Department of Ophthalmology, Faculty of Medicine, Erzincan University, 24100, Erzincan, Turkey.
Department of Pathology, Faculty of Medicine, Erzincan University, Erzincan, Turkey.
BMC Pharmacol Toxicol. 2019 Jul 5;20(1):40. doi: 10.1186/s40360-019-0319-5.
We aimed to determine the protective effects of thiamine pyrophosphate on ethanol induced optic neuropathy in an experimental model.
The rats were assigned into 4 groups, with 6 rats in each group as follows: healthy controls (HC group), only ethanol administered group (EtOH group), ethanol + thiamine pyrophosphate (20 mg/kg) administered group (TEt-20 group), and only thiamine pyrophosphate (20 mg/kg) (TPG group) administered group. To the rats in TEt-20 and TPG groups, 20 mg/kg thiamine pyrophosphate was administered via intraperitoneal route. To the rats in HC and EtOH groups, the same volume (0.5 ml) of distilled water as solvent was applied in the same manner. To the rats in TEt-20 and EtOH groups, one hour after application of thiamine pyrophosphate or distilled water, 32% ethanol with a dose of 5 g/kg was administered via oral gavage. This procedure was repeated once a day for 6 weeks. From the blood samples and tissues obtained from the rats, Malondialdehyde (MDA), reduced glutathione (GSH), interleukin 1 beta (IL-1β) and tumor necrosis factor alpha (TNF-α) levels were studied. Histopathological evaluations were performed to the optic nerve tissue.
Serum and tissue IL-1β, TNF-α and MDA levels were the highest in EtOH group which were significantly lower in thiamine pyrophosphate administered group (TEt-20 group) (p: 0.001). Serum and tissue reduced GSH levels were the lowest in EtOH group which were also significantly higher in TEt-20 group (p:0.001). In histopathological evaluations, in EtOH group there was obvious destruction and edema with hemorrhage and dilated blood vessels which were not present in any other groups.
There was an apparent destruction in ethanol administered group in histopathological analyses with an augmented level of oxidative stress markers and all those alterations were prevented with concomitant thiamine pyrophosphate administration. These protective effects of thiamine pyrophosphate are extremely important in chronic ethanol consumption. Clinical studies are warranted to define the exact role of thiamine pyrophosphate in prevention of ethanol induced optic neuropathy.
我们旨在确定焦磷酸硫胺素对乙醇诱导的实验性视神经病变的保护作用。
将大鼠分为 4 组，每组 6 只，如下：健康对照组（HC 组）、仅给予乙醇组（EtOH 组）、乙醇+焦磷酸硫胺素（20mg/kg）组（TEt-20 组）和仅给予焦磷酸硫胺素（20mg/kg）组（TPG 组）。TEt-20 组和 TPG 组大鼠腹腔内给予 20mg/kg 焦磷酸硫胺素。HC 组和 EtOH 组大鼠以相同体积（0.5ml）的蒸馏水作为溶剂以相同方式给药。TEt-20 组和 EtOH 组大鼠在给予焦磷酸硫胺素或蒸馏水 1 小时后，经口灌胃给予 32%乙醇 5g/kg，每天重复一次，共 6 周。从大鼠的血液样本和组织中，研究丙二醛（MDA）、还原型谷胱甘肽（GSH）、白细胞介素 1β（IL-1β）和肿瘤坏死因子α（TNF-α）水平。对视神经组织进行组织病理学评估。
血清和组织中 IL-1β、TNF-α 和 MDA 水平在 EtOH 组最高，而在给予焦磷酸硫胺素的组（TEt-20 组）中显著降低（p：0.001）。血清和组织中还原型 GSH 水平在 EtOH 组最低，而在 TEt-20 组中也显著升高（p：0.001）。组织病理学评估显示，EtOH 组视神经明显破坏，水肿伴出血，血管扩张，而其他组均未见这些改变。
在组织病理学分析中，乙醇给药组有明显的破坏，氧化应激标志物水平升高，同时给予焦磷酸硫胺素可预防所有这些改变。焦磷酸硫胺素的这种保护作用在慢性乙醇摄入中非常重要。需要进行临床研究以确定焦磷酸硫胺素在预防乙醇诱导的视神经病变中的确切作用。
