Inflammatory
cytokines and
neurotrophins play crucial roles in hypoxic-ischemic brain damage (HIBD), but the expression changes of these
proteins had not been systematically studied. In this article, we compared the levels of
tumor necrosis factor alpha (TNF-α),
intercellular adhesion molecule-1 (ICAM-1),
interleukin 1beta (IL-1β),
nerve growth factor (
NGF), and
brain-derived neurotrophic factor (
BDNF) in the progression of HIBD and analyzed their correlations with apoptosis. Seven-day-old pups of Sprague Dawley rats (n = 120) were randomly divided into two groups: the
sham-operated (control) group and the
hypoxia-
ischemia (HI) group. To establish the
hypoxic-ischemic encephalopathy model, the pups from the HI group were subjected to left common carotid artery
ligation followed by exposure to 8% O2 and 92% N2 for 2.5 hr. Pups from both the groups were sacrificed at 6, 24, 48, 72 hr and 7 days after
hypoxia. The levels of TNF-α,
ICAM-1, IL-1β,
NGF, and
BDNF in the brain tissues were measured by
enzyme-linked
immunosorbent assay. The neuronal apoptosis was examined by flow cytometry. We found that the levels of TNF-α,
ICAM-1, IL-1β,
NGF,
BDNF, and neuronal apoptosis rate in neonatal rats with HIBD significantly increased at 6, 24, 48, and 72 hr after
hypoxia compared to the control group (p < .05) and returned back to normal by 7 days. Furthermore, neuronal apoptosis rate was positively correlated with the levels of TNF-α,
ICAM-1, and IL-1β and negatively correlated with the levels of
NGF and
BDNF. In neonatal rats with HIBD, the brain reaches its peak levels of damage by 24-72 hr after the injury. Inflammatory
cytokines such as TNF-α,
ICAM-1, and IL-1β contribute to neuronal apoptosis induced by HIBD, whereas
neurotrophins NGF and
BDNF antagonize it.