The correlation between inducible nitric oxide synthase (iNOS) expression and level of malondialdehyde (MDA) on placenta tissue of pregnant mice in malaria infection with intra uteri growth restriction
DOI:
https://doi.org/10.30574/gscbps.2018.5.3.0139Keywords:
iNOS, Intra uteri growth restriction, Malaria, MalondialdehydeAbstract
Malaria infection in pregnant women can cause various clinical manifestations, one of them is fetus low birth weight. Sequestrations of infected erythrocytes and macrophages on intervillous space has been revealed by previous study, however the mechanism of this sequestration in placenta insufficiency is still unknown. We suggested that local immunity on placenta tissue can induce the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS) that can cause the destructions of placenta tissue due to the fetus low birth weight. This research was conducted to explore the path of immunity response on malaria placenta which involved the expression of inducible nitric oxide synthase (iNOS) and the level of malondialdehyde (MDA). This experimental laboratory study was done in pregnant Balb/c strain mice that infected with Plasmodium berghei in 9th day of pregnancy. Eighteen mice were divided into control group (pregnant mice) and treatment group (pregnant mice infected with Plasmodium berghei). iNOS expression was detected by using polyclonal antibody t iNOS, and level of MDA in the placenta tissue was measured by NTB assay. Fetal birth weight was measured on 15th day of pregnancy using analytic balance. The t-test independent showed a significant difference on iNOS expression between control group and treatment group (p<0.000), as well as fetal birth weight. (p<0.000). However there was no significant difference in the level of MDA between control group and treatment group (p = 0.101), The Pearson correlation test showed a significant correlation between iNOS expression with fetus birth weight (p<0.000); r=-0.925). It can be concluded that local immune response in placenta that involve nitric oxide pathway is responsible to placenta insufficiency.
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