Dynamics of inflammatory reaction and oxidative stress across maternal serum, placenta and amniotic fluid in laboratory rats and the role played by genistein aglycone

Background Genistein was reported to adversely influence fetal development although this is yet to be fully understood as a mechanism. Methods In this study, pregnant rats were divided into control (Cont.) and genistein force-fed (2-mg/kg and 4-mg/kg) groups. Each group was divided further into five subgroups: GD-0, GD-6, GD-13, GD-18, and GD-20 based on the terminal gestational day (GD). On the respective terminal GD, the rats were sacrificed and blood samples and amniotic fluid were carefully collected and separated and placenta homogenates were prepared. These samples were evaluated for oxidative stress and inflammatory reaction. The weights of embryonic implant and placenta tissue were also recorded. Heat shock protein (Hsp) (60 and 90), corticosterone, and oxidative stress biomarkers were determined in all the samples. Results Fetal and placental weights in all genistein-exposed groups were significantly decreased. A fluctuation in the level of the Hsp was recorded with a significant decrease recorded in Hsp90 level in the placenta and amniotic fluid towards GD-20 along with a concomitant increase in the corticosterone level in the amniotic fluid in all genistein groups compared to control. Maternal serum at GD-18 and GD -20 recorded a significant increase in antioxidant level (SOD, GSH, CAT) in all genistein-exposed groups. However, these antioxidants were significantly reduced in the placenta and the amniotic fluid compared to control. Conclusions Genistein enhances the placenta function in attenuating the risk of oxidative stress in the amniotic fluid and deferentially suppressed inflammatory activities in the placenta during early gestation and towards late gestation period.

Anti-Heat Shock Protein 90 is Increased in Acute Mania

Objective: The aim of this work was to examine autoantibodies in patients with bipolar disorder. Method: We enrolled 94 patients with acute bipolar mania, with 37 of them medicated and 57 unmedicated at the time of blood sampling. The samples also consisted of 44 patients in the remission state and another 48 normal controls. We first used human glioblastoma (U373 MG) cell lysate to screen the potential autoantibodies present in sera of bipolar mania patients, and anti-heat shock protein (anti-HSP) 60, 70 and 90 autoantibodies were identified. We then examined the serum levels of these autoantibodies by enzyme-linked immunosorbent assay. Results: The findings of this study showed that serum anti-HSP90 level was significantly higher in bipolar patients in acute mania than those in remission (p = 0.002). Conclusions: The data of this study suggest that increased anti-HSP90 might be a state marker for acute mania in patients with bipolar disorder.