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抑制谷胱甘肽系统和上调半胱天冬酶 3 依赖性细胞凋亡介导罗眠乐诱导的胃损伤。

Suppression of glutathione system and upregulation of caspase 3-dependent apoptosis mediate rohypnol-induced gastric injury.

机构信息

Reproductive Physiology and Bioinformatics Research Unit, Department of Physiology, Ladoke Akintola University of Technology, Ogbomoso, Nigeria.

Reproductive Biology and Toxicology Research Laboratories, Oasis of Grace Hospital, Osogbo, Nigeria.

出版信息

Redox Rep. 2022 Dec;27(1):111-118. doi: 10.1080/13510002.2022.2074128.

DOI:10.1080/13510002.2022.2074128
PMID:35535549
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9103675/
Abstract

This study investigated the impact of rohypnol on gastric tissue integrity. Forty male Wistar rats were randomized into control, low dose rohypnol-treated, high dose rohypnol-treated, low dose rohypnol-treated recovery and high dose rohypnol-treated recovery groups. Rohypnol caused significant rise in gastric malondialdehyde (MDA), oxidized glutathione (GSSG), nitric oxide (NO), tumour necrotic factor-α (TNF-α), and interleukin-6 (IL-6) levels. Also, rohypnol caused reductions in gastric reduced glutathione (GSH) (as well as GSH/GSSG), and activities of superoxide dismutase (SOD), catalase, glutathione-S-transferase (GST), glutathione peroxidase (GPx), cyclo-oxygenase (COX-2). Furthermore, rohypnol upregulated caspase 3 activity and induced gastric DNA damage, evident by a rise in 8-hydroxydeoxyguanosine (8-OHdG) and DNA fragmentation index (DFI) in gastric tissue. These alterations were coupled with reduced gastric weight and distorted gastric cytoarchitecture. Cessation of rohypnol caused a significant but not complete reversal of rohypnol-induced gastric damage. This study revealed that rohypnol induced gastric injury by suppressing glutathione content and COX-2 activity, and upregulating caspase 3-dependent apoptosis, which was partly reversed by rohypnol withdrawal.

摘要

本研究旨在探讨罗眠乐对胃组织完整性的影响。将 40 只雄性 Wistar 大鼠随机分为对照组、低剂量罗眠乐处理组、高剂量罗眠乐处理组、低剂量罗眠乐处理恢复组和高剂量罗眠乐处理恢复组。罗眠乐导致胃组织丙二醛（MDA）、氧化型谷胱甘肽（GSSG）、一氧化氮（NO）、肿瘤坏死因子-α（TNF-α）和白细胞介素-6（IL-6）水平显著升高。同时，罗眠乐还导致胃还原型谷胱甘肽（GSH）（以及 GSH/GSSG）减少，超氧化物歧化酶（SOD）、过氧化氢酶、谷胱甘肽-S-转移酶（GST）、谷胱甘肽过氧化物酶（GPx）和环氧化酶（COX-2）活性降低。此外，罗眠乐上调了 caspase 3 的活性，导致胃 DNA 损伤，胃组织 8-羟基脱氧鸟苷（8-OHdG）和 DNA 片段化指数（DFI）升高证实了这一点。这些改变伴随着胃重量的减少和胃细胞结构的扭曲。停止使用罗眠乐可显著（但不完全）逆转罗眠乐引起的胃损伤。本研究表明，罗眠乐通过抑制谷胱甘肽含量和 COX-2 活性，以及上调 caspase 3 依赖性细胞凋亡，引起胃损伤，而罗眠乐戒断可部分逆转这种损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac7b/9103675/02fbb657c427/YRER_A_2074128_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac7b/9103675/464181457189/YRER_A_2074128_F0001_OB.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac7b/9103675/4ba65eb352e1/YRER_A_2074128_F0002_OB.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac7b/9103675/9829cbe46229/YRER_A_2074128_F0003_OB.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac7b/9103675/02fbb657c427/YRER_A_2074128_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac7b/9103675/464181457189/YRER_A_2074128_F0001_OB.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac7b/9103675/4ba65eb352e1/YRER_A_2074128_F0002_OB.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac7b/9103675/9829cbe46229/YRER_A_2074128_F0003_OB.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac7b/9103675/02fbb657c427/YRER_A_2074128_F0004_OC.jpg

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