Exogenous H(2)S Ameliorates High Salt-Induced Hypertension by Alleviating Oxidative Stress and Inflammation in the Paraventricular Nucleus in Dahl S Rats.

Exogenous H(2)S Ameliorates High Salt-Induced Hypertension by Alleviating Oxidative Stress and Inflammation in the Paraventricular Nucleus in Dahl S Rats.
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外源性 H2S 通过减轻 Dahl S 大鼠室旁核的氧化应激和炎症来改善高盐诱发的高血压

DOI:
10.1007/s12012-022-09729-7
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发表时间:
2022-05
影响因子:
3.2
通讯作者:
Jiang E
Jiang E
中科院分区:
医学4区
文献类型:
--
作者:
Liao Y;Fan Y;He Q;Li Y;Wu D;Jiang E

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硫化氢(H2S)是调节动物心血管活动的重要气体信号分子。下丘脑室旁核(PVN)是参与血压(BP)调节的主要综合性区域。我们探讨了通过腹腔注射氢硫化钠(NaHS)外源性H2S是否能缓解高盐饮食(HSD)引起的血压升高以及PVN在达尔盐敏感(Dahl S)大鼠中的作用。将Dahl S大鼠按饮食方式(正常盐饮食[NSD]和高盐饮食[HSD])和治疗方法(每日腹腔注射NaHS或生理盐水)分为4组。我们监测血压、食物和水的摄取量以及体重,持续8周。实验结束时收集血浆、肾脏和脑组织。我们发现,外源性H2S不仅可以延缓血压升高,还可以减弱HSD Dahl S大鼠血浆中去甲肾上腺素、胱抑素C和尿素氮水平的升高。H2S还增强了PVN的总抗氧化能力、超氧化物歧化酶和谷胱甘肽过氧化物酶。外源性H2S降低了核因子-κB通路和促炎细胞因子的蛋白表达,HSD大鼠PVN中核因子-κB通路和促炎细胞因子的蛋白表达明显高于NSD大鼠。此外,外源性H2S可减轻HSD诱导的PVN神经元凋亡。这些发现表明,外源性H2S通过改善PVN中的氧化应激、炎症和凋亡来减轻HSD引起的高血压。这项研究为外周H2S治疗高血压的益处提供了证据。
Hydrogen sulfide (H2S) is an important gaseous signaling molecule that regulates cardiovascular activity in animals. The hypothalamic paraventricular nucleus (PVN) is a major integrative region involved in blood pressure (BP) regulation. We explored whether exogenous H2S application by intraperitoneal injection of sodium hydrosulfide (NaHS) alleviates BP increase induced by a high salt diet (HSD) and the role of PVN in Dahl salt-sensitive (Dahl S) rats. Dahl S rats were divided into four groups according to diet regime (normal salt diet [NSD] and HSD) and treatment method (daily intraperitoneal NaHS or saline injection). We monitored BP, food and water intake, and body weight for 8 weeks. Plasma, kidney, and brain tissues were collected at the end of the experiment. We found that exogenous H2S not only delayed BP elevation but also attenuated the increase in the levels of norepinephrine, cystatin C, and blood urea nitrogen in the plasma of Dahl S rats with an HSD. Furthermore, H2S enhanced the total antioxidant capacity, superoxide dismutase, and glutathione peroxidase in the PVN. Exogenous H2S attenuated the protein expression of the nuclear factor-κB pathway and proinflammatory cytokines, which were significantly higher in the PVN in rats with an HSD than in rats with an NSD. Additionally, exogenous H2S relieved PVN neuronal apoptosis induced by an HSD. These findings suggest that exogenous H2S attenuates hypertension caused by an HSD by ameliorating oxidative stress, inflammation, and apoptosis in the PVN. This study provides evidence of the benefits of peripheral H2S therapy for hypertension.
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