BACKGROUND We aimed to determine the protective effects of thiamine pyrophosphate on ethanol induced optic neuropathy in an experimental model. METHODS 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. RESULTS 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. CONCLUSIONS 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.

中文翻译：

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硫胺素焦磷酸对乙醇引起的视神经损伤的影响。

背景技术我们旨在确定焦磷酸硫胺素在实验模型中对乙醇诱发的视神经病变的保护作用。方法将大鼠分为4组，每组6只，分别为：健康对照组（HC组），仅乙醇组（EtOH组），乙醇+硫胺素焦磷酸酯（20 mg / kg）组（TEt-20）组），仅给予硫胺焦磷酸盐（20 mg / kg）（TPG组）。对TEt-20和TPG组的大鼠，通过腹膜内途径给予20 mg / kg硫胺素焦磷酸。以相同的方式对HC和EtOH组的大鼠使用相同体积（0.5 ml）的蒸馏水作为溶剂。在使用硫胺素焦磷酸或蒸馏水一小时后，对TEt-20和EtOH组的大鼠，经由管饲法施用32％乙醇，剂量为5g / kg。每天重复一次此过程，持续6周。从大鼠的血液样本和组织中，研究了丙二醛（MDA），还原型谷胱甘肽（GSH），白介素1β（IL-1β）和肿瘤坏死因子α（TNF-α）的水平。对视神经组织进行了组织病理学评估。结果EtOH组的血清和组织IL-1β，TNF-α和MDA水平最高，而硫胺素焦磷酸盐给药组（TEt-20组）则显着降低（p：0.001）。血清和组织中GSH含量的降低在EtOH组中最低，而在TEt-20组中也显着更高（p：0.001）。在组织病理学评估中，EtOH组有明显的破坏和水肿，并伴有出血和血管扩张，这是其他任何组别所没有的。结论在组织病理学分析中，乙醇给药组有明显的破坏，其氧化应激标志物水平升高，并且所有这些改变都可以通过硫胺素焦磷酸盐的给药来预防。硫胺素焦磷酸的这些保护作用在长期乙醇消费中极为重要。有必要进行临床研究来确定焦磷酸硫胺素在预防乙醇引起的视神经病变中的确切作用。结论在组织病理学分析中，乙醇给药组有明显的破坏，其氧化应激标志物水平升高，并且所有这些改变都可以通过硫胺素焦磷酸盐的给药来预防。硫胺素焦磷酸的这些保护作用在长期乙醇消费中极为重要。有必要进行临床研究来确定焦磷酸硫胺素在预防乙醇引起的视神经病变中的确切作用。结论在组织病理学分析中，乙醇给药组有明显的破坏，其氧化应激标志物水平升高，并且所有这些改变都可以通过硫胺素焦磷酸盐的给药来预防。硫胺素焦磷酸的这些保护作用在长期乙醇消费中极为重要。有必要进行临床研究来确定焦磷酸硫胺素在预防乙醇引起的视神经病变中的确切作用。