This study examines the effect of nanoparticles with zinc oxides (ZnONPs) on diabetic nephropathy, which is the primary cause of mortality for diabetic patients with end‐stage renal disease. Diabetes in adult male rats was induced via intraperitoneal injection of streptozotocin. ZnONPs were intraperitoneally administered to diabetic rats daily for 7 weeks. Diabetes was associated with increases in blood glucose level, 24‐h urinary albumin excretion rate, glomerular basement membrane thickness, renal oxidative stress markers, and renal mRNA or protein expression of transforming growth factor‐ β 1, fibronectin, collagen‐IV, tumour necrosis factor‐ α and vascular endothelial growth factor‐A. Moreover, the expression of nephrin and podocin, and the mRNA expression of matrix metalloproteinase‐9 were decreased in the diabetic group. These changes were not detected in the control group and were significantly prevented by ZnONP treatment. These results provide evidence that ZnONPs ameliorate the renal damage induced in a diabetic rat model of nephropathy through improving renal functionality; inhibiting renal fibrosis, oxidative stress, inflammation and abnormal angiogenesis; and delaying the development of podocyte injury. The present findings may help design the clinical application of ZnONPs for protection against the development of diabetic nephropathy.

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.

This study investigates the effect of myricetin as a therapeutic for benign prostatic hyperplasia (BPH) disease using a testosterone-induced BPH animal model. Forty adult male rats were randomly divided into four groups as follows: control group, BPH group that was injected with testosterone subcutaneously (3 mg/kg body weight/day), BPH + myricetin group, which received myricetin (50 mg/kg) subcutaneously every day with the BPH induction, and BPH + finasteride group, which administered finasteride orally with the BPH induction at a daily dose of 5 mg/kg. After 28 days, blood and prostate tissue samples were collected for analysis. Compared to the control group, treatment with myricetin improved the pathohistological signs of BPH and enhanced the antioxidant and anti-inflammatory capacity of the prostatic tissue, as evidenced by its ability to enhance the total antioxidant capacity (TAC) levels and reduce malondialdehyde (MDA) levels, decrease the levels of the inflammatory biomarkers tumor necrosis factor alpha (TNF-α) and interleukin-1 beta (IL1-β) levels, and reduce serum dihydrotestosterone (DHT) levels. In addition, myricetin treatment showed beneficial effects through its ability to reduce the prostatic mRNA expression levels of the anti-apoptotic protein Bcl2, the 5-α reductase enzyme, and the androgen receptor ( AR ), while simultaneously increasing the prostatic mRNA expression levels of the pro-apoptotic protein Bax . Myricetin treatment also exhibited anti-proliferative and anti-angiogenic effects, as evidenced by the reduced prostatic proliferating cell nuclear antigen (PCNA) and vascular endothelial growth factor-A ( VEGF-A ) mRNA expression levels. In summary, myricetin displays potential as a BPH therapy by diminishing inflammation and oxidative stress, hindering 5-α reductase / AR /DHT signaling, and endorsing pro-apoptotic over anti-apoptotic pathways.