9 research outputs found
HYPOXIC-ISCHEMIC BRAIN INJURY IN NEWBORN RAT : NEUROPROTECTIVE EFFECTS OF ACETAMINOPHEN AND THE INVOLVEMENT OF ACID SPHINGOMYELINASE ACTIVATION
Acetaminophen is widely used as an analgesic and antipyretic medication. Recently, acetaminophen has been shown as effective against neuronal cell death through its antioxidant and anti-inflammatory properties. In this study, we used the Rice-Vannucci model to examine whether the administration of acetaminophen was protective against hypoxic-ischemic brain injury in immature rat brain. Seven-day-old rat pups that had ligation of the right carotid artery received 20 mg/kg of acetaminophen intraperitoneally immediately before hypoxic exposure of 8% oxygen for 90 min. Compared to controls, acetaminophen treatment group showed decreased macroscopic brain injury scores at 48 h and 168 h after hypoxia-ischemia. Acetaminophen significantly decreased the number of apoptotic and necrotic cells in the cortex, caudate putamen, thalamus, and hippocampus. In addition, the percent brain damage of hypoxia-ischemia, which is another index for brain injury, was improved by the administration of acetaminophen. Our results suggested that acetaminophen inhibited apoptotic and necrotic cell death and played a role in neuroprotection after hypoxia-ischemia in immature rat brain. In addition, we showed that acid sphingomyelinase (ASM), which is as an important enzyme for cellular responses to reactive oxygen species (ROS), might be involved in brain injuries after hypoxie-ischemia. The activation of ASM after hypoxia-ischemia was attenuated by the administration of acetaminophen in our rat model. This attenuation might be caused by the antioxidant property of acetaminophen, supporting the suggestion of its neuroprotective effect on the hypoxic-ischemic brain injury