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| Molecular mechanisms of Sanhuang Fuyuan Decoction in the treatment of chronic renal failure rats with spleen-kidney yang deficiency pattern based on ferroptosis |
| Hits 164 Download times 48 Received:January 05, 2026 |
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| DOI
10.11656/j.issn.1673-9043.2026.05.11 |
| Key Words
Sanhuang Fuyuan Decoction;chronic renal failure of spleen-kidney yang deficiency pattern;ferroptosis;fibrosis;iron metabolism;ACSL4/SLC7A11/GPX4 pathway |
| Author Name | Affiliation | E-mail | | WANG Fengxian | Department of Nephrology, Hengshui Traditional Chinese Medicine Hospital, Hengshui 053000, China | | | LI Shanshan | Department of Nephrology, Hengshui Traditional Chinese Medicine Hospital, Hengshui 053000, China | 15616224663@163.com | | DU Yangyang | Department of Intensive Care Medicine, Hengshui Traditional Chinese Medicine Hospital, Hengshui 053000, China | | | HU Guomin | Taocheng District Disease Prevention and Control Center, Hengshui 053000, China | | | GAO Fushun | Nephrology Department of Hengshui Traditional Chinese Medicine Hospital, Hengshui 053000, China | |
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| Abstract
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| [Objective] To explore the potential mechanism of Sanhuang Fuyuan Decoction（SHFYD）in alleviating renal injury in rats with chronic renal failure（CRF）of spleen-kidney yang deficiency pattern，based on ferroptosis. [Methods] Forty-eight rats were randomly and equally divided into control，model，SHFYD，and SHFYD + ferroptosis inducer（Erastin）groups. Except for the control group，all groups received adenine gavage to establish the CRF model of spleen-kidney yang deficiency. Urinary 24-h protein，serum creatinine（Scr）and blood urea nitrogen（BUN）were determined by microplate assays；renal histopathology and fibrosis were evaluated by HE and Masson staining；renal levels of Fe2+，glutathione（GSH），malondialdehyde（MDA）and superoxide dismutase（SOD） were measured by biochemical methods；mitochondrial ultrastructure was observed under transmission electron microscopy；RT-qPCR was used to detect mRNA expression of iron regulatory protein 1（IRP1），transferrin receptor 1（TFR1）and ferroportin（FPN）；immunohistochemistry was employed to examine protein expression of long-chain- fatty-acid-CoA ligase 4（ACSL4），solute carrier family 7 member 11（SLC7A11）and glutathione peroxidase 4 （GPX4）. [Results] Compared with the control group，the model group showed severe renal pathological lesions and damaged mitochondrial ultrastructure，accompanied by increased 24-h proteinuria，Scr，BUN，collagen fraction， Fe2+，MDA，TFR1 and ACSL4（P<0.05），and decreased GSH，SOD，IRP1，FPN，SLC7A11 and GPX4（P<0.05）. Relative to the model group，SHFYD significantly attenuated renal injury，restored mitochondrial ultra structure， reduced 24-h proteinuria，Scr，BUN，collagen fraction，Fe2+，MDA，TFR1 and ACSL4（P<0.05），and elevated GSH， SOD，IRP1，FPN，SLC7A11 and GPX4（P<0.05）. These protective effects were partially reversed by Erastin（P<0.05）. [Conclusion] SHFYD effectively improves renal function and restrains pathological damage and ferroptosis in CRF rats with spleen-kidney yang deficiency，probably by modulating renal iron metabolism and regulating the ACSL4/SLC7A11/GPX4 pathway. |
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