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.

Abstract

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. 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, H2 O2 , 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. 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. Coenzyme Q10 attenuated placental inflammatory and oxidative stress, thereby protecting the rats against preeclampsia by activating the Nrf2/HO-1 pathway.