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.
This work demonstrated the feasibility of BOLD-MRI for detecting the VAT oxygenation status in ZDF rats, and the BOLD-MRI signals were associated with insulin resistance and systemic metaflammation in ZDF rats during the development of obesity.
Imbalanced iron status in patients on HD coexisted with abnormal lipid profiles, increased anaerobic activity and higher inflammatory status, which suggests that imbalanced iron status in HD patients may play a deleterious role in cardiovascular pathophysiology. Altered GH-IGF axis found in HD patients was more obvious than in IHD patients. This may imply that the GH-IGF axis system is modulated or adapted by HD.
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