长双歧杆菌(B.长)可以以Se-B的形式积累硒(Se)和纳米Se。longum和Nano-Se-B.longum,分别。在这项研究中,纳米Se-B的作用评估了糖尿病小鼠的长骨。生理和代谢参数,如血糖,体重,血清胰岛素水平,腹膜内葡萄糖耐量试验(IPGTT),食物摄入量,评估水消耗和尿量。通过蛋白质印迹法评估胰岛素信号通路相关蛋白的表达。苏木素和伊红(H&E)用于肝脏的组织学检查,胰腺和肾脏部分。测定血清肌酐(SCr)和血尿素氮(BUN)水平。纳米Se-B.在延缓糖尿病发作方面,长骨是最好的。纳米Se-B.与模型组相比,longum降低了血糖和体重。IPGTT,食物摄入量,与所有Nano-Se-B相比,模型组的水消耗和尿量显着增加,血清胰岛素水平显着降低。长处理的小鼠。组织学结果表明,Nano-Se-B.长脑组小鼠病理改变优于模型组小鼠。Nano-Se-B中胰岛素信号通路相关蛋白的表达上调。longum治疗组。模型组中SCr和BUN水平显著增加。本研究首次报道了Nano-Se-B的剂量依赖性预防作用。长对糖尿病和肾损害的发作。该机制可能与胰岛素信号的变化有关。
Bifidobacterium longum (B. longum) could accumulate Selenium (Se) and nano-Se in the form of Se-B. longum and Nano-Se-B. longum, respectively. In this study, the effect of Nano-Se-B. longum in diabetic mice was evaluated. Physiological and metabolic parameters such as blood glucose, body weight, serum insulin level, intraperitoneal glucose tolerance test (IPGTT), food intake, water consumption and urine output were evaluated. The expression of insulin signalling pathway-related proteins was evaluated by western blotting. Haematoxylin and eosin (H&E) was used for histological examination of the liver, pancreas and kidney sections. Creatinine levels in serum (SCr) and blood urea nitrogen (BUN) were measured. Nano-Se-B. longum was the best in terms of delaying the onset of diabetes. Nano-Se-B. longum decreased blood glucose and body weight compared with those noted for the model group. IPGTT, food intake, water consumption and urine output significantly increased and serum insulin levels significantly decreased in the model group compared with those in all the Nano-Se-B. longum-treated mice. Histological results showed that the Nano-Se-B. longum-treated mice were better than the model group mice in terms of pathological changes. The expression of insulin signalling pathway-related proteins was upregulated in the Nano-Se-B. longum-treated groups. A significant increase in SCr and BUN levels was noted in the model group. This study for the first time reported the dose-dependent preventive effect of Nano-Se-B. longum on the onset of diabetes and renal damage. The mechanism may be related to changes in insulin signalling.