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硫胺素通过下调肝细胞核因子 -kβ 及诱导乙二醛酶 -I 的活性来减轻大鼠的代谢综合征症状。

Thiamine reduced metabolic syndrome symptoms in rats via down-regulation of hepatic nuclear factor-kβ and induction activity of glyoxalase-I.

作者信息

Mahdavifard Sina, Dehghani Razieh, Jeddi Farhad, Najafzadeh Nowruz

机构信息

Department of Clinical Biochemistry, Ardabil University of Medical Sciences, Ardabil, Iran.

Department of Genetics and Pathology, School of Medicine, Ardabil University of Medical Sciences, Ardabil, Iran.

出版信息

Iran J Basic Med Sci. 2021 Mar;24(3):293-299. doi: 10.22038/ijbms.2021.53707.12086.

Abstract

OBJECTIVES

Metabolic syndrome (MS) is a cause of death worldwide. The hepatic nuclear factor- NF-kβ (NF-kβ) is the cardinal player of hepatic homeostasis, insulin sensitivity, and lipid metabolism. Thus, we investigated the effect of thiamine on hepatic gene expression of NF-kβ and its levels of activators in MS rats.

MATERIALS AND METHODS

Male Wistar rats were randomly divided into 4 equal groups (ten rats in each group): normal, MS, and two alike groups under thiamine treatment. MS was induced in rats with a high sucrose solution (40 % in drinking water) for 4 months. Treated groups of rats received 0.18 % of thiamine daily in drinking water. Hematoxylin-Eosin stains were employed to determine the histopathological changes of the liver. Metabolic profile, glycation products, oxidative stress, inflammatory markers, the activity of glyoxalase-I, as well as NF-kβ hepatic expression of all rat groups, were determined.

RESULTS

Acute hepatitis was not observed in the livers of the thiamine treated MS rats. Besides, the treatment showed an advantageous effect on glucose, lipid metabolism, and body weight via down-regulation of hepatic NF-kβ and induction of glyoxalase system activity. Furthermore, the treatment decreased diverse glycation, oxidative stress, and inflammatory markers (>0.001).

CONCLUSION

Thiamine decreased body weight and improved metabolism and activity of glyoxalase-I in MS rats with anti-glycation, antioxidant, and anti-inflammatory activities. Further, the treatment had a hepato-protective effect via reduction of NF-kβ signaling.

摘要

目的

代谢综合征(MS)是全球范围内的一个死亡原因。肝细胞核因子-NF-κB(NF-κB)是肝脏内环境稳定、胰岛素敏感性和脂质代谢的关键调节因子。因此,我们研究了硫胺素对MS大鼠肝脏中NF-κB基因表达及其激活剂水平的影响。

材料与方法

雄性Wistar大鼠随机分为4组,每组10只:正常组、MS组以及硫胺素治疗的两个相似组。通过给予大鼠高蔗糖溶液(饮用水中40%)4个月诱导MS。治疗组大鼠每天在饮用水中摄入0.18%的硫胺素。采用苏木精-伊红染色来确定肝脏的组织病理学变化。测定所有大鼠组的代谢概况、糖化产物、氧化应激、炎症标志物、乙二醛酶-I活性以及肝脏中NF-κB的表达。

结果

硫胺素治疗的MS大鼠肝脏中未观察到急性肝炎。此外,该治疗通过下调肝脏NF-κB和诱导乙二醛酶系统活性,对血糖、脂质代谢和体重产生了有益影响。此外,该治疗降低了多种糖化、氧化应激和炎症标志物(P>0.001)。

结论

硫胺素降低了MS大鼠的体重,改善了代谢和乙二醛酶-I的活性,具有抗糖化、抗氧化和抗炎活性。此外,该治疗通过减少NF-κB信号传导具有肝脏保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f0c/8087849/12a420a1ad2f/IJBMS-24-293-g001.jpg

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