Phytomedicine : international journal of phytotherapy and phytopharmacology · 2026
Portulaca oleracea L.-Derived extracellular vesicles alleviate renal lipotoxicity in diabetic kidney disease by regulating the NLRP3 pathway.
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Zhou Yao, Zhang Huijia, Li Yijing, Li Yingying, Tao Yupeng, Zhang Kejia, Liu Buhui, Wu Qi, Gao Kun
Аннотация
BACKGROUND: Diabetic kidney disease (DKD) remains a leading indication for renal replacement therapy, with existing drugs having many limitations. Portulaca oleracea L.-derived extracellular vesicles (PO-EVs) exhibit anti-inflammatory, antioxidant, and immune-regulatory properties. However, their function in DKD has yet to be fully elucidated.
OBJECTIVE: This investigation sought to examine the interplay between lipid metabolism and inflammation in renal tubular epithelial cells in DKD, and to clarify the role and underlying mechanism of PO-EVs in modulating lipid metabolism-inflammation crosstalk to mitigate DKD progression.
METHODS: PO-EVs underwent isolation via differential ultracentrifugation and characterization through transmission electron microscopy (TEM), particle size analysis, zeta potential measurement, and multi-omics analysis. In vivo, db/db mice (DKD model) were given PO-EVs intragastrically, with renal function and tissue indicators detected, and mechanisms explored by transcriptomics and proteomics. In vitro, palmitic acid (PA)-induced lipotoxicity in normal rat kidney tubular epithelial cells (NRK-52E) was used to explore the effects of PO-EVs.
RESULTS: PO-EVs significantly enhanced renal function and mitigated renal tissue lipid deposition in db/db mice. They also alleviated PA-induced cellular lipid accumulation and mitochondrial damage, inhibited NLRP3 inflammasome-related proteins, and enhanced fatty acid oxidation (FAO) and ATP synthesis. Suppressing NLRP3 expression markedly improved mitochondrial morphology, reduced lipid accumulation and increased peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) expression in NRK-52E.
CONCLUSION: PO-EVs disrupt the metabolism-inflammation vicious cycle by inhibiting NLRP3 and upregulating PGC-1α, thereby mitigating renal lipotoxicity and delaying DKD progression, providing a basis for DKD therapy.
OBJECTIVE: This investigation sought to examine the interplay between lipid metabolism and inflammation in renal tubular epithelial cells in DKD, and to clarify the role and underlying mechanism of PO-EVs in modulating lipid metabolism-inflammation crosstalk to mitigate DKD progression.
METHODS: PO-EVs underwent isolation via differential ultracentrifugation and characterization through transmission electron microscopy (TEM), particle size analysis, zeta potential measurement, and multi-omics analysis. In vivo, db/db mice (DKD model) were given PO-EVs intragastrically, with renal function and tissue indicators detected, and mechanisms explored by transcriptomics and proteomics. In vitro, palmitic acid (PA)-induced lipotoxicity in normal rat kidney tubular epithelial cells (NRK-52E) was used to explore the effects of PO-EVs.
RESULTS: PO-EVs significantly enhanced renal function and mitigated renal tissue lipid deposition in db/db mice. They also alleviated PA-induced cellular lipid accumulation and mitochondrial damage, inhibited NLRP3 inflammasome-related proteins, and enhanced fatty acid oxidation (FAO) and ATP synthesis. Suppressing NLRP3 expression markedly improved mitochondrial morphology, reduced lipid accumulation and increased peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) expression in NRK-52E.
CONCLUSION: PO-EVs disrupt the metabolism-inflammation vicious cycle by inhibiting NLRP3 and upregulating PGC-1α, thereby mitigating renal lipotoxicity and delaying DKD progression, providing a basis for DKD therapy.