Ghrelin inhibits sodium metabisulfite induced oxidative stress and apoptosis in rat gastric mucosa

Ghrelin inhibits sodium metabisulfite induced oxidative stress and apoptosis in rat gastric mucosa
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DOI:
10.1016/j.fct.2013.02.019
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发表时间:
2013-06-01
影响因子:
4.3
通讯作者:
Derin, Narin
Derin, Narin
中科院分区:
农林科学2区
文献类型:
--
作者:
Ercan, Sevim;Basaranlar, Goksun;Derin, Narin

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本研究旨在探讨生长素释放肽对亚硫酸盐诱导的大鼠胃粘膜氧化和凋亡变化的影响。将四十只雄性白化 ​​Wistar 大鼠随机分为对照组 (C)、焦亚硫酸钠 (Na2S2O5) 治疗组 (S)、生长素释放肽治疗组 (G) 和 Na2S2O5 + 生长素释放肽治疗组 (SG)。通过胃管饲给予焦亚硫酸钠(100mg/kg/天),并腹腔内给予生长素释放肽(20μg/kg/天),持续5周。 S组和SG组的血浆S-磺酸盐水平升高。钠-2。 S2O5 给药显着提高了胃粘膜中总氧化状态 (TOS) 水平,同时降低了总氧化状态 (TAS) 水平。与S组相比,Ghrelin显着降低SG组胃TOS水平。此外,发现 SG 组的 TAS 水平高于 S 组。 Na2S2O5 给药还显着增加胃粘膜细胞中凋亡细胞的数量、裂解的 caspase-3 和 PAR 表达(PARP 活性指标),并降低 Ki67 表达(细胞增殖指数)。在暴露于 Na2S2O5 的胃粘膜中,Ghrelin 处理减少了凋亡细胞数量、细胞色素 C 释放、PAR 和 caspase-3 表达,同时增加了 Ki67 表达。总之,我们认为 ghrelin 治疗可能会改善大鼠摄入 Na2S2O5 引起的由细胞凋亡和氧化应激引起的胃粘膜损伤。 (C) 2013 Elsevier Ltd. 保留所有权利。
This study aimed to investigate the effect of ghrelin administration on sulfite induced oxidative and apoptotic changes in rat gastric mucosa. Forty male albino Wistar rats were randomized into control (C), sodium metabisulfite (Na2S2O5) treated (S), ghrelin treated (G) and, Na2S2O5 + ghrelin treated (SG) groups. Sodium metabisulfite (100 mg/kg/day) was given by gastric gavage and, ghrelin (20 mu g/kg/day) was given intraperitoneally for 5 weeks. Plasma-S-sulfonate level was increased in S and SG groups. Na-2. S2O5 administration significantly elevated total oxidant status (TOS) levels while depleting total antioxidant status (TAS) levels in gastric mucosa. Ghrelin significantly decreased gastric TOS levels in the SG group compared with the S group. Additionally, TAS levels were found to be higher in SG group in reference to S group. Na2S2O5 administration also markedly increased the number of apoptotic cells, cleaved caspase-3 and PAR expression (PARP activity indicator) and, decreased Ki67 expression (cell proliferation index) in gastric mucosal cells. Ghrelin treatment decreased the number apoptotic cells, cytochrome C release, PAR and, caspase-3 expressions while increasing Ki67 expression in gastric mucosa exposed to Na2S2O5. In conclusion, we suggest that ghrelin treatment might ameliorate ingested-Na2S2O5 induced gastric mucosal injury stemming from apoptosis and oxidative stress in rats. (C) 2013 Elsevier Ltd. All rights reserved.