Purple sweet potato (PSP) powder with anthocyanins possesses the ability to reduce oxidative stress and inflammation. Studies have presumed a positive correlation between body fat and dry eye disease (DED) in adults. The regulation of oxidative stress and inflammation has been proposed as the mechanism underlying DED. This study developed an animal model of high fat diet (HFD)-induced DED. We added 5% PSP powder to the HFD to evaluate the effects and underlying mechanisms in mitigating HFD-induced DED. A statin drug, atorvastatin, was also added to the diet separately to assess its effect. The HFD altered the structure of lacrimal gland (LG) tissue, reduced LG secretory function, and eliminated the expression of proteins related to DED development, including α-smooth muscle actin and aquaporin-5. Although PSP treatment could not significantly reduce body weight or body fat, it ameliorated the effects of DED by preserving LG secretory function, preventing ocular surface erosion, and preserving LG structure. PSP treatment increased superoxide dismutase levels but reduced hypoxia-inducible factor 1-α levels, indicating that PSP treatment reduced oxidative stress. PSP treatment increased ATP-binding cassette transporter 1 and acetyl-CoA carboxylase 1 levels in LG tissue, signifying that PSP treatment regulated lipid homeostasis maintenance to reduce the effects of DED. In conclusion, PSP treatment ameliorated the effects of HFD-induced DED through the regulation of oxidative stress and lipid homeostasis in the LG.

Diabetic nephropathy (DN) is a major cause of morbidity and mortality among patients with diabetes mellitus (DM). Studies have highlighted the critical role of reactive oxygen species (ROS) in the pathogenesis of DM and its complications. Apple polyphenol (AP) has demonstrated antioxidant properties in various models. In this study, we investigated the effects of AP on DN in a rat model. Type 1 diabetes was induced in Sprague–Dawley rats via a single intraperitoneal injection of streptozotocin (65 mg/kg) (n = 8). Rats with blood glucose levels exceeding 250 mg/dL were treated with AP at dosages of 0.5%, 1%, or 2% (w/w) in drinking water for 10 weeks. AP administration significantly improved early-stage DN markers, including reductions in the blood urea nitrogen-to-creatinine ratio and the urinary albumin-to-creatinine ratio (ACR), in a dose-dependent manner. AP treatment also significantly lowered blood triglyceride levels and reduced lipid peroxidation in kidney tissues. Histological analysis revealed that AP attenuated renal hydropic change, reduced glomerular basement membrane thickening, and restored mitochondrial morphology in diabetic rats. Additionally, the upregulation of transforming growth factor-beta (TGF-β) observed in the diabetic kidney was attenuated by AP treatment. In H₂O₂-stimulated rat mesangial cells, AP reduced ROS levels, accompanied by a reduction in TGF-β expression. These findings suggest that AP exerts protective effects against DN by improving renal function and mitigating oxidative stress, indicating its potential as a nutraceutical supplement for slowing DN progression.