Serum Adropin Levels in a Preeclampsia Like L-Name Rat Model Treated with Sildenafil Citrate

Raafat, Nadine A.; Fathy, Maha A.

doi:10.21608/mjcu.2018.61490

Cited by 2 publications

(3 citation statements)

References 25 publications

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“…These results are in line with animal studies by Raafat and Fathy [40] and human studies by Masuyama et al [49], which demonstrated that insulin resistance is associated with preeclampsia. Additionally, Thadhani et al [50] stated that women with low levels of PlGF, a surrogate insulin resistance marker, in the first trimester have an increased risk of developing subsequent PE.…”

Section: Discussionsupporting

confidence: 90%

“…These results are in line with animal studies by Raafat and Fathy [40] and human studies by Carty et al [41] and Khoury et al [42], which demonstrated that the lipid levels in women with preeclampsia are higher than those in healthy pregnant women.…”

Section: Discussionsupporting

confidence: 89%

“…This may be due to blockage of the expression of eNOS in the placenta and the levels of NO and eNOS in the serum in PE, which causes peripheral insulin resistance, secondary to blockage of the hepatic parasympathetic reflex release of hepatic insulin sensitizing substance in response to insulin [40]. Thus, apelin helps to ameliorate these effects as it has a direct activating effect on the L-arginine/eNOS/NO pathway [35,51].…”

Section: Discussionmentioning

confidence: 99%

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RETRACTED: A Potential Role of Apelin-13 against Hepatic Injury and Metabolic Disorders in Preeclampsia Induced by L-NAME

et al. 2021

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Background: Hypertensive disorders of pregnancy, gestational hypertension, and preeclampsia (PE) are exceptionally challenging, as their pathologies and therapeutic management simultaneously influence the mother and embryo, sometimes putting their well-beings at odds with each other. Dysregulated lipid and glucose metabolism may be related to some cases of preeclampsia. Fluctuations in serum apelin levels may be attributed to changes in the serum levels of multiple interrelated factors such as insulin, insulin resistance, inflammatory cytokines, and nephritic damage. Previous studies demonstrated that apelin is an endogenous active peptide with vasodilatory and antioxidative-stress capabilities. Objective: We investigated the relationships among hepatic, nephrotic, and metabolic injuries in different preeclampsia-like mouse models and the potential effect of exogenous apelin administration on hepatic and nephrotic injuries and metabolic disorders in an N-nitro-L-arginine methyl ester (L-NAME) preeclampsia-like Sprague Dawley (SD) rat model. Materials and methods: Forty-three adult female and ten adult male SD rats were involved in this study. The male rats were used to induce pregnancy. The female rats were randomly divided into four equal groups: a non-pregnant group, a normal pregnant group, a group treated with L-NAME to induce preeclampsia, and a group treated with L-NAME and apelin. In all the groups, maternal blood was collected on the 21st day of gestation, and serum samples were used for the determination of systolic blood pressure; the serum uric acid, creatinine, nitric oxide (NO), xanthine oxidase, myeloperoxidase, insulin, glucose, cholesterol, triglyceride (TG), aspartate aminotransferase (AST) and alanine aspartate aminotransferase (ALT) levels; and the HOMA-insulin resistance (HOMA-IR). Results: In rats with pre-eclampsia, the systolic blood pressure; the concentrations of serum uric acid, creatinine, nitric oxide (NO), xanthine oxidase, myeloperoxidase, blood glucose, serum cholesterol, triglycerides, AST, and ALT; and the calculated HOMA-IR were significantly increased compared to those in the rats in the other groups. Additionally, apelin treatment significantly improved these parameters in the apelin-treated group. Conclusion: This study examined the potential mechanisms whereby apelin may act as a curative candidate to reduce hepatic injury and inhibit kidney damage and the development of metabolic disorders in an experimental model of preeclampsia.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 99%

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RETRACTED: A Potential Role of Apelin-13 against Hepatic Injury and Metabolic Disorders in Preeclampsia Induced by L-NAME

et al. 2021

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Correlation between Apelin and Some Angiogenic Factors in the Pathogenesis of Preeclampsia: Apelin-13 as Novel Drug for Treating Preeclampsia and Its Physiological Effects on Placenta

Hamza

Diab

Zahra

et al. 2021

International Journal of Endocrinology

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Preeclampsia (PE) is one of the commonest causes for maternal and fetal morbidity and mortality. Imbalances of angiogenic factors, oxidative stress, and inflammatory response have a role in the pathogenesis of PE. Data regarding the circulating apelin level and its role in PE remains controversial. This study was formulated to assess the serum apelin level in PE, investigate its correlation with some inflammatory, oxidative stress, and angiogenic proteins in a nitric oxide synthase inhibitor; the N (gamma)-nitro-L-arginine methyl ester (L-NAME)-induced rat model of PE and determine whether apelin administration could protect against development of PE. 40 healthy adult female albino rats and 10 adult male albino rats were used in this study. The pregnant female rats were randomly divided into three groups: group 1 (normal pregnant group), group 2 (PE-induced group), injected subcutaneously with 75 mg L-NAME/kg bodyweight/day starting from day 9 to 20 of gestation, and group 3 (PE-induced group supplemented with apelin (PE + apelin)); PE induced as before and simultaneously subcutaneously injected with apelin-13 (6 × 10−8 mol/kg bodyweight/twice daily) beginning from day 6 to 20 of gestation. In all groups, blood pressure and urine protein were determined at gestation days (GD) 0, 10, and 18. Moreover, serum apelin, placental growth factor (PLGF), vascular endothelial growth factor (VEGF), soluble fms-like tyrosine kinase-1 (sFlt-1), soluble endoglin (sEng), interferon-gamma (IFN-γ), and interleukin-10 (IL-10) levels and serum superoxide dismutase enzyme (SOD) and catalase (CAT) activities of all groups were estimated at the end of experiment. Placental histopathological examination was also performed. PE-induced rats showed significantly decreased serum apelin levels. Moreover, they showed significantly increased blood pressures, urine proteins, sFlt-1, sEng, and IFN-γ (mean arterial blood pressure, urine proteins, sFlt-1, sEng, and IFN-γ showed significant negative correlations with serum apelin level), but it showed significantly decreased VEGF, PLGF, IL-10, SOD, and CAT (VEGF, PLGF, IL-10, and SOD showed significant positive correlations with serum apelin level). In contrast, exogenous apelin administration significantly ameliorated these parameters together with improvement in the placental histoarchitecture in the apelin-supplemented PE group. This study demonstrated the protective effects of apelin administration on the pathogenesis of PE.

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Serum Adropin Levels in a Preeclampsia Like L-Name Rat Model Treated with Sildenafil Citrate

Cited by 2 publications

References 25 publications

RETRACTED: A Potential Role of Apelin-13 against Hepatic Injury and Metabolic Disorders in Preeclampsia Induced by L-NAME

RETRACTED: A Potential Role of Apelin-13 against Hepatic Injury and Metabolic Disorders in Preeclampsia Induced by L-NAME

Correlation between Apelin and Some Angiogenic Factors in the Pathogenesis of Preeclampsia: Apelin-13 as Novel Drug for Treating Preeclampsia and Its Physiological Effects on Placenta

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