI. Both mGluR2/3 agonists decreased area of ipsilateral hemisphere infraction. CONCLUSIONS: This study is the demonstration of the neuroprotective effect of mGluR2/3 agonist on neonatal HI brain injury. These data suggest the possibility that preconditioning reduces irreversible ischemic injury in part by decreasing apoptosis.

• Wydawca: -
• Czasopismo: Acta Neurobiologiae Experimentalis
• Rocznik: 2015
• Tom: 75
• Numer: Supl.
• Opis fizyczny: p.S101

Twórcy

autor

Bratek E.

• Department of Neurochemistry, Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland

autor

Ziembowicz A.

• Department of Neurochemistry, Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland

autor

Salinska E.

• Department of Neurochemistry, Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland