Xuan Rong-Rong, Niu Ting-Ting, Chen Hai-Min
Department of Gynecology and Obstetrics, The Affiliated Hospital of Medical College of Ningbo University, Ningbo, Zhejiang 315020, P.R. China.
School of Marine Science, Ningbo University, Ningbo, Zhejiang 315211, P.R. China.
Mol Med Rep. 2016 Sep;14(3):2697-704. doi: 10.3892/mmr.2016.5569. Epub 2016 Jul 28.
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.
研究虾青素对Nω-硝基-L-精氨酸甲酯（L-NAME）诱导的子痫前期大鼠的抗氧化作用。检测虾青素和过氧化氢处理的人脐静脉内皮细胞（HUVECs）的细胞存活率、活性氧（ROS）水平及线粒体膜电位（MMP）变化。通过注射L-NAME建立子痫前期的斯普拉格-道利（SD）大鼠模型并用虾青素进行处理。分析血清中丙二醛（MDA）、超氧化物歧化酶（SOD）和一氧化氮合酶（NOS）的活性。采用苏木精-伊红（H&E）染色检查病理变化。通过免疫组织化学检测子痫前期胎盘组织中核因子（NF）-κB、Rho相关蛋白激酶II（ROCK II）、血红素加氧酶-1（HO-1）和半胱天冬酶3的表达。虾青素显著降低过氧化氢诱导的HUVEC细胞死亡，降低ROS水平并提高MMP。虾青素显著降低子痫前期大鼠的血压和MDA含量，但显著提高SOD活性。尿蛋白以及NO和NOS水平也降低。H&E染色显示，虾青素处理后基底膜厚度增加，而滋养层细胞和螺旋动脉含量减少。免疫组织化学结果显示，虾青素处理后子痫前期胎盘组织中NF-κB、ROCK II和半胱天冬酶3的表达显著降低，而HO-1表达增加。总之，虾青素抑制过氧化氢诱导的HUVECs氧化应激。虾青素治疗显著改善L-NAME诱导的子痫前期症状，并减轻子痫前期胎盘组织的氧化应激和炎症损伤。虾青素治疗可能有效预防和治疗子痫前期。
