Al-Shwaheen Aseel, Aljabali Alaa A A, Alomari Ghada, Al Zoubi Mazhar, Alshaer Walhan, Al-Trad Bahaa, Tambuwala Murtaza M
Department of Biological Sciences, Faculty of Science, Yarmouk University, Irbid, 211-63, Jordan.
Department of Pharmaceutics and Pharmaceutical Technology, Faculty of Pharmacy, Yarmouk University, Irbid, Jordan.
Heliyon. 2022 Aug 21;8(9):e10358. doi: 10.1016/j.heliyon.2022.e10358. eCollection 2022 Sep.
This study aims to address the effects of gold nanoparticles (AuNPs) on diabetic myopathy in streptozotocin (STZ)-induced diabetic rats.
Adult male rats were separated into three groups (n = 15): non-diabetic control (ND), diabetic (D), and diabetic treated with AuNPs (2.5 mg/kg, D + AuNPs) intraperitoneally for 4 weeks. A single injection of 50 mg/kg STZ was used to induce diabetes.
Treatment with AuNPs lowered blood glucose levels. Skeletal muscle mRNA expression of two muscle-specific E3 ubiquitin-ligases enzymes, F-box-only protein 32 (FBXO32) and muscle RING-finger protein-1 (MuRF1) were upregulated in the D group. Diabetic rats showed significant increases in the skeletal muscle expression levels of plasminogen activator inhibitor-1 (PAI-1), tumor necrosis factor-α (TNF-α), transforming growth factor-β1 (TGF-β1), and a decrease in glucose transporter 4 (GLUT4) expression. Superoxide dismutase (SOD) activity decreased and malondialdehyde (MDA) level increased in skeletal muscles of D group. Compared to the D group, expression levels of FBXO32, MuRF1, PAI-1 TNF-α, and TGF-β1 were decreased in the D + AuNPs group, and mRNA of GLUT4 increased. Furthermore, in D + AuNPs group, skeletal muscle MDA levels decreased while SOD activity increased.
In experimental models, AuNPs can ameliorate muscle atrophy by reducing hyperglycemia, inflammation, and oxidative stress, and by suppressing the ubiquitin-proteasome proteolytic process.
本研究旨在探讨金纳米颗粒（AuNPs）对链脲佐菌素（STZ）诱导的糖尿病大鼠糖尿病性肌病的影响。
成年雄性大鼠分为三组（n = 15）：非糖尿病对照组（ND）、糖尿病组（D）和腹腔注射AuNPs（2.5 mg/kg）治疗4周的糖尿病组（D + AuNPs）。单次注射50 mg/kg STZ诱导糖尿病。
AuNPs治疗可降低血糖水平。D组中两种肌肉特异性E3泛素连接酶，即仅含F盒蛋白32（FBXO32）和肌肉环指蛋白1（MuRF1）的骨骼肌mRNA表达上调。糖尿病大鼠骨骼肌纤溶酶原激活物抑制剂-1（PAI-1）、肿瘤坏死因子-α（TNF-α）、转化生长因子-β1（TGF-β1）表达水平显著升高，葡萄糖转运蛋白4（GLUT4）表达降低。D组骨骼肌中超氧化物歧化酶（SOD）活性降低，丙二醛（MDA）水平升高。与D组相比，D + AuNPs组中FBXO32、MuRF1、PAI-1、TNF-α和TGF-β1的表达水平降低，GLUT4的mRNA增加。此外，在D + AuNPs组中，骨骼肌MDA水平降低而SOD活性增加。
在实验模型中，AuNPs可通过降低高血糖、炎症和氧化应激以及抑制泛素-蛋白酶体蛋白水解过程来改善肌肉萎缩。
