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Curcumin and dexmedetomidine prevents oxidative stress and renal injury in hind limb ischemia/reperfusion injury in a rat model

机译:姜黄素和右美托咪定可预防大鼠后肢缺血/再灌注损伤中的氧化应激和肾脏损伤

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Abstract Curcumin and dexmedetomidine have been shown to have protective effects in ischemia–reperfusion injury on various organs. However, their protective effects on kidney tissue against ischemia–reperfusion injury remain unclear. We aimed to determine whether curcumin or dexmedetomidine prevents renal tissue from injury that was induced by hind limb ischemia–reperfusion in rats. Fifty rats were divided into five groups: sham, control, curcumin (CUR) group (200?mg/kg curcumin, n?=?10), dexmedetomidine (DEX) group (25?μg/kg dexmedetomidine, n?=?10), and curcumin–dexmedetomidine (CUR–DEX) group (200?mg/kg curcumin and 25?μg/kg dexmedetomidine). Curcumin and dexmedetomidine were administered intraperitoneally immediately after the end of 4?h ischemia, just 5?min before reperfusion. The extremity re-perfused for 2?h and then blood samples were taken and total antioxidant capacity (TAC), total oxidative status (TOS) levels, and oxidative stress index (OSI) were measured, and renal tissue samples were histopathologically examined. The TAC activity levels in blood samples were significantly lower in the control than the other groups (p?0.01 for all comparisons). The TOS activity levels in blood samples were significantly higher in Control group and than the other groups (p??0.01 for all comparison). The OSI were found to be significantly increased in the control group compared to others groups (p?0.001 for all comparisons). Histopathological examination revealed less severe lesions in the sham, CUR, DEX, and CUR–DEX groups, compared with the control group (p? 0.01). Rat hind limb ischemia–reperfusion causes histopathological changes in the kidneys. Curcumin and dexmedetomidine administered intraperitoneally was effective in reducing oxidative stress and renal histopathologic injury in an acute hind limb I/R rat model.
机译:摘要姜黄素和右美托咪定已显示出对各种器官缺血再灌注损伤的保护作用。然而,它们对肾脏组织抵抗缺血-再灌注损伤的保护作用仍不清楚。我们旨在确定姜黄素或右美托咪定是否能防止大鼠后肢缺血再灌注引起的肾脏组织损伤。将50只大鼠分为5组:假手术,对照组,姜黄素(CUR)组(200μg/ kg姜黄素,n≥10),右美托咪定(DEX)组(25μg/ kg右美托咪定,n≥10)。 )和姜黄素-右美托咪定(CUR-DEX)组(200?mg / kg姜黄素和25?μg/ kg右美托咪定)。缺血4小时后立即腹膜内给予姜黄素和右美托咪定,仅在再灌注前5分钟。肢体再灌注2?h,然后取血样,测量总抗氧化能力(TAC),总氧化状态(TOS)水平和氧化应激指数(OSI),并对肾脏组织样品进行组织病理学检查。对照组的血样中TAC活性水平显着低于其他组(所有比较的P均0.01)。对照组和其他组的血液样本中的TOS活性水平均显着较高(所有比较的p ?? 0.01)。与其他组相比,对照组的OSI显着增加(所有比较均P <0.001)。组织病理学检查显示,与对照组相比,假手术,CUR,DEX和CUR-DEX组的病灶较轻(p <0.01)。大鼠后肢缺血-再灌注导致肾脏组织病理学改变。腹膜内给予姜黄素和右美托咪定可有效减轻急性后肢I / R大鼠模型的氧化应激和肾脏组织病理学损伤。

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