The role of vitamin A in preventing fetal injuries caused by Lipopolysaccharide injection of Escherichia coli

Lipopolysaccharide (LPS) is an important factor that induces adverse developmental outcome. They include intrauterine growth retardation (IUGR), intrauterine fetal death (IUFD), embryonic resorption, and preterm delivery in rodents, and were related LPS-induced oxidative stress. In this study, 48 pregnant female rats were divided into 4 groups and injected intraperitoneally from lipopolysaccharide to 15 and 17 days pregnant, respectively, to the first and second groups of 75 micrograms per kg body weight. The second and third groups received 100 mg / kg vitamin A intramuscularly a week before injection of lipopolysaccharide. The fourth group was the control group and placebo was injected to simulate injection stress. On the 18th day, all the rats were euthanized. The number of live fetuses, dead fetuses, and resorption sites was counted. Live fetuses in each litter were weighted. Crown-rump and tail lengths examined and skeletal development was evaluated. In addition, maternal liver, placenta, and fetal liver samples were excised for measurement of MDA and GSH contents. Results show administration of LPS significantly increase fetal mortality, decrease fetal weight and crown-rump and tail lengths of live fetuses and retarded skeletal ossification in caudal vertebrae, anterior and posterior phalanges and supraoccipital bone. Our study showed that co-treatment of vitamin A and LPS could decrease defects of LPS and improve injuries.