乳香提取物对糖尿病大鼠大脑皮层的抗氧化作用

Anwar Masoud , Mohammad Al-Ghazali , Fatima Al-Futini , Anisah Al-Mansori , Abdulalim Al-Subahi , Abdulrahman Farhan , Majdaldeen Al-Sharafi , Reham Al-absi , Sali Al-Matari
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引用次数: 4

摘要

糖尿病(DM)患者的数量是全世界关注的主要问题之一。由于氧化应激参与糖尿病病理的主要机制之一,我们在此研究乳香(FRN)的抗氧化能力,以治疗或减少糖尿病大鼠大脑皮层的糖尿病并发症。将动物分为4组,对照组、FRN组给予FRN 500 mg/kg剂量,连续5周;DM组给予单剂量150/kg / p的四氧嘧啶诱导糖尿病;DM + FRN组给予单剂量150/kg / p的四氧嘧啶诱导糖尿病,然后再给予FRN 500 mg/kg,连续5周。动物被献祭;他们的大脑皮层被切除并用于生化和组织病理学分析。糖尿病组的四氧嘧啶治疗显示过氧化氢酶(CAT)活性和其他非酶抗氧化剂(即硫醇群)显著降低,同时蛋白质和白蛋白水平降低,尿酸水平升高。然而,DM + FRN组DM + FRN组抗氧化剂恢复明显,DM + FRN组的硫醇含量(总硫醇、蛋白质硫醇和谷胱甘肽)较DM动物有所增加(p <0.05)。CAT活性恢复(p <0.05)与对照组基本持平,蛋白和白蛋白水平恢复(p <0.05)。DM组尿酸水平升高,经FRN治疗后恢复到对照组水平(p <0.05)。我们还观察到,FRN减轻了DM + FRN组四氧嘧啶引起的组织病理学损伤。综上所述,FRN具有减轻四氧嘧啶诱导的糖尿病大鼠皮质氧化损伤的有益作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Antioxidant effect of frankincense extract in the brain cortex of diabetic rats

The number of diabetes mellitus (DM) patients is one of the major concerns worldwide. As one of the main mechanisms of DM pathology is the involvement of oxidative stress, here we investigate the antioxidant capacities of frankincense (FRN) to treat or reduce the DM complications in the brain cortices of DM rats. Animals were segregated into four groups, the control group, FRN group given a dose of 500 mg of FRN/kg for 5 weeks, DM group given a single dose of 150/kg i.p of alloxan to induce diabetes and DM + FRN group given a single dose of 150/kg i.p to induce DM then followed by FRN 500 mg/kg for 5 weeks. The animals were sacrificed; their cerebral cortices were removed and used for biochemical and histopathological analyses.

Alloxan treatment in the DM group showed significant reductions in catalase (CAT) activity and other non-enzymatic antioxidants i.e. thiol groups, concomitant with decreases in the levels of protein and albumin and increasing the level of uric acid. However, FRN administration to DM animals in DM + FRN group showed significant recovery of antioxidants, the thiol contents (total thiols, protein thiols and glutathione) of DM + FRN group have been increased as compared with DM animals (p < 0.05). A recovery of CAT activity (p < 0.05) to almost the levels of control rats with the recovery in protein and albumin levels (p < 0.05) have been observed when FRN was administered. The uric acid level increased in DM group, came back to the levels of control after administration of FRN (p < 0.05). We also observed that FRN reduces the histopathological damage caused by alloxan in DM + FRN group. It is concluded that FRN shows a beneficial effects that can reduce the oxidative damage caused by alloxan induced DM in the cortex of rats.

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