Evaluation of blood vessel injury, oxidative stress and circulating inflammatory factors in an L‑NAME‑induced preeclampsia‑like rat model

Shu, Wen; Li, Hanying; Gong, Hao; Zhang, Mei; Niu, Xiulong; Ma, Yuanfang; Zhang, Xin; Cai, Wei; Gao, Yang; Wei, Minxin; Yang, Ning; Li, Yuming

doi:10.3892/etm.2018.6217

Cited by 37 publications

(45 citation statements)

References 46 publications

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“…In this study, we first established an animal model of preeclampsia. L‐NAME treatment induced the hypertension, increasing urine protein level, and reduced glomerular filtration rate and intrauterine growth restriction in rats 20 . These symptoms resembled those of preeclampsia patients.…”

Section: Discussionmentioning

confidence: 75%

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Implication of nuclear factor‐erythroid 2‐like 2/heme oxygenase 1 pathway in the protective effects of coenzyme Q10 against preeclampsia‐like in a rat model

Zhou

et al. 2020

Microcirculation

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Background: Preeclampsia has ranked as one of the leading causes of both maternal and prenatal morbidity and mortality around the world. The hypotensive effect of coenzyme Q10 has been widely reported in preeclampsia rat model. However, the detailed mechanism remains unclear. Methods: L-NAME was utilized to establish the preeclampsia rat model. Biomarker assessments were performed to identify the levels of vascular factors including soluble fms-like tyrosine kinase (sFlt-1) and placental growth factor (PlGF), the circulating cytokines including interleukin 6, tumor necrosis factor α and interleukin 1β, and oxidative stress factors including malondialdehyde, H 2 O 2 , glutathione, superoxide dismutase, glutathione peroxidase, and Catalase. QRT-PCR was used to demonstrate the levels of cytokines in placenta tissues, and Western blot was performed to estimate the nuclear factor-erythroid 2-like 2 (Nrf2) and heme oxygenase 1 (HO-1) protein levels. Results: Coenzyme Q10 treatment decreased the blood pressure in rat model with preeclampsia by regulating the circulating levels of sFlt-1 and PlGF. Coenzyme Q10 attenuated serum and placental inflammation and oxidative stress in L-NAME-induced preeclampsia rats. Coenzyme Q10 activated the placental Nrf2/HO-1 pathway in L-NAME-induced preeclampsia rats. Conclusion: Coenzyme Q10 attenuated placental inflammatory and oxidative stress, thereby protecting the rats against preeclampsia by activating the Nrf2/HO-1 pathway.

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Section: Discussionmentioning

confidence: 75%

“…L-NAME treatment induced the hypertension, increasing urine protein level, and reduced glomerular filtration rate and intrauterine growth restriction in rats. 20 These symptoms resembled those of preeclampsia patients. Therefore, we used L-NAME to build the preeclampsia model.…”

Section: Discussionmentioning

confidence: 81%

Implication of nuclear factor‐erythroid 2‐like 2/heme oxygenase 1 pathway in the protective effects of coenzyme Q10 against preeclampsia‐like in a rat model

Zhou

et al. 2020

Microcirculation

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“…The induction material for preeclampsia was using NOS inhibitors, L-NAME (C7H15N5O4 HCl) from Sigma-Aldrich (Merck KGaA, Darmstadt, Germany) (17). The L-Name dose given was 125 mg/kg BW starting from day 13 to day 18 intraperitoneally (18)(19). While, the EVOO "B" was given per oral gavage feeding tube from day 1 to day 18 of pregnancy.…”

Section: Preeclampsia Induction and Evoo Administrationmentioning

confidence: 99%

The Effect of Extra Virgin Olive Oil (EVOO) on Fetal Birth Weight in Preeclampsia Rat Model

Silvani

Maharani

Lovita

2020

JKB

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<p>Preeclampsia, as one of the most common pregnancy-specific diseases, causes high maternal-fetal morbidity and mortality in almost every country. Placental vascular abnormalities in preeclamptic women can cause chronic hypoxia and impaired fetal nutrition, so fetal growth retardation often occurs. EVOO has strong antioxidant effect is assumed to prevent nutritional disorders in the fetus. This study aimed to determine the effect of EVOO on fetal birth weight in a preeclampsia rat model. This research was laboratory research conducted in vivo with a Post Test Only Control Group design which consisted of five groups; negative control group, positive control group (pre-eclampsia rat model), dose 1, 2, and 3 groups that were preeclampsia rats given EVOO in 3 different doses (0.5 mL/day, 1 mL/day and 2 mL/day respectively). Blood pressure and proteinuria measurements were carried out at the 12, 15 and 19 day of pregnancy. After sacrificed, fetal weight was measured immediately using analytical balance. The result of this study showed that there was a significant reduction of fetal weight between negative control and positive control group (p=0.020), meanwhile no significant differences among positive control, dose 1 and dose 2 group (p=0.90 and p=0.142) but statistically significant to dose 3 group (p=0.005). EVOO administration increases fetal weight in doses group by its AA and DHA in Long-Chain Poly Unsaturated Fatty Acids (LCPUFA) within. The optimal dose of EVOO to increase fetal weight is 2 mL/day.</p>

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“…Animal models using rats or mice are very useful for the study of the pathogenesis, diagnosis, and treatment of preeclampsia. N-Nitro-L-arginine methyl Complications of Pregnancy ester (L-NAME) is an inhibitor of NO synthase, and it has been shown to promote arterial hypertension in pregnant rats [26,27].…”

Section: Animal Models For the Study Of Nitric Oxide During Pregnancymentioning

confidence: 99%

Maternal and Fetal Complications Due to Decreased Nitric Oxide Synthesis during Gestation

Jurado¹,

Saraiva²,

Marceliano³

et al. 2019

Complications of Pregnancy

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Nitric oxide (NO) is synthesized from L-arginine by the constitutive NO synthase in vascular endothelial cells and plays an important role in the regulation of blood pressure and coronary vasomotion. Normal pregnancy is associated with major adaptations in maternal cardiovascular function, which help the woman to accommodate the growing fetus. The vascular endothelium is stimulated during pregnancy to release increased amounts of NO, and the abnormality in the L-arginine NO pathway may play a role in the etiology of preeclampsia. The objective of this study is to discuss the importance of nitric oxide during gestation and the maternal and fetal complications associated with decreased NO synthesis during this period. Maternal arterial hypertension due to inhibition of nitric oxide synthesis during pregnancy impairs fetal development, mainly the reduction of the wall/lumen ratio of the cardiac and renal microvasculature as well as the reduction in the number of nephrons. These changes may contribute to the development of hypertension. Despite these findings, more studies are needed to understand the programming of fetal development, and the intrauterine environmental factors. influence this process.

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Evaluation of blood vessel injury, oxidative stress and circulating inflammatory factors in an L‑NAME‑induced preeclampsia‑like rat model

Cited by 37 publications

References 46 publications

Implication of nuclear factor‐erythroid 2‐like 2/heme oxygenase 1 pathway in the protective effects of coenzyme Q10 against preeclampsia‐like in a rat model

Implication of nuclear factor‐erythroid 2‐like 2/heme oxygenase 1 pathway in the protective effects of coenzyme Q10 against preeclampsia‐like in a rat model

The Effect of Extra Virgin Olive Oil (EVOO) on Fetal Birth Weight in Preeclampsia Rat Model

Maternal and Fetal Complications Due to Decreased Nitric Oxide Synthesis during Gestation

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