Prenatal immobility stress: Relationship with oxidative stress, inflammation, apoptosis, and intrauterine growth restriction in rats

Abstract

BackgroundPrenatal stress is a significant risk factor affecting pregnant women and fetal health. In the present study, we aimed to investigate the effect of immobility stress at different periods of pregnancy on oxidative stress, inflammation, placental apoptosis and intrauterine growth retardation in rats.MethodsFifty adult virgin female Wistar albino rats were used. Pregnant rats were exposed to 6 h/day immobilization stress in a wire cage at different stages of pregnancy. Groups I and II (Day 1–10 stress group) were sacrificed on the 10th day of pregnancy, and Group III, Group IV (10–19th‐day stress group), and Group V (1–19th‐day stress group) were sacrificed on the 19th day of pregnancy. Inflammatory cytokines, including interleukin‐6 (IL‐6) and interleukin‐10 (IL‐10), serum corticotropin‐releasing hormone (CRH), and corticosterone levels were measured by enzyme‐linked immunosorbent assay. Malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) levels in the placenta were spectrophotometrically measured. Histopathological analyses of the placenta were evaluated by hematoxylin and eosin staining. Tumor necrosis factor‐alpha (TNF‐α) and caspase‐3 immunoreactivity in placenta tissues were determined by the indirect immunohistochemical method. Placental apoptosis was determined by the TUNEL staining method.ResultsWe found that the immobility stress during pregnancy significantly increased serum corticosterone levels. Our results showed that the immobility stress diminished the number and weight of fetuses in rats compared to the non‐stress group. The immobility stress caused significant histopathological changes in the connection zone and labyrinth zone and increased placental TNF‐α and caspase‐3 immunoreactivity and placental apoptosis. In addition, immobility stress significantly increased the levels of pro‐inflammatory IL‐6 and MDA and caused a significant decrease in the levels of antioxidant enzymes such as SOD, CAT, and anti‐inflammatory IL‐10.ConclusionsOur data suggest that immobility stress causes intrauterine growth retardation by activating the hypothalamic‐pituitary‐adrenal axis and deteriorating placental histomorphology and deregulating inflammatory and oxidative processes.

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Gut Microbiota, Inflammation, and Probiotic Supplementation in Fetal Growth Restriction—A Comprehensive Review of Human and Animal Studies

“…Maternal food restriction during pregnancy causes IUGR and reduces the immunotolerant milieu in mouse placenta, which may affect immune tolerance and the immunologic pathways regulating ER stress and autophagy [63]. Prenatal immobility stress at different periods of pregnancy can cause IUGR in rodents, which results in increased levels of pro-inflammatory cytokines and decreased levels of antioxidant enzymes [64]. The administration of FK565, an innate immune receptor of Nod1, to pregnant C57BL/6 mice resulted in increased IUGR risk, which, in turn, can activate genes associated with inflammation and immune responses in fetal vascular tissues [65].…”