Journal of Traditional Chinese Medicine ›› 2026, Vol. 46 ›› Issue (4): 821-831.DOI: 10.19852/j.cnki.jtcm.2026.04.005
• Original Articles • Previous Articles Next Articles
Yigongsan decoction (异功散) ameliorates anemia of chronic disease by attenuating mothers against decapentaplegic homolog-signal transducer and activator of transcription 3 interaction to regulate iron homeostasis
ZHENG Qin1, ZHU Xiaoqin2, HU Jie3, BU Jingyang1, JI Yuting1, JIANG Yiling1, SHI Ling1, ZHANG Aiping1, WU Zhihao1, XU Haitao1, ZHANG Ruifeng1, YANG Yang4(
), LUO Meihong1
- 1
Department of Hematology ,Shanghai Baoshan Hospital of Integrated Traditional Chinese and Western Medicine (Baoshan Hospital, Shanghai University of Traditional Chinese Medicine) Shanghai 201999, China
2Department of Hematology ,Shanghai Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine Shanghai 200021, China
3Shanghai Huating Town Community Health Service Center Shanghai 201816, China
4Department of Science and Technology Experiment Center ,Shanghai University of Traditional Chinese Medicine Shanghai 201203, China
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Received:2025-10-06Accepted:2026-04-17Online:2026-08-15Published:2026-08-08 -
Contact:Prof. YANG Yang, Department of Science and Technology Experiment Center, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China. yyang_shutcm@126.com;
Prof. LUO Meihong, Department of Hematology, Shanghai Baoshan Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai 201999, China,Telephone: +86-13585703963 -
About author:First author contact:ZHENG Qin and ZHU Xiaoqin are co-first authors and contributed equally to this work
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Supported by:The Shanghai Oriental Talent Youth Program: Mechanism Study of Yigongsan Decoction in Improving Anemia of Chronic Disease by Downregulating Hepcidin Antimicrobial Peptide Through Histone Modification-mediated Crosstalk of Mothers Against Decapentaplegic Homolog/Signal Transducer and Activator of Transcription 3 Signaling Pathways(QNWS2024111);National Natural Science Foundation Youth Project: Mechanism Study of Yigongsan Decoction in Improving Iron Metabolism in Anemia of Chronic Disease by Regulating the Hepcidin-ferroportin Axis Through Activin B Competitive Binding to Bone Morphogenetic Protein Receptors(81804021);Construction of Key Medical Science (Specialty) Department in Baoshan District(BSZK-2023-Z01);Shanghai Key Discipline of Traditional Chinese Medicine (Clinical Type) Project(shzyyzdxk-2024208)
Cite this article
ZHENG Qin, ZHU Xiaoqin, HU Jie, BU Jingyang, JI Yuting, JIANG Yiling, SHI Ling, ZHANG Aiping, WU Zhihao, XU Haitao, ZHANG Ruifeng, YANG Yang, LUO Meihong. Yigongsan decoction (异功散) ameliorates anemia of chronic disease by attenuating mothers against decapentaplegic homolog-signal transducer and activator of transcription 3 interaction to regulate iron homeostasis[J]. Journal of Traditional Chinese Medicine, 2026, 46(4): 821-831.
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Figure 1 Effect of YGS on iron metabolism in mice A: representative Prussian blue staining images (× 200) of spleen sections in the CTL, LPS, YGS, and YGS + LPS groups; A1: CTL group; A2: LPS group; A3: YGS group; A4: YGS + LPS group; B: quantitative analysis of the percentage of iron-positive area in the spleen; C: serum iron level; D: liver HAMP mRNA relative expression; E: liver Fpn mRNA relative expression. CTL group: the same volume of water; LPS group: 1.5 mg/kg LPS on day 8; YGS group: YGS 15.413 g·kg-1·d-1; YGS + LPS group: YGS 15.413 g·kg-1·d-1 + 1.5 mg·kg-1 LPS. CTL: control; YGS: Yigongsan decoction; LPS: lipopolysaccharide; HAMP: hepcidin antimicrobial peptide; Fpn: ferroportin. Statistical analysis was performed using one-way analysis of variance followed by the least significant difference test for multiple comparisons. Data were presented as mean ± standard deviation (n = 6). Compared with the CTL group, aP < 0.05; compared with the LPS group, bP < 0.05.
Figure 1 Effect of YGS on iron metabolism in mice A: representative Prussian blue staining images (× 200) of spleen sections in the CTL, LPS, YGS, and YGS + LPS groups; A1: CTL group; A2: LPS group; A3: YGS group; A4: YGS + LPS group; B: quantitative analysis of the percentage of iron-positive area in the spleen; C: serum iron level; D: liver HAMP mRNA relative expression; E: liver Fpn mRNA relative expression. CTL group: the same volume of water; LPS group: 1.5 mg/kg LPS on day 8; YGS group: YGS 15.413 g·kg-1·d-1; YGS + LPS group: YGS 15.413 g·kg-1·d-1 + 1.5 mg·kg-1 LPS. CTL: control; YGS: Yigongsan decoction; LPS: lipopolysaccharide; HAMP: hepcidin antimicrobial peptide; Fpn: ferroportin. Statistical analysis was performed using one-way analysis of variance followed by the least significant difference test for multiple comparisons. Data were presented as mean ± standard deviation (n = 6). Compared with the CTL group, aP < 0.05; compared with the LPS group, bP < 0.05.
Figure 2 Effect of YGS-medicated serum on iron metabolism in vitro A: intracellular iron; B: extracellular iron; C: intracellular HAMP mRNA; D: intracellular Fpn mRNA expression; E: representative western blot of intracellular hepcidin and ferroportin; 1: 10% NC; 2: 10% NC + Activin B; 3: 10% YGS + Activin B; 4: 10% NC + IL-6; 5: 10% YGS + IL-6; 6: 10% NC + Activin B + IL-6; 7: 10% YGS + Activin B + IL-6; F: quantitative analysis of intracellular protein expression; F1: quantitative analysis of hepcidin intensity; F2: quantitative analysis of ferroportin intensity. 10% NC group: 10% normal serum; 10% NC + Activin B group: 10% normal serum with 50 ng/mL activin B; 10% YGS + Activin B group: 10% YGS-medicated serum with 50 ng/mL activin B; 10% NC + IL-6 group: 10% normal serum with 50 ng/mL IL-6; 10% YGS + IL-6 group: 10% YGS-medicated serum with 50 ng/mL IL-6; 10% NC + Activin B + IL-6 group: 10% normal serum with 50 ng/mL activin B and 50 ng/mL IL-6; 10% YGS + Activin B + IL-6 group: 10% YGS-medicated serum with 50 ng/mL activin B and 50 ng/mL IL-6. NC: negative control; YGS: Yigongsan decoction; HAMP: hepcidin antimicrobial peptide; Fpn: ferroportin; IL-6: interleukin-6. Statistical analysis was performed using one-way analysis of variance followed by the least significant difference test for multiple comparisons. Data were presented as mean ± standard deviation (n = 3). Compared with the 10% NC group, aP < 0.05; compared with the 10% NC + Activin B group, bP < 0.05; compared with the 10% NC + IL-6 group, cP < 0.05; compared with the 10% NC + Activin B + IL-6 group, dP < 0.05.
Figure 2 Effect of YGS-medicated serum on iron metabolism in vitro A: intracellular iron; B: extracellular iron; C: intracellular HAMP mRNA; D: intracellular Fpn mRNA expression; E: representative western blot of intracellular hepcidin and ferroportin; 1: 10% NC; 2: 10% NC + Activin B; 3: 10% YGS + Activin B; 4: 10% NC + IL-6; 5: 10% YGS + IL-6; 6: 10% NC + Activin B + IL-6; 7: 10% YGS + Activin B + IL-6; F: quantitative analysis of intracellular protein expression; F1: quantitative analysis of hepcidin intensity; F2: quantitative analysis of ferroportin intensity. 10% NC group: 10% normal serum; 10% NC + Activin B group: 10% normal serum with 50 ng/mL activin B; 10% YGS + Activin B group: 10% YGS-medicated serum with 50 ng/mL activin B; 10% NC + IL-6 group: 10% normal serum with 50 ng/mL IL-6; 10% YGS + IL-6 group: 10% YGS-medicated serum with 50 ng/mL IL-6; 10% NC + Activin B + IL-6 group: 10% normal serum with 50 ng/mL activin B and 50 ng/mL IL-6; 10% YGS + Activin B + IL-6 group: 10% YGS-medicated serum with 50 ng/mL activin B and 50 ng/mL IL-6. NC: negative control; YGS: Yigongsan decoction; HAMP: hepcidin antimicrobial peptide; Fpn: ferroportin; IL-6: interleukin-6. Statistical analysis was performed using one-way analysis of variance followed by the least significant difference test for multiple comparisons. Data were presented as mean ± standard deviation (n = 3). Compared with the 10% NC group, aP < 0.05; compared with the 10% NC + Activin B group, bP < 0.05; compared with the 10% NC + IL-6 group, cP < 0.05; compared with the 10% NC + Activin B + IL-6 group, dP < 0.05.
Figure 3 Effect of YGS on SMAD and STAT3 signaling pathway in vivo and vitro A: liver Inhbb mRNA relative expression; B: serum IL-6 level; C: representative Western blot of p-SMAD1/5/8, SMAD1, p-STAT3, STAT3 protein expressions in the liver; D: quantitative analysis of p-SMAD1/5/8/SMAD1 intensity ratio in the liver; E: quantitative analysis of p-STAT3/STAT3 intensity ratio in the liver; F: representative Western blot of intracellular p-SMAD1/5/8, SMAD1, p-STAT3, STAT3 protein expressions; 1: 10% NC; 2: 10% NC + Activin B; 3: 10% YGS + Activin B; 4: 10% NC + IL-6; 5: 10% YGS + IL-6; 6: 10% NC + Activin B + IL-6; 7: 10% YGS + Activin B + IL-6; G: quantitative analysis of intracellular p-SMAD1/5/8/SMAD1 intensity ratio; H: quantitative analysis of intracellular p-STAT3/STAT3 intensity ratio. CTL group: the same volume of water; LPS group: 1.5 mg·kg-1 LPS on day 8; YGS group: YGS 15.413 g·kg-1·d-1; YGS + LPS group: YGS 15.413 g·kg-1·d-1 + 1.5 mg/kg LPS. 10% NC group: 10% normal serum; 10% NC + Activin B group: 10% normal serum with 50 ng/mL activin B; 10% YGS + Activin B group: 10% YGS-medicated serum with 50 ng/mL activin B; 10% NC + IL-6 group: 10% normal serum with 50 ng/mL IL-6; 10% YGS + IL-6 group: 10% YGS-medicated serum with 50 ng/mL IL-6; 10% NC + Activin B + IL-6 group: 10% normal serum with 50 ng/mL activin B and 50 ng/mL IL-6; 10% YGS + Activin B + IL-6 group: 10% YGS-medicated serum with 50 ng/mL activin B and 50 ng/mL IL-6. CTL: control; YGS: Yigongsan decoction; LPS: lipopolysaccharide; NC: negative control; IL-6: interleukin-6; Inhbb: inhibin subunit beta B; SMAD: small mothers against decapentaplegic; STAT3: signal transducer and activator of transcription 3; p-: phosphorylated. Statistical analysis was performed using one-way analysis of variance followed by the least significant difference test for multiple comparisons. Data were presented as mean ± standard deviation (n = 6 for A-E, n = 3 for F-H). Compared with the CTL group, aP < 0.05; compared with the LPS group, b P < 0.05; compared with the 10% NC group, cP < 0.05; compared with the 10% NC + Activin B + IL-6 group, dP < 0.05; compared with the 10% NC + Activin B group, eP < 0.05; compared with the 10% NC + IL-6 group, fP < 0.05.
Figure 3 Effect of YGS on SMAD and STAT3 signaling pathway in vivo and vitro A: liver Inhbb mRNA relative expression; B: serum IL-6 level; C: representative Western blot of p-SMAD1/5/8, SMAD1, p-STAT3, STAT3 protein expressions in the liver; D: quantitative analysis of p-SMAD1/5/8/SMAD1 intensity ratio in the liver; E: quantitative analysis of p-STAT3/STAT3 intensity ratio in the liver; F: representative Western blot of intracellular p-SMAD1/5/8, SMAD1, p-STAT3, STAT3 protein expressions; 1: 10% NC; 2: 10% NC + Activin B; 3: 10% YGS + Activin B; 4: 10% NC + IL-6; 5: 10% YGS + IL-6; 6: 10% NC + Activin B + IL-6; 7: 10% YGS + Activin B + IL-6; G: quantitative analysis of intracellular p-SMAD1/5/8/SMAD1 intensity ratio; H: quantitative analysis of intracellular p-STAT3/STAT3 intensity ratio. CTL group: the same volume of water; LPS group: 1.5 mg·kg-1 LPS on day 8; YGS group: YGS 15.413 g·kg-1·d-1; YGS + LPS group: YGS 15.413 g·kg-1·d-1 + 1.5 mg/kg LPS. 10% NC group: 10% normal serum; 10% NC + Activin B group: 10% normal serum with 50 ng/mL activin B; 10% YGS + Activin B group: 10% YGS-medicated serum with 50 ng/mL activin B; 10% NC + IL-6 group: 10% normal serum with 50 ng/mL IL-6; 10% YGS + IL-6 group: 10% YGS-medicated serum with 50 ng/mL IL-6; 10% NC + Activin B + IL-6 group: 10% normal serum with 50 ng/mL activin B and 50 ng/mL IL-6; 10% YGS + Activin B + IL-6 group: 10% YGS-medicated serum with 50 ng/mL activin B and 50 ng/mL IL-6. CTL: control; YGS: Yigongsan decoction; LPS: lipopolysaccharide; NC: negative control; IL-6: interleukin-6; Inhbb: inhibin subunit beta B; SMAD: small mothers against decapentaplegic; STAT3: signal transducer and activator of transcription 3; p-: phosphorylated. Statistical analysis was performed using one-way analysis of variance followed by the least significant difference test for multiple comparisons. Data were presented as mean ± standard deviation (n = 6 for A-E, n = 3 for F-H). Compared with the CTL group, aP < 0.05; compared with the LPS group, b P < 0.05; compared with the 10% NC group, cP < 0.05; compared with the 10% NC + Activin B + IL-6 group, dP < 0.05; compared with the 10% NC + Activin B group, eP < 0.05; compared with the 10% NC + IL-6 group, fP < 0.05.
Figure 4 Effect of YGS on hepcidin-Fpn axis by the interaction between SMAD and STAT3 signaling pathway in vivo and vitro A: intracellular HAMP mRNA; B: intracellular Fpn mRNA expression; C: representative western blot of intracellular hepcidin and ferroportin; D: quantitative analysis of intracellular protein expression; D1: quantitative analysis of hepcidin intensity; D2: quantitative analysis of ferroportin intensity; E: in vivo co-IP assays demonstrating the interaction between p-SMAD1/5/8 and p-STAT3; E1: liver lysates were immunoprecipitated with an anti-p-STAT3 antibody or normal IgG (negative control), followed by immunoblotting with antibodies against p-SMAD1/5/8 and p-STAT3; E2: reciprocal co-IP was performed using an anti-p-SMAD1/5/8 antibody for immunoprecipitation, followed by immunoblotting with antibodies against p-STAT3 and p-SMAD1/5/8; F: in vitro co-IP assays confirming the interaction between p-SMAD1/5/8 and p-STAT3; F1: cell lysates were immunoprecipitated with an anti-p-STAT3 antibody or normal IgG, followed by immunoblotting for p-SMAD1/5/8 and p-STAT3; F2: reciprocal co-IP was performed using an anti-p-SMAD1/5/8 antibody for immunoprecipitation, followed by immunoblotting for p-STAT3 and p-SMAD1/5/8. 1: 10% NC + Activin B + IL-6 group; 2: 10% YGS + Activin B + IL-6 group,10% NC + siRNA-NC group: siRNA-NC transfection + 10% normal serum; 10% YGS + siRNA-NC group: siRNA-NC transfection + 10% YGS-medicated serum; 10% NC + siRNA-STAT3 group: siRNA-STAT3 transfection + 10% normal serum; 10% YGS + siRNA-STAT3 group: siRNA-STAT3 transfection + 10% YGS-medicated serum; 10% NC + siRNA-SMAD1 group: siRNA-SMAD1 transfection + 10% normal serum; 10% YGS + siRNA-SMAD1 group: siRNA-SMAD1 transfection + YGS-medicated serum. CTL group: the same volume of water; LPS group: 1.5 mg/kg LPS on day 8; YGS group: YGS 15.413 g·kg-1·d-1; YGS + LPS group: YGS 15.413 g·kg-1·d-1 + 1.5 mg·kg-1 LPS. 10% NC + Activin B + IL-6 group: 10% normal serum with 50 ng/mL activin B and 50 ng/mL IL-6; 10% YGS + Activin B + IL-6 group: 10% YGS-medicated serum with 50 ng/mL activin B and 50 ng/mL IL-6. CTL: control; YGS: Yigongsan decoction; LPS: lipopolysaccharide; NC: negative control; IL-6: interleukin-6; SMAD: small mothers against decapentaplegic; STAT3: signal transducer and activator of transcription 3; p-: phosphorylated; siRNA: small interfering RNA; co-IP: co-immunoprecipitation. Statistical analysis was performed using one-way analysis of variance followed by the least significant difference test for multiple comparisons. Data were presented as mean ± standard deviation (n = 3). Compared with the 10% NC + siRNA-NC group, aP < 0.05; compared with the 10% NC + siRNA-STAT3 group, bP < 0.05; compared with the 10% NC + siRNA-SMAD1 group, cP < 0.05.
Figure 4 Effect of YGS on hepcidin-Fpn axis by the interaction between SMAD and STAT3 signaling pathway in vivo and vitro A: intracellular HAMP mRNA; B: intracellular Fpn mRNA expression; C: representative western blot of intracellular hepcidin and ferroportin; D: quantitative analysis of intracellular protein expression; D1: quantitative analysis of hepcidin intensity; D2: quantitative analysis of ferroportin intensity; E: in vivo co-IP assays demonstrating the interaction between p-SMAD1/5/8 and p-STAT3; E1: liver lysates were immunoprecipitated with an anti-p-STAT3 antibody or normal IgG (negative control), followed by immunoblotting with antibodies against p-SMAD1/5/8 and p-STAT3; E2: reciprocal co-IP was performed using an anti-p-SMAD1/5/8 antibody for immunoprecipitation, followed by immunoblotting with antibodies against p-STAT3 and p-SMAD1/5/8; F: in vitro co-IP assays confirming the interaction between p-SMAD1/5/8 and p-STAT3; F1: cell lysates were immunoprecipitated with an anti-p-STAT3 antibody or normal IgG, followed by immunoblotting for p-SMAD1/5/8 and p-STAT3; F2: reciprocal co-IP was performed using an anti-p-SMAD1/5/8 antibody for immunoprecipitation, followed by immunoblotting for p-STAT3 and p-SMAD1/5/8. 1: 10% NC + Activin B + IL-6 group; 2: 10% YGS + Activin B + IL-6 group,10% NC + siRNA-NC group: siRNA-NC transfection + 10% normal serum; 10% YGS + siRNA-NC group: siRNA-NC transfection + 10% YGS-medicated serum; 10% NC + siRNA-STAT3 group: siRNA-STAT3 transfection + 10% normal serum; 10% YGS + siRNA-STAT3 group: siRNA-STAT3 transfection + 10% YGS-medicated serum; 10% NC + siRNA-SMAD1 group: siRNA-SMAD1 transfection + 10% normal serum; 10% YGS + siRNA-SMAD1 group: siRNA-SMAD1 transfection + YGS-medicated serum. CTL group: the same volume of water; LPS group: 1.5 mg/kg LPS on day 8; YGS group: YGS 15.413 g·kg-1·d-1; YGS + LPS group: YGS 15.413 g·kg-1·d-1 + 1.5 mg·kg-1 LPS. 10% NC + Activin B + IL-6 group: 10% normal serum with 50 ng/mL activin B and 50 ng/mL IL-6; 10% YGS + Activin B + IL-6 group: 10% YGS-medicated serum with 50 ng/mL activin B and 50 ng/mL IL-6. CTL: control; YGS: Yigongsan decoction; LPS: lipopolysaccharide; NC: negative control; IL-6: interleukin-6; SMAD: small mothers against decapentaplegic; STAT3: signal transducer and activator of transcription 3; p-: phosphorylated; siRNA: small interfering RNA; co-IP: co-immunoprecipitation. Statistical analysis was performed using one-way analysis of variance followed by the least significant difference test for multiple comparisons. Data were presented as mean ± standard deviation (n = 3). Compared with the 10% NC + siRNA-NC group, aP < 0.05; compared with the 10% NC + siRNA-STAT3 group, bP < 0.05; compared with the 10% NC + siRNA-SMAD1 group, cP < 0.05.
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