Omrani Hasan, Alipour Mohammad Reza, Farajdokht Fereshteh, Ebrahimi Hadi, Mesgari Abbasi Mehran, Mohaddes Gisou
1 Drug Applied Research Center of Tabriz University of Medical Sciences , Tabriz, Iran .
2 Neurosciences Research Center of Tabriz University of Medical Sciences , Tabriz, Iran .
High Alt Med Biol. 2017 Jun;18(2):145-151. doi: 10.1089/ham.2016.0132. Epub 2017 Mar 21.
Omrani, Hasan, Mohammad Reza Alipour, Fereshteh Farajdokht, Hadi Ebrahimi, Mehran Mesgari Abbasi, and Gisou Mohaddes. Effects of chronic ghrelin treatment on hypoxia-induced brain oxidative stress and inflammation in a rat normobaric chronic hypoxia model. High Alt Med Biol. 18:145-151, 2017.
This study aimed to evaluate the probable antioxidant effects of ghrelin in the brain and serum and its effect on tumor necrosis factor-alpha (TNF-α) levels in the brain in a model of chronic systemic hypoxia in rats.
Systemic hypoxia was induced by a normobaric hypoxic chamber (O 11%) for ten days. Adult male Wistar rats were divided into control (C), chronic ghrelin (80 μg/kg/10 days) (Ghr), chronic hypoxia (CH), and CH and ghrelin (80 μg/kg/ip/10 days) (CH + Gh) groups. The activity of superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), and malondialdehyde (MDA), total antioxidant capacity, and TNF-α levels were assessed in the serum and brain tissue.
Our results showed that chronic ghrelin administration attenuated the CH-increased oxidative stress by decreasing MDA levels in the serum and brain tissue. Moreover, ghrelin enhanced the antioxidant defense against hypoxia-induced oxidative stress in the serum and brain tissue. Brain TNF-α levels in CH did not change significantly; however, ghrelin significantly (p < 0.001) decreased it.
These results indicated that ghrelin promoted antioxidative and anti-inflammatory defense under chronic exposure to hypoxia. Therefore, ghrelin might be used as a potential therapy in normobaric hypoxia and oxidative stress induced by CH.
奥姆拉尼，哈桑，穆罕默德·礼萨·阿里普尔，费雷什特·法拉吉多赫特，哈迪·易卜拉欣米，梅赫兰·梅斯加里·阿巴西，以及吉苏·莫哈德斯。慢性胃饥饿素治疗对大鼠常压慢性缺氧模型中缺氧诱导的脑氧化应激和炎症的影响。《高海拔医学与生物学》。2017年第18卷，第145 - 151页。
本研究旨在评估胃饥饿素在大鼠慢性全身缺氧模型中对脑和血清可能的抗氧化作用及其对脑肿瘤坏死因子-α（TNF-α）水平的影响。
通过常压缺氧舱（氧含量11%）诱导全身缺氧10天。成年雄性Wistar大鼠分为对照组（C）、慢性胃饥饿素组（80μg/kg/10天）（Ghr）、慢性缺氧组（CH）以及慢性缺氧加胃饥饿素组（80μg/kg腹腔注射/10天）（CH + Gh）。评估血清和脑组织中超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GPx）、过氧化氢酶（CAT）、丙二醛（MDA）的活性、总抗氧化能力以及TNF-α水平。
我们的结果表明，慢性给予胃饥饿素通过降低血清和脑组织中的MDA水平减轻了慢性缺氧增加的氧化应激。此外，胃饥饿素增强了血清和脑组织中针对缺氧诱导的氧化应激的抗氧化防御。慢性缺氧组脑TNF-α水平无显著变化；然而，胃饥饿素使其显著降低（p < 0.001）。
这些结果表明，胃饥饿素在慢性缺氧暴露下促进了抗氧化和抗炎防御。因此，胃饥饿素可能作为常压缺氧和慢性缺氧诱导的氧化应激的一种潜在治疗方法。
