Astaxanthin blocks preeclampsia progression by suppressing oxidative stress and inflammation.

To investigate the antioxidative effect of astaxanthin on Nω-nitro-L-arginine methyl ester (L-NAME)-induced preeclamptic rats. Cell survival, the level of reactive oxygen species (ROS) and the changes in mitochondrial membrane potential (MMP) were examined in astaxanthin and H2O2-treated human umbilical vein endothelial cells (HUVECs). The preeclamptic Sprague-Dawley (SD) rat model was established by injection of L‑NAME and treatment with astaxanthin. The activities of malondialdehyde (MDA), superoxide dismutase (SOD) and nitric oxide synthase (NOS) in serum were analyzed. Pathological changes were examined by hematoxylin and eosin (H&E) staining. The expression of nuclear factor (NF)‑κB, Rho‑associated protein kinase II (ROCK II), heme oxygenase‑1 (HO‑1) and caspase 3 in preeclamptic placentas were examined by immunohistochemistry. Astaxanthin significantly reduced H2O2‑induced HUVEC cell death, decreased ROS and increased MMP. Astaxanthin significantly reduced blood pressure and the content of MDA, but significantly increased the activity of SOD in preeclamptic rats. The urinary protein and the level of NO and NOS were also decreased. H&E staining revealed that the thickness of the basilar membrane was increased, while the content of trophoblast cells and spiral arteries were reduced following astaxanthin treatment. Immunohistochemistry results showed that the expression of NF‑κB, ROCK II and caspase 3 in preeclamptic placentas was significantly decreased after astaxanthin treatment, while HO‑1 expression was increased. In conclusion, astaxanthin inhibited H2O2‑induced oxidative stress in HUVECs. Astaxanthin treatment significantly improved L‑NAME‑induced preeclamptic symptoms and reduced the oxidative stress and inflammatory damages in preeclamptic placentas. Astaxanthin treatment may effectively prevent and treat preeclampsia.