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首页> 外文期刊>Clinical and experimental pharmacology & physiology >Effects of captopril, telmisartan and bardoxolone methyl (CDDO-Me) in ischemia-reperfusion-induced acute kidney injury in rats: An experimental comparative study
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Effects of captopril, telmisartan and bardoxolone methyl (CDDO-Me) in ischemia-reperfusion-induced acute kidney injury in rats: An experimental comparative study

机译：卡托普利，替米沙坦和甲基巴多索隆（CDDO-Me）在缺血再灌注诱导的大鼠急性肾损伤中的作用：实验比较研究

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Renal ischemia-reperfusion (IR) injury is one of the most common causes of acute kidney injury. This study investigated the effects of captopril (CAP), telmisartan (TEL) and bardoxolone methyl (BM) in animals with renal IR injury. Adult male Wistar-Albino rats were divided into six groups: control, vehicle, IR, IR with CAP, IR with TEL and IR with BM. Before IR was induced, drugs were administered by oral gavage. After a 60-min ischemia and a 120-min reperfusion period, bilateral nephrectomies were performed. Serum urea, creatinine, neutrophil gelatinase-associated lipocalin (NGAL) levels, tissue total oxidant status (TOS), total antioxidant status (TAS), total thiol (TT), asymmetric dimethylarginine (ADMA) levels, superoxide dismutase (SOD) activity and glutathione peroxidase (GSH-Px) activity were measured. Tissue mRNA expression levels of peroxisome proliferator-activated receptor-γ(phonetic) (PPAR-γ(phonetic)), nuclear factor erythroid 2-related factor 2 (Nrf2) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) were analyzed. In addition, renal tissues were evaluated histopathologically and immunohistochemically. All tested drugs reduced renal damage, apoptosis, urea, creatinine, NGAL, TOS, nitric oxide (NO) and ADMA levels, NF-κB, inducible nitric oxide synthase (iNOS) and endothelin-1 (ET-1) expressions (P < 0.001). All tested drugs increased SOD activity, GSH-Px activity, TAS levels, TT levels, endothelial nitric oxide synthase (eNOS) expression, dimethylarginine dimethylaminohydrolases (DDAHs) expression, Nrf2 expression and PPAR-γ(phonetic) expression (P < 0.001, P < 0.003). These results suggest that CAP, TEL and BM pretreatment could reduce renal IR injury via anti-inflammatory, antioxidant and anti-apoptotic effects.
机译：肾缺血再灌注（IR）损伤是急性肾损伤的最常见原因之一。这项研究调查了卡托普利（CAP），替米沙坦（TEL）和甲基巴多索隆（BM）在肾IR损伤动物中的作用。将成年雄性Wistar-Albino大鼠分成六组：对照组，媒介物，IR，具有CAP的IR，具有TEL的IR和具有BM的IR。在诱发IR之前，通过管饲法给药。缺血60分钟和再灌注120分钟后，进行双侧肾切除术。血清尿素，肌酐，中性粒细胞明胶酶相关的脂蛋白（NGAL）水平，组织总氧化剂状态（TOS），总抗氧化剂状态（TAS），总硫醇（TT），不对称二甲基精氨酸（ADMA）水平，超氧化物歧化酶（SOD）活性和测定了谷胱甘肽过氧化物酶（GSH-Px）的活性。过氧化物酶体增殖物激活受体-γ（语音）（PPAR-γ（语音）），核因子红系2相关因子2（Nrf2）和核因子κ轻链增强子的组织mRNA表达水平（ NF-κB）进行了分析。此外，对肾脏组织进行了组织病理学和免疫组织化学评估。所有测试的药物均降低了肾脏损害，细胞凋亡，尿素，肌酐，NGAL，TOS，一氧化氮（NO）和ADMA水平，NF-κB，诱导型一氧化氮合酶（iNOS）和内皮素1（ET-1）的表达（P < 0.001）。所有测试的药物均增加了SOD活性，GSH-Px活性，TAS水平，TT水平，内皮型一氧化氮合酶（eNOS）表达，二甲基精氨酸二甲基氨基水解酶（DDAHs）表达，Nrf2表达和PPAR-γ（语音）表达（P <0.001，P <0.003）。这些结果表明，CAP，TEL和BM预处理可通过抗炎，抗氧化和抗凋亡作用减少肾脏IR损伤。

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