Post-anoxic level of HIF-1alpha and BDNF in neonatal rat brain depends on body temperature

• Autorzy: Rogalska J. , Kletkiewicz H. , Hyjek M. , Jaworski K. , Siejka A. , Nowakowska A.
• Języki publikacji: EN

Abstrakty

EN

INTRODUCTION: Complications after neonatal asphyxia are the most common cause of subsequent neurological disorders. Transcriptional hypoxia‑inducible factor‑1α (HIF‑1α) plays the fundamental role in adaptive processes in response to hypoxia. Moreover, the most crucial role in neuronal plasticity is attributed to brain-derived neurotrophic factor (BDNF). Newborn mammals showing reduced physiological body temperature are protected against perinatal asphyxia-induced neurotoxicity. The processes underlying neuroprotective effects of decreased body temperature might include the increased levels of HIF‑1α and BDNF. AIM(S): Therefore, we aimed at experimental verification of the hypothesis, that the body temperature during perinatal anoxia affects the level of HIF‑1α and BDNF. METHOD(S): Two-day-old newborn rats were exposed to anoxia in 100% nitrogen atmosphere for 10 min in different thermal conditions, which allow them to regulate the rectal temperature at the level of i. 33°C (physiological to rat neonates), ii. 37°C (level typical of healthy adult rats), or iii. 39°C (febrile adult rats). Hippocampal and cortex levels of HIF‑1α and BDNF were determined 1) immediately after anoxia, 2) 3 days after anoxia, and 3) 7 days after anoxia. RESULTS: There were no postanoxic changes in the level of BDNF in newborn rats kept at body temperature of 33°C. In contrast, at hyperthermic thermal conditions the level of the neurotrophin was decreased. Thermal conditions during neonatal anoxia affected the cerebral level of HIF‑1α. The highest level of anoxia‑induced HIF‑1α production was recorded in animals having physiological body temperature in comparison with that in hyperthermic animals. CONCLUSIONS: Since HIF-1 and BDNF have been recently regarded as promising therapeutical targets against brain lesions due to hypoxia/ischemia, presented data imply that to achieve a full effect of neuroprotection, the thermal conditions during and after the insult should be taken into consideration. FINANCIAL SUPPORT: Research on this paper was supported by grant from National Science Centre, Poland, no 2016/21/N/NZ7/00399.

• Wydawca: -
• Czasopismo: Acta Neurobiologiae Experimentalis
• Rocznik: 2017
• Tom: 77
• Numer: Suppl.1
• Opis fizyczny: p.71

Twórcy

autor

Rogalska J.

• Department of Animal Physiology, Faculty of Biology and Environmental Protection, Nicolaus Copernicus University, Torun, Poland

autor

Kletkiewicz H.

• Department of Animal Physiology, Faculty of Biology and Environmental Protection, Nicolaus Copernicus University, Torun, Poland

autor

Hyjek M.

• Department of Cell Biology, Faculty of Biology and Environmental Protection, Nicolaus Copernicus University, Torun, Poland
• Centre For Modern Interdisciplinary Technologies, Nicolaus Copernicus University, Torun, Poland

autor

Jaworski K.

• Chair of Plant Physiology and Biotechnology, Nicolaus Copernicus University, Torun, Poland

autor

Siejka A.

• Department of Animal Physiology, Faculty of Biology and Environmental Protection, Nicolaus Copernicus University, Torun, Poland

autor

Nowakowska A.

• Department of Animal Physiology, Faculty of Biology and Environmental Protection, Nicolaus Copernicus University, Torun, Poland