Senol Sefika Pinar, Temiz Meryem, Guden Demet Sinem, Cecen Pelin, Sari Ayse Nihal, Sahan-Firat Seyhan, Falck John R, Dakarapu Rambabu, Malik Kafait U, Tunctan Bahar
Department of Pharmacology, Faculty of Pharmacy, Yenisehir Campus, Mersin University, 33169, Mersin, Turkey.
Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Inflamm Res. 2016 May;65(5):367-87. doi: 10.1007/s00011-016-0922-5. Epub 2016 Feb 13.
We have previously demonstrated that downregulation of the MyD88/TAK1-dependent signaling pathway associated with increased CYP4A1 expression and 20-HETE formation participates in the protective effect of N-(20-hydroxyeicosa-5[Z],14[Z]-dienoyl)glycine (5,14-HEDGE), a 20-HETE mimetic, against vascular hyporeactivity, hypotension, tachycardia, inflammation, and mortality in a rodent model of septic shock. The aim of this study was to determine whether increased renal and cardiovascular expression of PPARα/β/γ and RXRα associated with decreased expression and/or activity of AP-1 and importin-α3 participates in the protective effect of 5,14-HEDGE in response to systemic administration of lipopolysaccharide (LPS).
Conscious male Wistar rats received saline (4 ml/kg) or LPS (10 mg/kg) at time 0. Blood pressure and heart rate were measured using a tail-cuff device. Separate groups of LPS-treated rats were given 5,14-HEDGE (30 mg/kg) 1 h after injection of saline or LPS. The rats were killed 4 h after saline or LPS administration and the kidney, heart, thoracic aorta, and superior mesenteric artery were collected for measurement of protein expression.
Blood pressure fell by 33 mmHg and heart rate rose by 72 beats/min at 4 h after LPS administration. In LPS-treated rats, tissue protein expressions of cytosolic/nuclear PPARα/β/γ and nuclear RXRα, in addition to nuclear translocation of PPARα/β/γ proteins, were decreased, while cytosolic/nuclear AP-1 subunit c-jun/phosphorylated c-jun and importin-α3 protein expression as well as their nuclear translocation were increased. The LPS-induced changes were prevented by 5,14-HEDGE.
The results suggest that an increase in the expression of PPARα/β/γ and RXRα as well as a decrease in AP-1 and importin-α3 expression/activity participates in the protective effect of 5,14-HEDGE against hypotension, tachycardia, and inflammation during endotoxemia and thus have a beneficial effect in septic shock treatment.
我们之前已经证明,与CYP4A1表达增加和20-羟基二十碳四烯酸(20-HETE)形成相关的MyD88/TAK1依赖性信号通路的下调参与了N-(20-羟基二十碳-5[Z],14[Z]-二烯酰)甘氨酸(5,14-HEDGE,一种20-HETE模拟物)对脓毒症休克啮齿动物模型中血管反应性降低、低血压、心动过速、炎症和死亡率的保护作用。本研究的目的是确定PPARα/β/γ和RXRα在肾脏和心血管中的表达增加以及与AP-1和importin-α3表达和/或活性降低相关,是否参与了5,14-HEDGE对全身给予脂多糖(LPS)的保护作用。
清醒雄性Wistar大鼠在时间0时接受生理盐水(4 ml/kg)或LPS(10 mg/kg)。使用尾套装置测量血压和心率。在注射生理盐水或LPS 1小时后,将单独的LPS处理大鼠组给予5,14-HEDGE(30 mg/kg)。在给予生理盐水或LPS 4小时后处死大鼠,并收集肾脏、心脏、胸主动脉和肠系膜上动脉用于测量蛋白质表达。
LPS给药4小时后,血压下降33 mmHg,心率上升72次/分钟。在LPS处理的大鼠中,胞质/核PPARα/β/γ和核RXRα的组织蛋白表达,以及PPARα/β/γ蛋白的核转位均降低,而胞质/核AP-1亚基c-jun/磷酸化c-jun和importin-α3蛋白表达及其核转位增加。5,14-HEDGE可预防LPS诱导的变化。
结果表明,PPARα/β/γ和RXRα表达增加以及AP-1和importin-α3表达/活性降低参与了5,14-HEDGE对内毒素血症期间低血压、心动过速和炎症的保护作用,因此对脓毒症休克治疗具有有益作用。