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Astaxanthin Ameliorates Blood Pressure in Salt-Induced Prehypertensive Rats Through ROS/MAPK/NF-κB Pathways in the Hypothalamic Paraventricular Nucleus
Cardiovascular Toxicology ( IF 3.4 ) Pub Date : 2021-09-18 , DOI: 10.1007/s12012-021-09695-6
Hong-Li Gao 1 , Xiao-Jing Yu 1 , Yan Zhang 1 , Chen-Long Wang 1 , Yi-Ming Lei 1 , Jia-Yue Yu 1 , Dong-Miao Zong 1 , Kai-Li Liu 1 , Dong-Dong Zhang 1 , Ying Li 1 , Hua Tian 1 , Nian-Ping Zhang 2 , Yu-Ming Kang 1
Affiliation  

Astaxanthin (AST) has a variety of biochemical effects, including anti-inflammatory, antioxidative, and antihypertensive functions. The aim of the present study was to determine whether AST ameliorates blood pressure in salt-induced prehypertensive rats by ROS/MAPK/NF-κB pathways in hypothalamic paraventricular nucleus.

To explore the central effects of AST on the development of blood pressure, prehypertensive rats were induced by a high-salt diet (HS, 8% NaCl) and its control groups were treated with normal-salt diet (NS, 0.3% NaCl). The Dahl salt-sensitive (S) rats with HS diet for 6 weeks received AST or vehicle by gastric perfusion for 6 weeks. Compared to those with NS diet, rats with HS diet exhibited increased mean arterial pressure (MAP) and heart rate (HR). These increases were associated with higher plasma level of norepinephrine (NE), interleukin 1β (IL-1β), and interleukin 6 (IL-6); elevated PVN level of reactive oxygen species (ROS), NOX2, and NOX4, that of IL-1β, IL-6, monocyte chemotactic protein 1 (MCP-1), tyrosine hydroxylase (TH), phosphorylation extracellular-signal-regulated kinase (p-ERK1/2), phosphorylation Jun N-terminal kinases (p-JNK), nuclear factor-kappa B (NF-κB) activity; and lower levels of IL-10, superoxide dismutase (SOD), and catalase (CAT) in the PVN. In addition, our data demonstrated that chronic AST treatment ameliorated these changes in the HS but not NS diet rats. These data suggested that AST could alleviate prehypertensive response in HS-induced prehypertension through ROS/MAPK/NF-κB pathways in the PVN.



中文翻译:


虾青素通过下丘脑室旁核中的 ROS/MAPK/NF-κB 通路改善盐诱导的高血压前期大鼠的血压



虾青素 (AST) 具有多种生化作用,包括抗炎、抗氧化和抗高血压功能。本研究的目的是确定 AST 是否通过下丘脑室旁核中的 ROS/MAPK/NF- κ B 通路改善盐诱导的高血压前期大鼠的血压。


为了探讨AST对血压发展的中枢作用,采用高盐饮食(HS,8% NaCl)诱导高血压前期大鼠,对照组给予正常盐饮食(NS,0.3% NaCl)。采用 HS 饮食 6 周的 Dahl 盐敏感 (S) 大鼠通过胃灌注接受 AST 或载体 6 周。与NS饮食的大鼠相比,HS饮食的大鼠表现出平均动脉压(MAP)和心率(HR)增加。这些增加与去甲肾上腺素 (NE)、白细胞介素 1 β (IL-1 β ) 和白细胞介素 6 (IL-6) 血浆水平升高有关; PVN 活性氧 (ROS)、NOX2 和 NOX4 水平升高,IL-1 β 、IL-6、单核细胞趋化蛋白 1 (MCP-1)、酪氨酸羟化酶 (TH)、磷酸化细胞外信号调节激酶水平升高(p-ERK1/2)、磷酸化 Jun N 末端激酶 (p-JNK)、核因子-κ B (NF-κB) 活性; PVN 中 IL-10、超氧化物歧化酶 (SOD) 和过氧化氢酶 (CAT) 水平较低。此外,我们的数据表明,长期 AST 治疗可以改善 HS 大鼠的这些变化,但不能改善 NS 饮食大鼠的这些变化。这些数据表明,AST 可以通过 PVN 中的 ROS/MAPK/NF-κB 通路减轻 HS 诱导的高血压前期反应。

更新日期:2021-09-19
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