Effect of Irisin on Experimentally-Induced Preeclampsia in Female Albino Rats

Abstract
Background: Preeclampsia is a syndrome associated with pregnancy and characterized by new onset hypertension and proteinuria that might result from hypoxic placenta which secretes pathogenic factors that enter the maternal blood stream and result in endothelial dysfunction. Irisin is a myokine that improves endothelial dysfunction and has anti-oxidant and anti-inflammatory effects. Therefore, the current study aims to explore the possible effects of irisin on a model of preeclampsia induced experimentally in adult female albino rats and to explain the possible underlying mechanisms.
Material and Methods: 24 adult female albino rats were divided into three groups: Group I (control pregnant rats): That were injected daily with saline solution from 7th day to 14th day of gestation, Group II (preeclamptic rats): In which pregnant rats were injected daily with L-NAME starting from the 7th day to 14th day of gestation, and Group III (irisin-treated preeclamptic rats): In which L-NAME-induced preec-lamptic rats were treated daily with intravenous irisin; 2μg/kg; from 10th day to 19th day of gestation. In all groups, systolic and diastolic Blood Pressure (BP), Total Urinary Proteins/24 hour (TUP), number of living pups and serum Endothelin-1 (ET-1), Interleukin-6 (IL-6), Nitric Oxide (NO), Placental Growth Factor (PGF), insulin, glucose, Super Oxide Dismutase (SOD), Malondialdehyde (MDA) were measured and HOMA-IR was calculated.
Results: Irisin-treated preeclamptic rats showed significant decrease in systoilic BP, diastolic BP, TUP, ET-1, IL-6, HOMA-IR, MDA and significant increase in the number of living pups, NO, PGF, SOD in comparison to preeclamptic rats.
Conclusion: Irisin may be a promising molecule for treatment of vascular complications of preeclampsia, as manifested by the improvement of hypertension and proteinuria in preeclamptic rats, through several mechanisms that may involve decreasing the oxidative stress, IL-6, ET-1 and insulin resistance or increasing the levels of PGF and NO.