Phytomedicine : international journal of phytotherapy and phytopharmacology · 2025
Mechanism of Eucalyptus oil in alleviating UUO-induced renal fibrosis revealed by transcriptomics and metabolomics.
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Li Na, Qi Huili, Li Jiacun, Cheng Xiaoling, Li Xin, Zhang Ke, Aimaier Shabaaiti, Wang Yanli, Li Jialu, Guo Yaping, Yao Dahong, Wang Hangyu, Wang Jinhui
Аннотация
BACKGROUND: Renal fibrosis (RF), a major contributor to the progression of chronic kidney disease (CKD), is an important therapeutic target. Eucalyptus oil (EO), a volatile extract derived from traditional Chinese herbal medicine with known anti-inflammatory and antioxidant properties, has shown potential in CKD treatment. However, its efficacy and mechanisms in preventing kidney injury induced by unilateral ureteral obstruction (UUO) remain unclear.
PURPOSE: This study aimed to evaluate the protective effects of EO against renal injury in UUO rats and to investigate its underlying mechanisms of action.
METHODS: A UUO-induced rat model of RF was established to assess the antifibrotic effects of EO. Integrated multi-omics approaches, including genomic and metabolomic analyses, along with molecular docking and experimental validation using Western blot and qPCR, were employed to systematically elucidate the molecular mechanisms and pharmacodynamic basis of EO in alleviating RF.
RESULTS: EO significantly reduced RF in the UUO model by concurrently inhibiting the transforming growth factor-beta 1 (TGF-β1)/Smad3 signaling pathway and the tryptophan metabolism-aryl hydrocarbon receptor (AhR) axis. Specifically, EO suppressed Smad3 phosphorylation, fibroblast activation, and extracellular matrix (ECM) accumulation. It also inhibited AhR nuclear translocation and reduced the expression of cytochrome P450 1A1 (Cyp1A1), cytochrome P450 1B1 (Cyp1B1), and aryl hydrocarbon receptor nuclear translocator (ARNT). These molecular effects were associated with improvements in renal function indicators, including reductions in serum creatinine (SCR), blood urea nitrogen (BUN), and kidney injury molecule-1 (KIM-1). EO also mitigated histological damage and decreased oxidative stress markers-malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH)-as well as inflammatory mediators-monocyte chemoattractant protein-1 (MCP-1), interleukin-1 beta (IL-1β), and tumor necrosis factor-alpha (TNF-α). These findings highlight the multitarget antifibrotic potential of EO.
CONCLUSION: EO suppresses renal fibrosis by inhibiting both the TGF-β1/Smad3 signaling pathway and the tryptophan metabolism-AhR pathway, thereby reducing abnormal ECM accumulation.
PURPOSE: This study aimed to evaluate the protective effects of EO against renal injury in UUO rats and to investigate its underlying mechanisms of action.
METHODS: A UUO-induced rat model of RF was established to assess the antifibrotic effects of EO. Integrated multi-omics approaches, including genomic and metabolomic analyses, along with molecular docking and experimental validation using Western blot and qPCR, were employed to systematically elucidate the molecular mechanisms and pharmacodynamic basis of EO in alleviating RF.
RESULTS: EO significantly reduced RF in the UUO model by concurrently inhibiting the transforming growth factor-beta 1 (TGF-β1)/Smad3 signaling pathway and the tryptophan metabolism-aryl hydrocarbon receptor (AhR) axis. Specifically, EO suppressed Smad3 phosphorylation, fibroblast activation, and extracellular matrix (ECM) accumulation. It also inhibited AhR nuclear translocation and reduced the expression of cytochrome P450 1A1 (Cyp1A1), cytochrome P450 1B1 (Cyp1B1), and aryl hydrocarbon receptor nuclear translocator (ARNT). These molecular effects were associated with improvements in renal function indicators, including reductions in serum creatinine (SCR), blood urea nitrogen (BUN), and kidney injury molecule-1 (KIM-1). EO also mitigated histological damage and decreased oxidative stress markers-malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH)-as well as inflammatory mediators-monocyte chemoattractant protein-1 (MCP-1), interleukin-1 beta (IL-1β), and tumor necrosis factor-alpha (TNF-α). These findings highlight the multitarget antifibrotic potential of EO.
CONCLUSION: EO suppresses renal fibrosis by inhibiting both the TGF-β1/Smad3 signaling pathway and the tryptophan metabolism-AhR pathway, thereby reducing abnormal ECM accumulation.