AIM: To examine the dynamic changes of TNF-α, IL-6, IL-10, and GDNF (glial cell-derived neurotrophic factor) in serum or brain tissues of neonatal rat with hypoxic-ischemic encephalopathy and to explore their roles in neuronal apoptosis. MATERIALS AND METHODS: A total of 80 Wistar rats were randomly divided into the sham-operated (control) group and the hypoxia-ischemia (HI) group. To establish the hypoxic-ischemic encephalopathy (HIE) model, the pups from the HI group were subjected to left common carotid artery ligation followed by exposure to 8% O2 and 92% N2. The concentration of TNF-α, IL-6, IL-10, and GDNF in serum or brain tissues was measured by enzyme linked immunosorbent assay (ELISA). Neuronal apoptosis was examined by flow cytometry (FC). Statistical analysis was performed using the SPSS13.0 software. RESULTS: We found that the neuronal apoptosis rate and the levels of TNF-α and IL-6 in rat with hypoxic-ischemic brain damage (HIBD) were significantly increased at 6 h, 24 h, 48 h, and 72 h after hypoxia compared to the control group (p < 0.05). We also found that the neuronal apoptosis rate was positively correlated with the levels of TNF-α and IL-6, and negatively correlated with IL-10 and GDNF. CONCLUSIONS: In neonatal rats with HIE, the brain reaches its peak levels of damage by 24~72 h after the injury. Inflammatory cytokines such as TNF-α and IL-6 promote HIE-induced neuronal apoptosis, whereas IL-10 and GDNF antagonize it.
AIM: To examine the dynamic changes of TNF-α, IL-6, IL-10, and GDNF (glial cell-derived neurotrophic factor) in serum or brain tissues of neonatal rat with hypoxic-ischemicencephalopathy and to explore their roles in neuronal apoptosis. MATERIALS AND METHODS: A total of 80 Wistar rats were randomly divided into the sham-operated (control) group and the hypoxia-ischemia (HI) group. To establish the hypoxic-ischemicencephalopathy (HIE) model, the pups from the HI group were subjected to left common carotid artery ligation followed by exposure to 8% O2 and 92% N2. The concentration of TNF-α, IL-6, IL-10, and GDNF in serum or brain tissues was measured by enzyme linked immunosorbent assay (ELISA). Neuronal apoptosis was examined by flow cytometry (FC). Statistical analysis was performed using the SPSS13.0 software. RESULTS: We found that the neuronal apoptosis rate and the levels of TNF-α and IL-6 in rat with hypoxic-ischemic brain damage (HIBD) were significantly increased at 6 h, 24 h, 48 h, and 72 h after hypoxia compared to the control group (p < 0.05). We also found that the neuronal apoptosis rate was positively correlated with the levels of TNF-α and IL-6, and negatively correlated with IL-10 and GDNF. CONCLUSIONS: In neonatal rats with HIE, the brain reaches its peak levels of damage by 24~72 h after the injury. Inflammatory cytokines such as TNF-α and IL-6 promote HIE-induced neuronal apoptosis, whereas IL-10 and GDNF antagonize it.
Authors: Nienke Wagenaar; Caroline G M de Theije; Linda S de Vries; Floris Groenendaal; Manon J N L Benders; Cora H A Nijboer Journal: Pediatr Res Date: 2017-11-01 Impact factor: 3.756
Authors: Davide M Croci; Stefan Wanderer; Fabio Strange; Basil E Grüter; Sivani Sivanrupan; Lukas Andereggen; Daniela Casoni; Michael von Gunten; Hans Rudolf Widmer; Stefano Di Santo; Javier Fandino; Luigi Mariani; Serge Marbacher Journal: Transl Stroke Res Date: 2021-01-06 Impact factor: 6.829
Authors: Felipe Kawa Odorcyk; R T Ribeiro; A C Roginski; L E Duran-Carabali; N S Couto-Pereira; C Dalmaz; M Wajner; C A Netto Journal: Mol Neurobiol Date: 2021-01-08 Impact factor: 5.590