Wu Wei, Chen Hai-min
Affiliated Hospital of Ningbo University, China.
Yao Xue Xue Bao. 2014 Oct;49(10):1400-5.
The effect of astaxanthin on N(Ω)-nitro-L-arginine methyl ester (L-NAME) induced preeclampsia disease rats was investigated. Thirty pregnant Sprague-Dawley rats were randomly divided into three groups (n = 10): blank group, L-NAME group and astaxanthin group. From day 5 to 20, astaxanthin group rats were treated with astaxanthin (25 mg x kg(-1) x d(-1) x bw(-1)) from pregnancy (day 5). To establish the preeclamptic rat model, L-NAME group and astaxanthin group rats were injected with L-NAME (125 mg x kg(-1) x d(-1) x bw(-1)) from days 10-20 of pregnancy. The blood pressure and urine protein were recorded. Serum of each group was collected and malondialdehyde (MDA), superoxide dismutase (SOD) and nitric oxide synthase (NOS) activities were analyzed. Pathological changes were observed with HE stain. The expression of NF-κB (nuclear factor kappa B), ROCK II (Rho-associated protein kinase II), HO-1 (heme oxygenase-1) and Caspase 3 were analyzed with immunohistochemistry. L-NAME induced typical preeclampsia symptoms, such as the increased blood pressure, urinary protein, the content of MDA, etc. Astaxanthin significantly reduced the blood pressure (P < 0.01), the content of MDA (P < 0.05), and increased the activity of SOD (P < 0.05) of preeclampsia rats. The urinary protein, NO, and NOS were also decreased. HE stain revealed that after treated with astaxanthin, the thickness of basilal membrane was improved and the content of trophoblast cells and spiral arteries was reduced. Immunohistochemistry results revealed that the expressions of NF-κB, ROCK II and Caspase 3 in placenta tissue were effectively decreased, and HO-1 was increased. Results indicated that astaxanthin can improve the preeclampsia symptoms by effectively reducing the oxidative stress and inflammatory damages of preeclampsia. It revealed that astaxanthin may be benefit for prevention and treatment of preeclampsia disease.
研究了虾青素对N（Ω）-硝基-L-精氨酸甲酯（L-NAME）诱导的子痫前期疾病大鼠的影响。将30只怀孕的Sprague-Dawley大鼠随机分为三组（n = 10）：空白组、L-NAME组和虾青素组。从妊娠第5天至20天，虾青素组大鼠从妊娠（第5天）开始用虾青素（25 mg·kg⁻¹·d⁻¹·bw⁻¹）进行治疗。为建立子痫前期大鼠模型，L-NAME组和虾青素组大鼠在妊娠第10 - 20天注射L-NAME（125 mg·kg⁻¹·d⁻¹·bw⁻¹）。记录血压和尿蛋白。收集每组血清并分析丙二醛（MDA）、超氧化物歧化酶（SOD）和一氧化氮合酶（NOS）活性。用苏木精-伊红（HE）染色观察病理变化。用免疫组织化学分析核因子κB（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。L-NAME诱导了典型的子痫前期症状，如血压升高、尿蛋白增加、MDA含量升高等。虾青素显著降低了子痫前期大鼠的血压（P < 0.０1）、MDA含量（P < 0.０5），并提高了SOD活性（P < 0.０5）。尿蛋白、一氧化氮（NO）和NOS也降低。HE染色显示，用虾青素治疗后，基底膜厚度得到改善，滋养层细胞和螺旋动脉含量减少。免疫组织化学结果显示，胎盘组织中NF-κB、ROCK II和半胱天冬酶3的表达有效降低，而HO-1增加。结果表明，虾青素可通过有效降低子痫前期的氧化应激和炎症损伤来改善子痫前期症状。这表明虾青素可能有助于子痫前期疾病的预防和治疗。
