Histopathological study of diclofenac induced acute renal failure under lipoic acid and bosentan therapy in male albino rats

L. B. Qasim, G. A. Jasim, Ihsan Rabeea, مساق تجهب, يلع ثيغ, عيبر حلاص ناسحا
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引用次数: 2

Abstract

Acute kidney injury (AKI), formly known as acute renal failure (ARF), is an abrupt and reversible decrease in kidney function as indicated by the glomerular filtration rate (GFR). Diclofenac-induced AKI is due to toxic effect of it on renal glomeruli, resulting in glomerular lesions. Furthermore, diclofenac causes autolysis, which increase renal intracellular osmolarity that leads to proximal renal tubular dilatations. Lipoic acid (LA) has antioxidant and anti-inflammatory activities. Bosentan is a competitive endothelin A (ETA) and endothelin B (ETB) receptors antagonist. In this study, the evaluation of effectiveness of lipoic acid and bosentan against diclofenac-induced AKI was done by histopathological examination. The results showed that diclofenac caused histopathological changes include; retracted glomerulus, tubular cast, tubule-interstitial inflammation and tubular necrosis. Lipoic acid or bosentan alone could not reduce the histopathological alterations caused by diclofenac. Meanwhile, the combination therapy was able to reduce the histopathological changes significantly (p>0.05). Therefore, the combination therapy of lipoic acid and bosentan showed promising ameliorative effect against diclofenac-induced AKI
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硫辛酸与波生坦联合治疗双氯芬酸致雄性白化大鼠急性肾功能衰竭的组织病理学研究
急性肾损伤(AKI),正式称为急性肾功能衰竭(ARF),是肾小球滤过率(GFR)显示的肾功能突然和可逆性下降。双氯芬酸所致AKI是由于其对肾小球的毒性作用,导致肾小球病变。此外,双氯芬酸引起自溶,增加肾脏细胞内渗透压,导致近端肾小管扩张。硫辛酸(LA)具有抗氧化和抗炎活性。波生坦是一种竞争性内皮素a (ETA)和内皮素B (ETB)受体拮抗剂。本研究通过组织病理学检查评价硫辛酸和波生坦对双氯芬酸诱导的AKI的疗效。结果显示双氯芬酸引起的组织病理学改变包括;肾小球缩回,小管铸造,小管间质炎症和小管坏死。单用硫辛酸或波生坦不能减轻双氯芬酸引起的组织病理学改变。同时,联合治疗能显著降低组织病理学改变(p>0.05)。因此,硫辛酸与波生坦联合治疗对双氯芬酸诱导的AKI有良好的改善作用
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