Phytomedicine : international journal of phytotherapy and phytopharmacology · 2026
Lithocarpus litseifolius and trilobatin ameliorate diabetic nephropathy through alleviating carbonyl stress by inhibiting AGEs/RAGE/NF-κB pathway.
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Chen Xue-Min, Chen Jie-Xin, Chen Xiao-Mei, Gao Yu-Xin, Zeng Chen-Yue, Chen Die-Yi, Xiang Xiao-Qiang, Hao Xiao-Tong, Wang Shu-Mei, Tang Dan
Аннотация
BACKGROUND: Diabetic nephropathy (DN) is a major complication of diabetes, and reactive carbonyl species (RCS) that induce carbonyl stress are key mediators in its pathogenesis. Lithocarpus litseifolius (LI), also known as Lithocarpus polystachyus, possesses both edible and medicinal properties with a history of use as "sweet tea" in China spanning over 1600 years. However, its beneficial effects and bioactive components for the treatment of DN remain unclear.
PURPOSE: This study aimed to elucidate the beneficial effects and potential action mechanisms of LI in ameliorating DN, and identify its primary bioactive component.
METHODS: A High-fat diet (HFD)/streptozotocin (STZ)-induced DN mouse model was used to evaluate the renoprotective effects of LI in diabetic mice. UPLC-Q-Orbitrap HRMS/MS and HPLC were employed for the qualitative and quantitative analysis of LI. Carbonyl stress stimulated cellular model was further utilized to investigate the protective effects of LI-derived components against methylglyoxal (MGO) induced HK2 cell injury, and to explore the underlying mechanisms.
RESULTS: The study demonstrated that LI ameliorated dyslipidemia, renal dysfunction, and kidney pathological damage in DN model mice, concurrently alleviating carbonyl stress and inflammation. A total of 39 chemical components were identified in LI, with dihydrochalcone derivatives identified as principal active compounds by UPLC-Q-Orbitrap HRMS/MS analysis. In vitro experiments revealed that dihydrochalcone derivatives, specifically trilobatin, could effectively modulate the AGEs/RAGE/NF-κB and downstream pyroptosis signaling pathways, which are closely associated with carbonyl stress. This modulation resulted in the mitigation of MGO-induced HK2 cell damage, thereby exerting protective effects against DN.
CONCLUSION: Our study demonstrates that Lithocarpus litseifolius and its primary component, trilobatin, mitigate carbonyl stress by inhibiting the AGEs/RAGE/NF-κB signaling pathway, thereby mitigating inflammation and pyroptosis and exhibiting therapeutic effects on DN.
PURPOSE: This study aimed to elucidate the beneficial effects and potential action mechanisms of LI in ameliorating DN, and identify its primary bioactive component.
METHODS: A High-fat diet (HFD)/streptozotocin (STZ)-induced DN mouse model was used to evaluate the renoprotective effects of LI in diabetic mice. UPLC-Q-Orbitrap HRMS/MS and HPLC were employed for the qualitative and quantitative analysis of LI. Carbonyl stress stimulated cellular model was further utilized to investigate the protective effects of LI-derived components against methylglyoxal (MGO) induced HK2 cell injury, and to explore the underlying mechanisms.
RESULTS: The study demonstrated that LI ameliorated dyslipidemia, renal dysfunction, and kidney pathological damage in DN model mice, concurrently alleviating carbonyl stress and inflammation. A total of 39 chemical components were identified in LI, with dihydrochalcone derivatives identified as principal active compounds by UPLC-Q-Orbitrap HRMS/MS analysis. In vitro experiments revealed that dihydrochalcone derivatives, specifically trilobatin, could effectively modulate the AGEs/RAGE/NF-κB and downstream pyroptosis signaling pathways, which are closely associated with carbonyl stress. This modulation resulted in the mitigation of MGO-induced HK2 cell damage, thereby exerting protective effects against DN.
CONCLUSION: Our study demonstrates that Lithocarpus litseifolius and its primary component, trilobatin, mitigate carbonyl stress by inhibiting the AGEs/RAGE/NF-κB signaling pathway, thereby mitigating inflammation and pyroptosis and exhibiting therapeutic effects on DN.