Meng-Hsun Yu
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Meng-Hsun Yu has a total of 15 co-authors. Here are the top co-authors by number of shared publications:
- Chau-Jong Wang
Department of Health Diet and Industry Management, Chung Shan Medical University, Taichung 402, Taiwan
2 shared publications - Chieh-Yu Wang
School of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan
1 shared publication - Chih-Ying Wang
Department of Biochemistry, School of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan
1 shared publication - Dai-Lin Wu
School of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan
1 shared publication - Dong-Hui Chen
Institute of Medicine, Chung Shan Medical University, Taichung, 402, Taiwan
1 shared publication - Hsin-Wen Liang
Department of Medical Research, Chung Shan Medical University Hospital, Taichung 40201, Taiwan
1 shared publication
Latest Publications
- 21 May 2026
- Published by Royal Society of Chemistry (RSC) in Food & Function
- Vol. 17 (12) , 5506-5520
Neochlorogenic acid attenuates endothelial injury in diabetic ApoE −/− mice by suppressing NF-κB mediated NLRP3 inflammasome activation
Diabetes mellitus (DM) significantly increases global morbidity and mortality through cardiovascular complications, particularly atherosclerosis, characterized by chronic inflammation, oxidative stress, and endothelial dysfunction.
- 21 May 2026
- Published by Royal Society of Chemistry (RSC) in Food & Function
- Vol. 17 (12) , 5506-5520
Neochlorogenic acid attenuates endothelial injury in diabetic ApoE −/− mice by suppressing NF-κB mediated NLRP3 inflammasome activation
Diabetes mellitus (DM) significantly increases global morbidity and mortality through cardiovascular complications, particularly atherosclerosis, characterized by chronic inflammation, oxidative stress, and endothelial dysfunction.
- Open Access
- 23 January 2025
- Published by MDPI AG in Antioxidants
- Vol. 14 (2) , 130
Apple Polyphenol Mitigates Diabetic Nephropathy via Attenuating Renal Dysfunction with Antioxidation in Streptozotocin-Induced Diabetic Rats
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.
- 23 January 2025
- Published by MDPI AG in Antioxidants
- Vol. 14 (2) , 130
Open AccessApple Polyphenol Mitigates Diabetic Nephropathy via Attenuating Renal Dysfunction with Antioxidation in Streptozotocin-Induced Diabetic Rats
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.
- Open Access
- 22 January 2024
- Published by Elsevier in Journal of Traditional and Complementary Medicine
- Vol. 14 (3) , 266-275
Mulberry leaf extract inhibits obesity and protects against diethylnitrosamine-induced hepatocellular carcinoma in rats
- 22 January 2024
- Published by Elsevier in Journal of Traditional and Complementary Medicine
- Vol. 14 (3) , 266-275
Open AccessMulberry leaf extract inhibits obesity and protects against diethylnitrosamine-induced hepatocellular carcinoma in rats