(+)‐Catechins Play a Protective Role in Diabetic Kidney Disease by Alleviating EMT through Multiple Pathways

• Published in: Molecular nutrition & food research 2024-09, Vol.68 (17), p.e2400387-n/a
• Main Authors: Ni, Ying, Zhu, Dina, Chen, Chao, Wang, Fan, Miu, Yanyan, Zhang, Wensheng
• Format: Article
• Language: English
• Subjects: (+)‐Catechin; Animals; Calcium channels (voltage-gated); Catechin - pharmacology; Cell Line; Diabetes; Diabetes mellitus; Diabetes Mellitus, Experimental - complications; Diabetic Nephropathies - drug therapy; diabetic nephropathy; Epithelial-Mesenchymal Transition - drug effects; epithelial‐mesenchymal transition; Gene regulation; Global health; Humans; Hyperglycemia; Kidney diseases; Male; Mice; Mice, Inbred C57BL; mRNA; Nephropathy; NF-kappa B - metabolism; Public health; RAGE; Receptor for Advanced Glycation End Products - genetics; Receptor for Advanced Glycation End Products - metabolism; Renal function; Signal transduction; Signal Transduction - drug effects
• ISSN: 1613-4125; 1613-4133; 1613-4133
• DOI: 10.1002/mnfr.202400387

Scope Diabetic nephropathy (DN), a complication of diabetes mellitus, is becoming a significant global health concern, with no complete cure currently available. Tea is regarded as an essential component of a balanced diet and contains (+)‐Catechin (CE), which exert a range of pharmacological effects. Consequently, CE may be a potential treatment for DN. The objective of this study is to examine the protective effects and underlying mechanisms of CE on DN, with a particular focus on the epithelial‐mesenchymal transition (EMT) process, which plays a pivotal role in regulating DN. Methods and results In this study db/db mice are treated with catechins. The results demonstrate that CE reduces obesity and hyperglycemia, improves renal dysfunction and morphological changes in diabetic mice, and inhibits the development of DN through the RAGE/NF‐κB signaling pathway. Among them differentially expressed messenger RNA (mRNA) results, those related to EMT, including Cav1, grem2, macrod2, and kap, are identified. To further validate the results, the same experiments are performed on HK‐2 cells. Conclusions The research results offer novel perspectives by emphasizing the anti‐inflammatory properties of CE and their potential role in mitigating DN through the regulation of EMT‐related genes such as RAGE, Cav1, grem2, macrod2, and kap. (+)‐Catechin exerts an inhibitory effect on the NF‐κB pathway through multiple pathways, thereby exerting an anti‐inflammatory effect and improving the process of EMT in DN. (By Figdraw.)