s-1743 and Ischemia

Preeclampsia (PE) is a pregnancy-specific hypertensive disorder with end-organ damage that presents after 20 wk of gestation. PE pathophysiology often includes vascular dysfunction and increased inflammation that continues to damage patient health even after PE resolves. Currently, there is no cure for PE beyond delivery of the fetal-placental unit. Previous clinical studies have identified elevated placental NLRP3 expression in patients with PE and suggest NLRP3 as a potential therapeutic target. In this study, we examined the effect of NLRP3 inhibition on PE pathophysiology in the reduced uterine perfusion pressure (RUPP) model rat using MCC950 (20 mg/kg/day) or esomeprazole (3.5 mg/kg/day). We hypothesized that increased NLRP3 in response to placental ischemia impairs anti-inflammatory IL-33 signaling to induce T-helper 17 cell (T

Topics: Animals; Blood Pressure; Esomeprazole; Female; Humans; Hypertension; Inflammation; Interleukin-33; Ischemia; NLR Family, Pyrin Domain-Containing 3 Protein; Placenta; Pre-Eclampsia; Pregnancy; Rats; Rats, Sprague-Dawley

Topics: Aged; Anti-Ulcer Agents; Body Mass Index; Duodenal Ulcer; Duodenitis; Esomeprazole; Humans; Hypertension, Portal; Ischemia; Liver Cirrhosis, Alcoholic; Male; Risk Factors; Stomach Ulcer; Treatment Outcome