Journal of ethnopharmacology · 2026
Identifying the active components and mechanisms of Toona sinensis pericarps for the treatment of diabetic kidney disease using network pharmacology and experimental verification.
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Zhang Yufeng, Li Huiting, Sun Weining, Wang Rongshen, Li Zhongxin, Chen Ying, Lan Shuying, Wang Yuxin, Liu Wenshan, Li Wanzhong
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Toona sinensis is used to treat diabetic kidney disease (DKD). However, the potential bioactive components and effects of T. sinensis pericarps dichloromethane extracts (DCME) on DKD are poorly understood.
AIM OF THE STUDY: This study aimed to determine the therapeutic effects and active components of DCME on DKD using network pharmacology and experimental verification.
MATERIALS AND METHODS: Interactions between DCME components and disease targets were determined and verified using network pharmacology, molecular docking, and molecular dynamics simulations. DKD was induced in mice with a high-fat, high-glucose diet and streptozotocin to explore the therapeutic effects of DCME. High-glucose was administered to glomerular mesangial cells to explore the therapeutic mechanisms of strongly active DCME compounds identified by molecular docking.
RESULTS: Twenty-one active DCME compounds and 325 potential targets were identified using network pharmacology. The GO and KEGG analyses revealed that DCME modulates multiple biological processes. Fasting blood glucose, and liver and kidney indices were significantly reduced in mice after treatment with DCME. DCME decreased MDA, NF-κB, TGF-β1, TNF-α, and IL-6 levels, and increased SOD, Nrf2, and HO-1 levels, ameliorating inflammation and oxidative stress. Pathological glomerular and tubule structures were restored by DCME. C2, C3, C4, C6, C7, and C19 were identified as core DCME components, and TNF, ALB, EGFR, CASP3, STAT3, BCL2, SRC, PPARG, JUN, and NFκB1 were identified as core targets. C6 and C7 formed stable hydrogen-bond interactions with NF-κB and TNF-α. C6 significantly attenuated increased NF-κB and TNF-α levels and activated Nrf2 and HO-1 better than C7.
CONCLUSION: DCME and C6, potential candidates for the treatment of DKD, may inhibit the NF-κB pathway and activate the Nrf2 pathway to improve DKD.
AIM OF THE STUDY: This study aimed to determine the therapeutic effects and active components of DCME on DKD using network pharmacology and experimental verification.
MATERIALS AND METHODS: Interactions between DCME components and disease targets were determined and verified using network pharmacology, molecular docking, and molecular dynamics simulations. DKD was induced in mice with a high-fat, high-glucose diet and streptozotocin to explore the therapeutic effects of DCME. High-glucose was administered to glomerular mesangial cells to explore the therapeutic mechanisms of strongly active DCME compounds identified by molecular docking.
RESULTS: Twenty-one active DCME compounds and 325 potential targets were identified using network pharmacology. The GO and KEGG analyses revealed that DCME modulates multiple biological processes. Fasting blood glucose, and liver and kidney indices were significantly reduced in mice after treatment with DCME. DCME decreased MDA, NF-κB, TGF-β1, TNF-α, and IL-6 levels, and increased SOD, Nrf2, and HO-1 levels, ameliorating inflammation and oxidative stress. Pathological glomerular and tubule structures were restored by DCME. C2, C3, C4, C6, C7, and C19 were identified as core DCME components, and TNF, ALB, EGFR, CASP3, STAT3, BCL2, SRC, PPARG, JUN, and NFκB1 were identified as core targets. C6 and C7 formed stable hydrogen-bond interactions with NF-κB and TNF-α. C6 significantly attenuated increased NF-κB and TNF-α levels and activated Nrf2 and HO-1 better than C7.
CONCLUSION: DCME and C6, potential candidates for the treatment of DKD, may inhibit the NF-κB pathway and activate the Nrf2 pathway to improve DKD.