Resistin is expressed in human placenta and has been postulated to play a role in regulating energy metabolism in pregnancy. However, changes in serum resistin levels in normal pregnancy and in the setting of pre-eclampsia are far from understood. The purpose of the present study was to clarify the alterations in serum resistin level in normal pregnancy and pre-eclampsia. Blood samples were taken from 28 healthy non-pregnant women, 27 women in the first, 26 in the second and 26 in the third trimesters of normal pregnancy and 25 women with pre-eclampsia. Serum resistin concentrations were determined by using an ELISA, and mean serum resistin levels were compared with one-way ANOVA. Serum resistin levels were not significantly different among non-pregnant women and women in the first and second trimesters of pregnancy (P>0.05 for all). Serum resistin was significantly elevated in the third trimester of normal pregnancy compared with non-pregnant women (P<0.01) and women in the first (P<0.001) and second (P<0.001) trimesters of pregnancy. Serum resistin level was significantly lower in women with pre-eclampsia than women in the third trimester of normal pregnancy (P<0.001), but was comparable with those of non-pregnant women and women in the first and second trimesters of pregnancy (P>0.05 for all). In conclusion, we found an increase in serum resistin in the third trimester of normal pregnancy, but this increase was not present in pre-eclampsia. We postulate that these associations may offer insight into the mechanisms of maternal adaptation to pregnancy and the pathogenesis of pre-eclampsia.

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BackgroundEarly pregnancy loss (EPL) is a frustrating clinical problem, whose mechanisms are not completely understood. DNA methylation, which includes maintenance methylation and de novo methylation directed by DNA methyltransferases (DNMTs), is important for embryo development. Abnormal function of these DNMTs may have serious consequences for embryonic development.MethodsTo evaluate the possible involvement of DNA methylation in human EPL, the expression of DNMT proteins and global methylation of DNA were assessed in villous or decidua from EPL patients. The association of maintenance methylation with embryo implantation and development was also examined.ResultsWe found that DNMT1 and DNMT3A were both expressed in normal human villous and decidua. DNMT1 expression and DNA global methylation levels were significantly down-regulated in villous of EPL. DNMT3A expression was not significantly changed in the EPL group compared to controls in either villous or decidua. We also found that disturbance of maintenance methylation with a DNMT1 inhibitor may result in a decreased global DNA methylation level and impaired embryonic development in the mouse model, and inhibit in vitro embryo attachment to endometrial cells.ConclusionsOur results demonstrate that defects in DNA maintenance methylation in the embryo, not in the mother, are associated with abnormal embryonic implantation and development. The findings of the current study provide new insights into the etiology of EPL.

Resveratrol, a plant-derived polyphenolic compound and a phytoestrogen, was shown to possess multiple protective effects including anti-inflammatory response and anti-oxidative stress. Hypoxic pulmonary hypertension (HPH) is a progressive disease characterized by sustained vascular resistance and marked pulmonary vascular remodeling. The exact mechanisms of HPH are still unclear, but inflammatory response and oxidative stress was demonstrated to participate in the progression of HPH. The present study was designed to investigate the effects of resveratrol on HPH development. Sprague-Dawley rats were challenged by hypoxia exposure for 28 days to mimic hypoxic pulmonary hypertension along with treating resveratrol (40 mg/kg/day). Hemodynamic and pulmonary pathomorphology data were then obtained, and the anti-proliferation effect of resveratrol was determined by in vitro assays. The anti-inflammation and anti-oxidative effects of resveratrol were investigated in vivo and in vitro. The present study showed that resveratrol treatment alleviated right ventricular systolic pressure and pulmonary arterial remodeling induced by hypoxia. In vitro experiments showed that resveratrol notably inhibited proliferation of pulmonary arterial smooth muscle cells in an ER-independent manner. Data showed that resveratrol administration inhibited HIF-1 α expression in vivo and in vitro, suppressed inflammatory cells infiltration around the pulmonary arteries, and decreased ROS production induced by hypoxia in PAMSCs. The inflammatory cytokines' mRNA levels of tumor necrosis factor α, interleukin 6, and interleukin 1β were all suppressed by resveratrol treatment. The in vitro assays showed that resveratrol inhibited the expression of HIF-1 α via suppressing the MAPK/ERK1 and PI3K/AKT pathways. The antioxidant axis of Nuclear factor erythroid-2 related factor 2/ Thioredoxin 1 (Nrf-2/Trx-1) was up-regulated both in lung tissues and in cultured PASMCs. In general, the current study demonstrated that resveratrol may prevent pulmonary hypertension through its anti-proliferation, anti-inflammation and antioxidant effects. Hence, the present data may offer novel targets and promising pharmacological perspective for treating hypoxic pulmonary hypertension.

A decrease in visfatin level was demonstrated in pre-eclampsia, suggesting that visfatin and adipokine-associated metabolic abnormalities are involved in the pathogenesis of the disease.