DH Wang, JB Lei

Neonatal rats were subjected to unilateral carotid artery ligation followed by three hours of hypoxia. Magnesium sulphate or ligustrazin was given 30 minutes before the hypoxic insult. Levels of superoxide dismutase (SOD) and MDA were measured in the cortex, as was serum MDA. The levels of SOD and MDA in the cerebral cortex and of MDA in the serum were significantly increased in the hypoxic insult group compared to the control group. All three levels were lower in the rats treated with magnesium sulphate than in the hypoxic insult group (P < 0.05). The cortical level of MDA was lower in the ligustrazin-treated group than in the hypoxic insult group (P < 0.05). Neuropathological examination of the hypoxic insult group showed pyknotic or karyorrhexic neurons in the white matter and hippocampus. Swollen or vacuous mitochondria and axons were revealed using an electron microscope. These changes were less serious in the two drug-treated groups. Our results indicate that: 1) free radical formation is one of the pathogenic factors of brain damage caused by hypoxic insult; 2) SOD activity in the cerebral cortex can compensate in the early stages of such damage; 3) magnesium sulphate and ligustrazin may prevent hypoxic insult damage by indirect antioxidation.