Prazosin Protects the Liver Against Renal Ischemia/Reperfusion Injury in Rats

被引:1
作者
Khajepour, Fatemeh [1 ]
Mahmoodpoor, Fariba [2 ,3 ]
Jafari, Elmira [1 ]
Kakaei, Farzad [4 ]
Bahraminia, Farina [1 ]
Aghajani, Shadi [1 ]
Vahed, Sepideh Zununi [2 ]
Bagheri, Yasin [2 ,5 ]
机构
[1] Islamic Azad Univ, Fac Vet Med, Tabriz Branch, Tabriz, Iran
[2] Tabriz Univ Med Sci, Kidney Res Ctr, Tabriz, Iran
[3] Zanjan Univ Med Sci, Sch Med, Dept Persian Med, Zanjan, Iran
[4] Tabriz Univ, Dept Gen & Vasc Surg, Med Sci, Tabriz, Iran
[5] Tabriz Univ Med Sci, Kidney Res Ctr, Tabriz 5166614756, Iran
关键词
acute kidney injury; prazosin; liver injury; distant organs; ACUTE KIDNEY INJURY; PARACETAMOL-INDUCED HEPATOTOXICITY; ISCHEMIA-REPERFUSION; GAMMA-ORYZANOL;
D O I
10.1055/a-2015-7976
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
Acute kidney injury (AKI) is a common subsequent problem after many medical conditions. AKI is associated with distant organ dysfunction where systemic inflammation and oxidative stress play major roles. In this study, the effect of Prazosin, an alpha 1-Adrenergic receptor antagonist, was investigated on the liver injury induced by kidney ischemia-reperfusion (I/R) in rats. Male adult Wistar rats (n = 21) were divided into three groups: sham, kidney I/R, and kidney I/R pre-treated with Prazosin (1 mg/kg). Kidney I/R was induced by vascular clamping of the left kidney for 45 min to reduce the blood flow. Oxidative and antioxidant factors along with apoptotic (Bax, Bcl-2, caspase3), and inflammatory (NF-kappa beta, IL-1 beta, and IL-6) factors were measured in the liver at protein levels. Prazosin could reserve liver function (p < 0.01) and increase glutathione level (p < 0.05) after kidney I/R significantly. Malonil dialdehyde (MDA), a lipid peroxidation marker, was diminished more significantly in Prazosin-treated rats compared to the kidney I/R group (p < 0.001). Inflammatory and apoptotic factors were diminished by Prazosin pre-treatment in the liver tissue (p < 0.05). Pre-administration of Prazosin could preserve liver function and decrease its inflammatory and apoptotic factors under kidney I/R conditions.
引用
收藏
页码:289 / 295
页数:7
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