Effects of SAC on oxidative stress and NO availability in placenta: Potential benefits to preeclampsia

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• 作者：J. Yu ^{yjtj2010@163.com} ; L. Feng ; ^{lfengtjmu@163.com} ; Y. Hu ^{yhutjmu@163.com} ; Y. Zhou ^{yzhoutjmu@163.com}
• 关键词：Preeclampsia ; S-allyl-l-cysteine ; Placental explants ; Nitric oxide ; Oxidative stress ; Hydrogen peroxide
• 刊名：Placenta
• 出版年：2012
• 期刊代码：260_01434004
• 类别：med
• 出版时间：June, 2012
• 卷：33
• 期：6
• 页码：487-494
• 文件大小：1066 K

摘要

Preeclampsia (PE) is a major cause of fetal growth restriction and perinatal mortality, which involves oxidative stress and vasodilator signaling disorder. S-allyl-l-cysteine (SAC) is one of the most abundant compounds in garlic extracts, and possesses several biological activities. This research was designed to investigate the protective effects of SAC against H₂O₂-induced oxidative insults, as well as the effects on NO/cGMP signaling pathway in placenta. We used TEV-1 cells and placental explants to detect the effects of SAC. TEV-1 cells and human placental explants were separately exposed to SAC, H₂O₂, or a combination of H₂O₂ and SAC. Intracellular ROS was detected by flow cytometry; the NO level was detected by an NO metabolites (NOx) assay; the cGMP level was simultaneously measured by the method of radioimmunoassay; the expression of eNOS in TEV-1 cells was measured by immunochemistry and Western blot. Our findings showed that H₂O₂ treatment increased ROS productions in TEV-1 cells and significantly decreased cGMP and NO level either in TEV-1 cells or explants compared to the control groups (p聽<聽0.05). The expression of eNOS in TEV-1 cells also significantly decreased in H₂O₂ treated group compared to the control group (p聽<聽0.05). Co-treatment of H₂O₂ and SAC significantly decreased ROS productions, and increased NO, cGMP and eNOS level compared to the H₂O₂ treated alone groups (p聽<聽0.05), which were all reverted back to near control levels. Further more, SAC treatment increased NO and cGMP level of TEV-1 cells and explants in a dose-dependent manner even at non-oxidative stress status (p聽<聽0.05). However, when the TEV-1 cells were cultured in the presence of NOS inhibitor (L-NAME) and NO donor (SNP), additional SAC treatment still significantly increased the NO level in comparison with SAC non-treated group (p聽<聽0.05). In conclusion, these results demonstrate that ROS (H₂O₂-mediated) can induce insults to NO/cGMP pathway, while SAC could antagonize this insult. And SAC also possesses the ability to increase NO and cGMP level at non-oxidative stress status in TEV-1 cells and placenta explants. SAC is therefore hypothesized to be a potential drug for PE treatment.