Hyperbaric Oxygen Preconditioning Upregulates Heme OxyGenase-1 and Anti-Apoptotic Bcl-2 Protein Expression in Spontaneously Hypertensive Rats with Induced Postischemic Acute Kidney Injury.

Hyperbaric Oxygen Preconditioning Upregulates Heme OxyGenase-1 and Anti-Apoptotic Bcl-2 Protein Expression in Spontaneously Hypertensive Rats with Induced Postischemic Acute Kidney Injury.
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DOI:
10.3390/ijms22031382
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发表时间:
2021-01-30
影响因子:
5.6
通讯作者:
Miloradovic Z
Miloradovic Z
中科院分区:
生物学2区
文献类型:
--
作者:
Nesovic Ostojic J;Ivanov M;Mihailovic-Stanojevic N;Karanovic D;Kovacevic S;Brkic P;Zivotic M;Vajic UJ;Jovovic D;Jeremic R;Ljubojevic-Holzer S;Miloradovic Z

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肾缺血再灌注(I/R)损伤是引起急性肾损伤(AKI)的最常见原因。缺血后AKI的发病机制涉及血流动力学改变、氧化应激、炎症过程、钙离子超载、细胞凋亡和坏死。到目前为止,治疗AKI的治疗方法极其有限。因此,本研究旨在探讨高压氧(HBO)预适应对正常血压Wistar和自发性高血压大鼠(SHR)脑缺血后急性脑损伤(AKI)中保护酶、血红素氧合酶-1(HO-1)、促凋亡的Bax和抗凋亡的Bcl2蛋白表达的影响。动物随机分为假手术Wistar大鼠(W-sham)、大鼠脑缺血再灌注损伤(W-AKI)和高压氧预适应(W-AKI+HBO)组。另一方面,SHR大鼠也分为三组:SHR-Sham组、SHR-AKI组和SHR-AKI+HBO组。我们发现高压氧预适应上调了Wistar和SH大鼠HO-1和抗细胞凋亡的Bcl2蛋白的表达。此外,高压氧预适应改善了肾小球滤过率,通过显著增加两个品系大鼠的肌酐、尿素和磷酸盐清除来支持这一点。考虑到我们的结果,我们还可以说,即使在高血压的情况下,我们也可以期待高压氧预适应对实验性AKI的保护作用。
Renal ischemia and reperfusion (I/R) injury is the most common cause of acute kidney injury (AKI). Pathogenesis of postischemic AKI involves hemodynamic changes, oxidative stress, inflammation process, calcium ion overloading, apoptosis and necrosis. Up to date, therapeutic approaches to treat AKI are extremely limited. Thus, the aim of this study was to evaluate the effects of hyperbaric oxygen (HBO) preconditioning on citoprotective enzyme, heme oxygenase-1 (HO-1), pro-apoptotic Bax and anti-apoptotic Bcl-2 proteins expression, in postischemic AKI induced in normotensive Wistar and spontaneously hypertensive rats (SHR). The animals were randomly divided into six experimental groups: SHAM-operated Wistar rats (W-SHAM), Wistar rats with induced postischemic AKI (W-AKI) and Wistar group with HBO preconditioning before AKI induction (W-AKI + HBO). On the other hand, SHR rats were also divided into same three groups: SHR-SHAM, SHR-AKI and SHR-AKI + HBO. We demonstrated that HBO preconditioning upregulated HO-1 and anti-apoptotic Bcl-2 protein expression, in both Wistar and SH rats. In addition, HBO preconditioning improved glomerular filtration rate, supporting by significant increase in creatinine, urea and phosphate clearances in both rat strains. Considering our results, we can also say that even in hypertensive conditions, we can expect protective effects of HBO preconditioning in experimental model of AKI.
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