Tags

Type your tag names separated by a space and hit enter

Inhibition of nitric oxide synthase lowers fatty acid oxidation in preeclampsia-like mice at early gestational stage.
Chin Med J (Engl). 2011 Oct; 124(19):3141-7.CM

Abstract

BACKGROUND

Preeclampsia is one of hypertensive disorders in pregnancy. It is associated with abnormal lipid metabolism, including fatty acid oxidation metabolism. Long chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD) plays an indispensable role in the oxidation of fatty acids. It has been reported that nitric oxide (NO) is one of the regulatory factors of the fatty acid oxidation pathway. The aim of this research was to investigate whether the nitric oxide synthase (NOS) inhibitor L-NAME may cause down-regulation of LCHAD in the pathogenesis of preeclampsia.

METHODS

Pregnant wild-type (WT) mice were treated with L-NAME or normal saline (NS) during gestation days 7 - 18 (early group), days 11 - 18 (mid group) and days 16 - 18 (late group), and apoE-/- mice served as a control. Systolic blood pressure (SBP), urine protein, feto-placental outcome, plasma lipid levels and NO concentrations were measured, and the expression of mRNA and protein for LCHAD in placental tissue were determined by real-time polymerase chain reaction (RT-PCR) and Western blotting, respectively.

RESULTS

In WT and apoE-/- mice, SBP and urinary protein increased following L-NAME injection. Fetal and placental weights and NO concentrations were reduced and total cholesterol, triglycerides and free fatty acid levels were increased in early and mid L-NAME groups in WT and apoE-/- mice, compared with the NS group. There was no significant difference between the late L-NAME group and NS group. RT-PCR and Western blotting analysis showed that the mRNA and protein levels of LCHAD expression were significantly down-regulated in the early and mid L-NAME groups but not in the late L-NAME group in the WT and apoE-/- mice compared with the corresponding NS groups.

CONCLUSIONS

Inhibition of NO in early and mid gestation in mice may cause hyperlipidemia and suppression of fatty acid oxidation, whereas preeclampsia-like conditions in late gestation may be a maternal vascular response to inhibition of NO.

Authors+Show Affiliations

Department of Obstetrics and Gynecology, Peking University Third Hospital, Beijing 100191, China.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22040569

Citation

Ma, Rui-Qiong, et al. "Inhibition of Nitric Oxide Synthase Lowers Fatty Acid Oxidation in Preeclampsia-like Mice at Early Gestational Stage." Chinese Medical Journal, vol. 124, no. 19, 2011, pp. 3141-7.
Ma RQ, Sun MN, Yang Z. Inhibition of nitric oxide synthase lowers fatty acid oxidation in preeclampsia-like mice at early gestational stage. Chin Med J (Engl). 2011;124(19):3141-7.
Ma, R. Q., Sun, M. N., & Yang, Z. (2011). Inhibition of nitric oxide synthase lowers fatty acid oxidation in preeclampsia-like mice at early gestational stage. Chinese Medical Journal, 124(19), 3141-7.
Ma RQ, Sun MN, Yang Z. Inhibition of Nitric Oxide Synthase Lowers Fatty Acid Oxidation in Preeclampsia-like Mice at Early Gestational Stage. Chin Med J (Engl). 2011;124(19):3141-7. PubMed PMID: 22040569.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inhibition of nitric oxide synthase lowers fatty acid oxidation in preeclampsia-like mice at early gestational stage. AU - Ma,Rui-Qiong, AU - Sun,Min-Na, AU - Yang,Zi, PY - 2011/11/2/entrez PY - 2011/11/2/pubmed PY - 2012/3/27/medline SP - 3141 EP - 7 JF - Chinese medical journal JO - Chin Med J (Engl) VL - 124 IS - 19 N2 - BACKGROUND: Preeclampsia is one of hypertensive disorders in pregnancy. It is associated with abnormal lipid metabolism, including fatty acid oxidation metabolism. Long chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD) plays an indispensable role in the oxidation of fatty acids. It has been reported that nitric oxide (NO) is one of the regulatory factors of the fatty acid oxidation pathway. The aim of this research was to investigate whether the nitric oxide synthase (NOS) inhibitor L-NAME may cause down-regulation of LCHAD in the pathogenesis of preeclampsia. METHODS: Pregnant wild-type (WT) mice were treated with L-NAME or normal saline (NS) during gestation days 7 - 18 (early group), days 11 - 18 (mid group) and days 16 - 18 (late group), and apoE-/- mice served as a control. Systolic blood pressure (SBP), urine protein, feto-placental outcome, plasma lipid levels and NO concentrations were measured, and the expression of mRNA and protein for LCHAD in placental tissue were determined by real-time polymerase chain reaction (RT-PCR) and Western blotting, respectively. RESULTS: In WT and apoE-/- mice, SBP and urinary protein increased following L-NAME injection. Fetal and placental weights and NO concentrations were reduced and total cholesterol, triglycerides and free fatty acid levels were increased in early and mid L-NAME groups in WT and apoE-/- mice, compared with the NS group. There was no significant difference between the late L-NAME group and NS group. RT-PCR and Western blotting analysis showed that the mRNA and protein levels of LCHAD expression were significantly down-regulated in the early and mid L-NAME groups but not in the late L-NAME group in the WT and apoE-/- mice compared with the corresponding NS groups. CONCLUSIONS: Inhibition of NO in early and mid gestation in mice may cause hyperlipidemia and suppression of fatty acid oxidation, whereas preeclampsia-like conditions in late gestation may be a maternal vascular response to inhibition of NO. SN - 2542-5641 UR - https://www.unboundmedicine.com/medline/citation/22040569/Inhibition_of_nitric_oxide_synthase_lowers_fatty_acid_oxidation_in_preeclampsia_like_mice_at_early_gestational_stage_ L2 - https://Insights.ovid.com/pubmed?pmid=22040569 DB - PRIME DP - Unbound Medicine ER -