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Fibroblast growth factor 1 ameliorates diabetes-induced splenomegaly via suppressing inflammation and oxidative stress.
Biochemical and Biophysical Research Communications ( IF 2.5 ) Pub Date : 2020-05-29 , DOI: 10.1016/j.bbrc.2020.05.145
Yanqing Wu 1 , Gaili Jia 2 , Beini Wang 2 , Jun Xiong 2 , Jingyu Xu 3 , Peipei Zheng 2 , Yuan Yuan 2 , Yiyang Li 2 , Ting Jiang 2 , Abdullah Al Mamun 2 , Ke Xu 3 , Yaqian Liu 2 , Hong Cao 2 , Jian Xiao 2
Affiliation  

Type-2 diabetes (T2D) is a common metabolic disorder, which causes several physiological and pathological complications. Spleen is regarded as an important organ, which regulates immune system and iron metabolism in the body. Precious few studies have been conducted to explore the pathological and deleterious roles of diabetes on spleen. In our current study, we have explored and confirmed the pathological effects of diabetes on spleen in db/db experimental mice model. In our current study, 0.5 mg/kg fibroblast growth factor 1 (FGF1) dose was intraperitoneally administrated to db/db mice. We found that diabetes evidently induced spleen enlargement and fibrosis progression in the db/db mice. Additionally, our studies demonstrate that iron has hugely deposited in the spleen in db/db mice. Several studies have documented that diabetes largely disrupts the inflammatory cells distribution, immune homeostasis, proliferation and oxidative stress with the down-regulation of anti-inflammatory cytokines and antioxidant activities. Moreover, we have observed that FGF1 administration significantly reversed the deleterious effect of diabetes on spleen enlargement and dysfunction. In summary, these substantial findings clearly demonstrate that diabetes plays deleterious roles in maintaining the spleen structure and functions. Therefore, our investigations suggest that FGF1 can effectively prevent diabetes-mediated splenomegaly progression.



中文翻译:

成纤维细胞生长因子1通过抑制炎症和氧化应激可改善糖尿病引起的脾肿大。

2型糖尿病(T2D)是一种常见的代谢紊乱,会引起多种生理和病理并发症。脾脏被认为是调节人体免疫系统和铁代谢的重要器官。很少有研究探索糖尿病对脾脏的病理和有害作用。在我们目前的研究中,我们已经探索并证实了db / db实验小鼠模型中糖尿病对脾脏的病理作用。在我们目前的研究中,对db / db小鼠腹膜内给予0.5 mg / kg的成纤维细胞生长因子1(FGF1)剂量。我们发现糖尿病显然在db / db小鼠中引起脾脏增大和纤维化进展。此外,我们的研究表明,铁已大量沉积在db / db小鼠的脾脏中。数项研究表明,糖尿病会通过下调抗炎细胞因子和抗氧化剂的活性来破坏炎性细胞的分布,免疫稳态,增殖和氧化应激。此外,我们已经观察到,FGF1的给药显着逆转了糖尿病对脾脏肿大和功能障碍的有害作用。总之,这些实质性发现清楚地表明,糖尿病在维持脾脏结构和功能中起有害作用。因此,我们的研究表明FGF1可有效预防糖尿病介导的脾肿大进展。我们已经观察到,施用FGF1可显着逆转糖尿病对脾脏肿大和功能障碍的有害作用。总之,这些实质性发现清楚地表明,糖尿病在维持脾脏结构和功能中起有害作用。因此,我们的研究表明FGF1可以有效预防糖尿病介导的脾肿大进展。我们已经观察到,施用FGF1可显着逆转糖尿病对脾脏肿大和功能障碍的有害作用。总之,这些实质性发现清楚地表明,糖尿病在维持脾脏结构和功能中起有害作用。因此,我们的研究表明FGF1可以有效预防糖尿病介导的脾肿大进展。

更新日期:2020-05-29
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