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Melatonin regulates neurodegenerative complications associated with NAFLD via enhanced neurotransmission and cellular integrity: a correlational study.
Metabolic Brain Disease ( IF 3.6 ) Pub Date : 2020-07-21 , DOI: 10.1007/s11011-020-00593-4
Gehad A Abdel Jaleel 1 , Sally A Al-Awdan 1 , Rania F Ahmed 1 , Omar A H Ahmed-Farid 2 , Dalia O Saleh 1
Affiliation  

Nonalcoholic fatty liver disease (NAFLD) is recognized globally as the leading cause of chronic liver diseases whose patients are asymptomatic and are diagnosed incidentally. It increases the rate of mortality which is usually related to cardiovascular events; however, scarce attention has been addressed to brain damage. This study was designed to investigate the impact of melatonin (MEL; 10 mg/kg) on overcoming the hepato and neuro-complications associated with high fat, high fructose (HFHF) diet induced-NAFLD in rats. NAFLD was induced by HFHF diet for 8 consecutive weeks. MEL was given orally for the last 10 days. Rats’ general behavior was assessed by; open field test (OFT) and forced swimming test (FST). On biochemical level; serum levels of glucose, insulin, alanine transaminase and aspartate transaminase as well as the hepatic levels of triglycerides and total cholesterol were evaluated. Monoamines’ brain levels, their metabolites in addition to the brain level of 8-hydroxyguanosine (8-OHdG) were evaluated. Moreover, the levels of tumor necrosis factor-α (TNF-α), malondialdehyde (MDA), reduced glutathione (GSH) and nitric oxide (NOx) were measured in both the liver and brain tissues. Oral treatment of NAFLD induced rats with MEL for ten consecutive days managed to increase the activity of the rats in the OFT and decrease the immobility period in the FST. Moreover, MEL reduced monoamines turnover and elevated brain 8-OHdG level. It also had the ability to counteract the elevated levels of GSH, NOx, MDA, and TNF- α in liver and brain tissues. MEL can be suggested to be a promising candidate for treating the neuronal side effects related to NAFLD.



中文翻译:

褪黑激素通过增强神经传递和细胞完整性调节与 NAFLD 相关的神经退行性并发症:一项相关研究。

非酒精性脂肪性肝病 (NAFLD) 是全球公认的慢性肝病的主要原因,其患者无症状且被偶然诊断。它会增加死亡率,而死亡率通常与心血管事件有关;然而,很少有人关注脑损伤。本研究旨在研究褪黑激素 (MEL; 10 mg/kg) 对克服与高脂肪、高果糖 (HFHF) 饮食诱导的大鼠 NAFLD 相关的肝和神经并发症的影响。NAFLD 由 HFHF 饮食诱导连续 8 周。在过去的 10 天内口服 MEL。大鼠的一般行为通过以下方式评估;野外试验(OFT)和强迫游泳试验(FST)。在生化水平上;血清葡萄糖、胰岛素水平,评估了丙氨酸转氨酶和天冬氨酸转氨酶以及甘油三酯和总胆固醇的肝脏水平。除了 8-羟基鸟苷 (8-OHdG) 的大脑水平外,还评估了单胺的大脑水平、它们的代谢物。此外,还测量了肝脏和脑组织中肿瘤坏死因子-α (TNF-α)、丙二醛 (MDA)、还原型谷胱甘肽 (GSH) 和一氧化氮 (NOx) 的水平。连续 10 天对 NAFLD 诱导的大鼠进行 MEL 口服治疗,设法增加了大鼠在 OFT 中的活动并减少了 FST 中的不动期。此外,MEL 减少了单胺周转并提高了大脑 8-OHdG 水平。它还具有抵消肝脏和脑组织中 GSH、NOx、MDA 和 TNF-α 水平升高的能力。

更新日期:2020-07-21
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