ABSTRACT
BACKGROUND: Circular RNA plays a critical role in cell proliferation, differentiation, and autophagy. However, the role and mechanism of circRNA in preeclampsia is yet to be clarified. The present study investigated the function and mechanism of circ-0002814 in preeclampsia. METHODS: The expression level of circ-0002814, microRNA 210 (miR210), Notch receptor 1 (Notch1), or cytoplasmic polyadenylation element-binding protein 2 (CPEB2) was investigated by Reverse transcription Real-time Quantitative PCR (RT-qPCR). The level of Notch1, CPEB2, and FUS (FUS RNA-binding protein) proteins was detected by western blot. The localization of circ-0002814 and miR-210 was determined by FISH assay. Cell proliferation and invasion were detected by EdU and transwell assays, respectively. The interaction between circ-0002814 and FUS protein was detected by RNA pulldown assay, while that between circ-0002814 and miR-210 was detected by dual-luciferase reporter assay. RESULTS: The expression of circ-0002814 was decreased in the placenta and plasma of patients with preeclampsia. The ectopic expression of circ-0002814 promoted the invasion and proliferation of HTR8 cells compared to the control group (p < 0.05). Silencing circ-0002814 suppressed the invasion and proliferation of JEG3 cells compared to the control group (p < 0.05). circ_0002814-regulated Notch1 and CPEB2 by interaction with miR-210 and also regulated FUS/VEGF axis in HTR8 and JEG3 cells. CONCLUSION: A low expression of circ-0002814 was detected in the plasma and placental tissue in preeclampsia patients. circ-0002814 participated in the proliferation and invasion of HTR8 and JEG3 cells. Thus, circ-0002814 may be considered as a potential diagnostic marker and therapeutic target for preeclampsia.
Subject(s)
MicroRNAs , Pre-Eclampsia , RNA, Circular , Cell Line, Tumor , Cell Movement/genetics , Cell Proliferation/genetics , Female , Humans , MicroRNAs/genetics , MicroRNAs/metabolism , Placenta/metabolism , Pre-Eclampsia/genetics , Pregnancy , RNA, Circular/genetics , RNA-Binding Protein FUS/genetics , RNA-Binding Protein FUS/metabolism , Vascular Endothelial Growth Factor A/metabolismABSTRACT
BACKGROUND: To investigate the risk factors and changes in serum inflammatory factors in puerperal infection, and propose clinical prevention measures. METHODS: A total of 240 subjects with suspected puerperal infection treated in our hospital from January 2017 to December 2017 were collected, among which puerperal infection was definitely diagnosed in 40 cases, and it was excluded in 40 cases. Levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and high-sensitivity C-reactive protein (hs-CRP) were compared between the two groups, and the change trends of IL-6 and hs-CRP were recorded. RESULTS: Levels of IL-6, hs-CRP, and TNF-α in puerperal infection group were higher than those in non-infection group (P < .05). Levels of IL-6 and hs-CRP at enrollment and 1-3 days after enrollment in infection group were higher than those in non-infection group (P < .05). The body mass index >25, placenta previa, placenta accreta, postpartum hemorrhage, premature rupture of membrane, gestational diabetes mellitus, and anemia during pregnancy were relevant and independent risk factors for puerperal infection. Puerperal infection occurred in uterine cavity, vagina, pelvic peritoneum, pelvic tissue, incision, urinary system, etc, and gram-negative (G+) bacteria were dominated in pathogens. CONCLUSION: The inflammatory response of patients with puerperal infection is significantly enhanced.
Subject(s)
Inflammation Mediators/blood , Puerperal Infection/blood , Puerperal Infection/prevention & control , Adult , C-Reactive Protein/metabolism , Female , Humans , Interleukin-6/blood , Logistic Models , Multivariate Analysis , Puerperal Infection/epidemiology , Puerperal Infection/microbiology , Risk Factors , Young AdultABSTRACT
Gestational diabetes mellitus (GDM) is a common disorder characterized by abnormal glucose metabolism during pregnancy, affecting 2% to 5% of pregnant women. Currently, clinical treatment for GDM is very limited. The present study was designed to investigate the effect and underlying molecular mechanism of tertiary butylhydroquinone (TBHQ) in a pregnant C57BL/KsJ-Lep db/+ (referred to as db+) GDM mouse model. The results showed that nonpregnant db/+ mice did not show a diabetic phenotype, and TBHQ had no effect on glucose and insulin tolerance in these mice. Moreover, in db/+ pregnant mice exhibiting typical diabetes symptoms, such as hyperglycemia and hypoinsulinemia, TBHQ could remarkably decrease the blood glucose level, increase insulin level, and improve glucose and insulin intolerance. The results also revealed that TBHQ could inhibit oxidative stress in pregnant db/+ mice. Furthermore, TBHQ greatly improved offspring survival rate, glucose metabolism, and insulin tolerance. In addition, TBHQ inhibited oxidative stress by reducing malondialdehyde (MDA) and reactive oxygen species (ROS) levels and increased superoxide dismutase (SOD), and glutathione peroxidase (GPx) activities. Moreover, we found that TBHQ activated the nuclear factor erythroid 2-related factor 2 (Nrf2), thereby increasing the levels of Nrf2, and ultimately upregulating the expression of heme oxygenase 1 (NO-1) and superoxide dismutase 2 (SOD2). In conclusion, our findings demonstrated that TBHQ alleviated GDM via Nrf2 activation.
