Estrogen inhibits lipid peroxidation after hypoxic-ischemic brain damage in neonatal rats

摘要

Sprague-Dawley neonatal rats within 7 days after birth were used in this study. The left common carotid artery was occluded and rats were housed in an 8% O ₂ environment for 2 hours to establish a hypoxic-ischemic brain damage model. 17β-estradiol (1 × 10 -5 M) was injected into the rat abdominal cavity after the model was successfully established. The left hemisphere was obtained at 12, 24, 48, 72 hours after operation. Results showed that malondialdehyde content in the left brain of neonatal rats gradually increased as modeling time prolonged, while malondialdehyde content of 17β-estrodial-treated rats significantly declined by 24 hours, reached lowest levels at 48 hours, and then peaked at 72 hours after injury. Nicotinamide-adenine dinucleotide phosphate histochemical staining showed the nitric oxide synthase-positive cells and fibers dyed blue/violet and were mainly distributed in the cortex, hippocampus and medial septal nuclei. The number of nitric oxide synthase-positive cells peaked at 48 hours and significantly decreased after 17β-estrodial treatment. Our experimental findings indicate that estrogen plays a protective role following hypoxic-ischemic brain damage by alleviating lipid peroxidation through reducing the expression of nitric oxide synthase and the content of malondialdehyde. Research Highlights Estrogen was observed to have a neuroprotective effect against hypoxic-ischemic brain damage in neonatal rats, which was most likely due to its antioxidant capacity.The expression of malondialdehyde and nitric oxide synthase in brain tissue of neonatal rats peaked at 48 hours after hypoxic-ischemic brain damage. Sham surgery was able to induce an increase in malondialdehyde expression.Estrogen inhibited the expression of malondialdehyde and nitric oxide synthase in ischemic brain tissue of neonatal rats following hypoxic-ischemic brain damage. Abbreviation TTC, 2,3,5-triphenyltetrazolium chloride