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Article

Investigating the Mechanism of Emodin in Rheumatoid Arthritis Through the HIF-1α/NLRP3 Pathway and Mitochondrial Autophagy

by
Dehao Du
1,
Linlan Zhou
1,
Jiayu Tian
1,
Lianying Cheng
1,
Han Zhang
2,
Yifu Tang
2,
Zexuan Qiu
1,
Tingdan Zhang
1 and
Xiaofeng Rong
1,*
1
Department of Integrated Traditional Chinese and Western Medicine, Sci-Tech Innovation Center, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China
2
School of Basic Medical Sciences, Chongqing Medical University, Chongqing 400016, China
*
Author to whom correspondence should be addressed.
Curr. Issues Mol. Biol. 2025, 47(7), 486; https://doi.org/10.3390/cimb47070486
Submission received: 13 May 2025 / Revised: 18 June 2025 / Accepted: 21 June 2025 / Published: 25 June 2025
(This article belongs to the Special Issue Therapeutic Effects of Natural Bioactive Compounds in the Management of Human Diseases)
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Abstract

In this study, we investigated the inhibitory effects of emodin on pyroptosis in rheumatoid arthritis (RA) synovial cells by modulating the HIF-1α/NLRP3 inflammasome pathway and mitochondrial autophagy. By employing a chemically induced hypoxia model with CoCl2, we established experimental groups including normal control, model group, and emodin-treated groups at different concentrations (5 μM, 10 μM, and 20 μM). We optimized the CoCl2 concentration via CCK-8 assay to ensure cell viability. ELISA, Western blotting, transmission electron microscopy, and immunofluorescence were employed to assess HIF-1α, IL-1β, and IL-18 levels, pyroptosis-related proteins, autophagy markers, and NLRP3 fluorescence intensity. Statistical analysis revealed that increased CoCl2 concentrations led to a significant cell viability reduction (p < 0.05), with 300 μM CoCl2 causing ~50% inhibition at 24 h. Transmission electron microscopy confirmed autophagosome formation in emodin-treated groups, while Western blotting showed dose-dependent downregulation of HIF-1α, NLRP3, BNIP3, and related proteins. Immunofluorescence revealed reduced NLRP3 fluorescence intensity with increasing emodin doses (p < 0.05), alongside dose-dependent cell viability recovery (p < 0.05). Our findings demonstrate that emodin alleviates RA synovitis through dual mechanisms: inhibition of mitochondrial autophagy to regulate the balance between mitochondrial autophagy and pyroptosis, and suppression of HIF-1α/NLRP3-mediated pyroptosis signaling, thereby reducing IL-1β and IL-18 release and inhibiting synovial cell proliferation. This study provides innovative approaches for targeted RA therapy.
Keywords: rheumatoid arthritis; emodin; cobalt chloride; hypoxia; pyroptosis; mitochondrial autophagy rheumatoid arthritis; emodin; cobalt chloride; hypoxia; pyroptosis; mitochondrial autophagy

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MDPI and ACS Style

Du, D.; Zhou, L.; Tian, J.; Cheng, L.; Zhang, H.; Tang, Y.; Qiu, Z.; Zhang, T.; Rong, X. Investigating the Mechanism of Emodin in Rheumatoid Arthritis Through the HIF-1α/NLRP3 Pathway and Mitochondrial Autophagy. Curr. Issues Mol. Biol. 2025, 47, 486. https://doi.org/10.3390/cimb47070486

AMA Style

Du D, Zhou L, Tian J, Cheng L, Zhang H, Tang Y, Qiu Z, Zhang T, Rong X. Investigating the Mechanism of Emodin in Rheumatoid Arthritis Through the HIF-1α/NLRP3 Pathway and Mitochondrial Autophagy. Current Issues in Molecular Biology. 2025; 47(7):486. https://doi.org/10.3390/cimb47070486

Chicago/Turabian Style

Du, Dehao, Linlan Zhou, Jiayu Tian, Lianying Cheng, Han Zhang, Yifu Tang, Zexuan Qiu, Tingdan Zhang, and Xiaofeng Rong. 2025. "Investigating the Mechanism of Emodin in Rheumatoid Arthritis Through the HIF-1α/NLRP3 Pathway and Mitochondrial Autophagy" Current Issues in Molecular Biology 47, no. 7: 486. https://doi.org/10.3390/cimb47070486

APA Style

Du, D., Zhou, L., Tian, J., Cheng, L., Zhang, H., Tang, Y., Qiu, Z., Zhang, T., & Rong, X. (2025). Investigating the Mechanism of Emodin in Rheumatoid Arthritis Through the HIF-1α/NLRP3 Pathway and Mitochondrial Autophagy. Current Issues in Molecular Biology, 47(7), 486. https://doi.org/10.3390/cimb47070486

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