Protective and anti-inflammatory effect of trans-cinnamic acid on hippocampus cell damage and fetal forebrain neuroinflammation in preeclampsia model rats

Pre-eclampsia (PE) can cause brain damage before birth. However, its mechanism is not clear. The present study evaluated the effect of cinnamic acid (CIN) on the expression of inflammatory cytokines of the forebrain and neuronal damage in the hippocampus of PE model fetuses induced with l-NAME.

25 pregnant female rats were randomly divided into 5 groups: control group (no treatment), PE+NS group (daily injection of 250 mg l-NAME from embryonic day (ED) 15 to 20 to induce PE and then one hour later normal saline gavage), PE+CIN25, PE+CIN50 and PE+CIN100 groups (CIN gavage with doses of 25, 50 and 100 mg, respectively, one hour after l-NAME injection). On the ED21, after cesarean section, the fetal brain was dissected. The content of tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6) and interleukin-1 beta (IL-1β) in the forebrain and cell density in the CA1 and CA3 regions of the fetal hippocampus were measured.

A significant increase in TNF-α, IL-6 and IL-1β in the forebrain along with a decrease in neuronal density in the CA1/CA3 regions was seen in the PE+NS group compared to the control group (p<0.05). While in the groups receiving CIN, they showed a significant decrease in TNF-α, IL-6 and IL-1β in the forebrain and an increase in CA1/CA3 neuronal density compared to the PE+NS group (p<0.05).

CIN improved the inflammation and reduced cell damage in the hippocampus of PE model fetuses through modulating the level of anti-inflammatory cytokines in the fetal forebrain.