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

Abstract

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.