| Effects of SAC on oxidative stress and NO availability in placenta: Potential benefits to preeclampsia. | |
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MedLine Citation:
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PMID: 22405339 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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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 H(2)O(2)-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, H(2)O(2), or a combination of H(2)O(2) 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 H(2)O(2) 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 < 0.05). The expression of eNOS in TEV-1 cells also significantly decreased in H(2)O(2) treated group compared to the control group (p < 0.05). Co-treatment of H(2)O(2) and SAC significantly decreased ROS productions, and increased NO, cGMP and eNOS level compared to the H(2)O(2) treated alone groups (p < 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 < 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 < 0.05). In conclusion, these results demonstrate that ROS (H(2)O(2)-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. |
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Authors:
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J Yu; L Feng; Y Hu; Y Zhou |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2012-3-7 |
Journal Detail:
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Title: Placenta Volume: - ISSN: 1532-3102 ISO Abbreviation: - Publication Date: 2012 Mar |
Date Detail:
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Created Date: 2012-3-12 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8006349 Medline TA: Placenta Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Copyright Information:
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Copyright © 2012 Elsevier Ltd. All rights reserved. |
Affiliation:
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Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PR China. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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