Preeclampsia is a pregnancy-specific disease characterized by hypertension as well as proteinuria after the 20th week of pregnancy. Animal models are effective tools for studying the pathogenesis, diagnostic criteria and treatment methods of preeclampsia. The present study sought to establish and evaluate a preeclampsia-like Sprague Dawley (SD) rat model using N-nitro-L-arginine methyl ester (L-NAME). Rats were randomly assigned to 7 groups (n=10 in each): Control rats and rats treated with low-dose L-NAME (40 mg/kg body weight/day) starting from gestational day (GD) 9, medium-L-NAME (75 mg/kg body weight/day) starting from GD 9 (9D ML group), high-dose L-NAME (125 mg/kg body weight/day) starting from GD 9, low-dose L-NAME starting from GD 10, medium-dose L-NAME starting from GD 10 and high-dose L-NAME starting from GD 10. Blood pressure (BP), 24-h proteinuria, fetal intrauterine growth, histopathological changes, the plasma soluble fms-like tyrosine kinase-1 (sFlt-1)/placental growth factor (PLGF) ratio and cytokine levels were evaluated. Elevated BP, increased urinary albumin excretion, severe endotheliosis, mesangial expansion and increased sFlt-1/PLGF ratios were observed in the experimental groups compared with the control group (P<0.05), particularly in the 9D ML group. The results of the present study may optimize the conditions of the previously established L-NAME-induced preeclampsia SD rat model and aid further study into the pathogenesis of preeclampsia.

Graphical abstract LBP attenuated myocardial ischemia/reperfusion injury by restoring redox status, ultimately improving cardiac function. CAT: catalase; GPX: glutathione peroxidase; HO1: heme oxygenase 1; IL-6: interleukin-6; I/R: ischemia/reperfusion; LBP: Lycium barbarum polysaccharides; Nrf2: nuclear factor erythroid 2-related factor 2; NQO1: NADPH dehydrogenase quinone 1; ROS: reactive oxygen species; SOD: superoxide dismutase; TNF-α: tumor necrosis factor α.