Abstract
Resveratrol has been shown to be a therapeutic agent for cardiovascular disorders by maintaining a lower redox level in vivo through its anti-oxidant properties. Resveratrol can prevent cells from p53- and reactive oxygen species-dependent apoptosis induced by interleukin-1b. We identified an inhibitory effect of resveratrol against oxidative stress and apoptosis using the TUNEL assay in NG-Nitro-l-arginine methyl ester-induced preeclampsia in rats. To investigate a possible association between resveratrol and the apoptosis caused by oxidative stress in vitro, assays for superoxide dismutase and malondialdehyde as well as flow cytometric analyses were conducted in HTR-8/SVneo cells after hypoxic treatment with or without resveratrol for 24 h. These data suggest that resveratrol significantly opposes the effects of oxidative stress in vivo and in vitro.
Highlights
Preeclampsia (PE) is a pregnancy-specific disease with a worldwide prevalence of 7%–12% [1].As one of the most common pathologic complications of pregnancy, it is a leading contributor to pregnancy-associated mortality, and can cause serious damage to the heart, brain, kidneys, and other organs
The indicators of blood pressure (BP), urine volume, and creatinine level were normal before treatment
Results suggested that the NG-Nitro-L-arginine methyl ester (L-NAME) (n = 10)-injected group exhibited significant increases in BP and levels of protein/creatinine compared with the control (n = 8) and
Summary
Preeclampsia (PE) is a pregnancy-specific disease with a worldwide prevalence of 7%–12% [1]. As one of the most common pathologic complications of pregnancy, it is a leading contributor to pregnancy-associated mortality, and can cause serious damage to the heart, brain, kidneys, and other organs. The underlying pathogenesis of PE is usually considered to be insufficient perfusion of the uterus and placenta from the mother, which contributes to the ischemic and hypoxic microenvironment of placental trophoblasts. Recent evidence suggests that placental oxidative stress might be involved in the pathophysiologic characteristics of PE [2]. Oxidative stress activates several signaling pathways that restore homeostasis but, in case of failure, apoptotic machinery might be activated [3]. Several studies have found an increased level of apoptosis of villous trophoblasts in PE [4]
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