Glutathione improves the prognosis of Intrauterine Growth Restriction via downregulated hepatic and renal TNFα expression in Wistar rats

Abstract

Objective: Oxidative stress is requisite for the development of IUGR, with subsequent manifestation in the reduced levels of antioxidants enzymes. Glutathione protects against free radical-mediated injury, therefore we elucidated on its role in protecting against oxidative stress-induced consequences of IUGR. In order to improve the prognosis of IUGR in affected infants, we investigated the protective role of glutathione in rats exposed to IUGR. Method: Ten female Sprague-Dawley rats were mated overnight. The pregnant rats were divided into 2 groups of 5 rats each. From gestational day 9 until parturition, group A received normal saline while group B received 50 mg/kg daily of L-NAME. Pups from group A were allowed free access to food and water, while group B pups were randomly assigned into 3 groups; G1 pups were left untreated; 1.5g/kg of gluthatione was administered to G2 pups from PND 4-10 and G3 pups from PND 25-31. We measured the body weight of rats; immunolocalized and further quantified TNFα expression in the hepatic and renal tissues. Results: Postnatal GSH administration increased body weight in treated groups exposed to IUGR more significantly from days 4-10 as opposed to days 25-31. IUGR resulted in a significant increase in the TNFα immunoreactivity in the hepatic and renal tissues of the untreated group of rats when compared with the control and treated groups. GSH significantly reduced TNFα immunoreactivity in the kidney and liver of the treated groups, especially the days 4-10. Conclusions: Oral GSH administration regulates the inflammatory response in IUGR at the early neonatal period.