Islam, J., Haque, M., Rahaman, A., Hossain, S.
Intrauterine hypoxia-reperfusion is an important cause of neonatal brain injury. Thus, we tested whether S. cumini seed extract (SE) protects the incidence of embryofoetal oxidative toxicity in rat fetal brains produced by intrauterine hypoxia-reperfusion injury. Hypoxia was induced by uteroplacental occlusion followed by reperfusion. Brain proinflammatory tumor necrosis factor alpha (TNF-α), the levels of lipid peroxides (LPO) and reduced glutathione (GSH), activities of catalase (CAT) and superoxide dismutase (SOD) and acetylcholine esterase (AChE) enzymes were assessed. Histology of the fetal brain slices was studied after hematoxylene/eosin staining. The hypoxia-reperfusion increased the levels of TNF-α, LPO and decreased the activities of CAT and SOD enzymes and levels of GSH in the fetal brains. The oral preadministration of the S. cumini (L.) seed extract to the mother rats, however, significantly inhibited the rises of the levels of TNF-α and the oxidative stress in the fetal brains and increased the activities of CAT and SOD enzymes and levels of GSH in the fetal brains concurrently. Histological studies revealed decreased structural disintegration and inflammatory necrosis in the fetal brains of S. cumini + hypoxic mothers. We, therefore, conclude that oral preadministration of S. cumini (L.) seed extract to pregnant rats might prevent reproductive and fetal development impairments caused by intrauterine proinflammatory and hypoxia-reperfusion injury.
Oxidative stress, TNF-α, embryofoetal brain, hypoxia, Syzygium cumini (L.), antioxidative enzymes
Cite This Article
Islam, J., Haque, M., Rahaman, A., & Hossain, S. (2014). Syzygium cumini (L.) Seed Extract Protects Embryofoetal Brains against Intrauterine Oxidative Toxicity in Rats during Hypoxia-reperfusion Injury. International Journal for Pharmaceutical Research Scholars (IJPRS), 3(3), 170-177.