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已发表论文
复方葶苈子汤含药血清通过 SIRT3 相关的 AIM2 分子伴侣介导的自噬抑制心肌细胞 PANoptosis
Authors Huang R, Tang J, Huang W, Shang Y, Liu W, Long H, Wan R
Received 14 May 2025
Accepted for publication 18 October 2025
Published 14 November 2025 Volume 2025:18 Pages 6975—6987
DOI https://doi.org/10.2147/IJGM.S540452
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Redoy Ranjan
Ren Huang,1,* Junyu Tang,2,* Wenjuan Huang,1 Yan Shang,1 Wenli Liu,1 Huajun Long,1 Rongwen Wan1
1Department of Intensive Care Medicine, The Affiliated Hospital of Hunan Academy of Traditional Chinese Medicine, Changsha, Hunan, People’s Republic of China; 2Department of Geriatric Medicine, The Affiliated Hospital of Hunan Academy of Traditional Chinese Medicine, Changsha, Hunan, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Rongwen Wan, Department of Intensive Care Medicine, The Affiliated Hospital of Hunan Academy of Traditional Chinese Medicine, 58 Lushan Road, Yuelu District, Changsha, Hunan, 410006, People’s Republic of China, Email wanrongwen007@163.com
Background: Septic cardiomyopathy (SCM) is a life-threatening complication of sepsis with no specific therapeutic options. Recent evidence suggests that PANoptosis, a programmed cell death pathway, contributes to myocardial injury in sepsis. Compound Tinglizi Decoction (CTLZC), a traditional Chinese herbal formula, has shown potential cardioprotective effects, yet the underlying biochemical mechanisms remain unclear.
Methods: A rat model of SCM was established to investigate the effect of CTLZC-containing serum on myocardial injury. Primary cardiomyocytes were treated with CTLZC-containing serum, and SIRT3 expression was modulated via overexpression and knockdown plasmids. Cell viability, PANoptosis markers, and chaperone-mediated autophagy (CMA) proteins were assessed through CCK-8, TUNEL staining, RT-qPCR, Western blotting, ELISA, and Co-IP assays.
Results: CTLZC-containing serum enhanced cardiomyocyte viability and significantly upregulated SIRT3 expression. It inhibited the expression of PANoptosis-related molecules (AIM2, ZBP1, RIPK1, RIPK3, FADD, and caspase-8) and promoted the expression of CMA-related proteins HSC70 and LAMP2A. SIRT3 knockdown reversed these effects and increased the release of biochemical markers of myocardial injury (LDH, CK-MB) and inflammatory cytokines (TNF-α, IL-1β, IL-18). Co-IP confirmed that AIM2 interacts with HSC70, indicating lysosomal degradation via CMA.
Conclusion: CTLZC-containing serum attenuates inflammatory and cell death responses in septic cardiomyopathy, likely through a SIRT3-associated modulation of chaperone-mediated autophagy and PANoptosis. These findings highlight the biochemical regulatory role of SIRT3 in mediating autophagic and inflammatory pathways during SCM, offering new insights into potential therapeutic targets.
Keywords: compound tinglizi decoction, cardiomyocytes, SIRT3, chaperone-mediated autophagy, PANoptosis
1Department of Intensive Care Medicine, The Affiliated Hospital of Hunan Academy of Traditional Chinese Medicine, Changsha, Hunan, People’s Republic of China; 2Department of Geriatric Medicine, The Affiliated Hospital of Hunan Academy of Traditional Chinese Medicine, Changsha, Hunan, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Rongwen Wan, Department of Intensive Care Medicine, The Affiliated Hospital of Hunan Academy of Traditional Chinese Medicine, 58 Lushan Road, Yuelu District, Changsha, Hunan, 410006, People’s Republic of China, Email wanrongwen007@163.com
Background: Septic cardiomyopathy (SCM) is a life-threatening complication of sepsis with no specific therapeutic options. Recent evidence suggests that PANoptosis, a programmed cell death pathway, contributes to myocardial injury in sepsis. Compound Tinglizi Decoction (CTLZC), a traditional Chinese herbal formula, has shown potential cardioprotective effects, yet the underlying biochemical mechanisms remain unclear.
Methods: A rat model of SCM was established to investigate the effect of CTLZC-containing serum on myocardial injury. Primary cardiomyocytes were treated with CTLZC-containing serum, and SIRT3 expression was modulated via overexpression and knockdown plasmids. Cell viability, PANoptosis markers, and chaperone-mediated autophagy (CMA) proteins were assessed through CCK-8, TUNEL staining, RT-qPCR, Western blotting, ELISA, and Co-IP assays.
Results: CTLZC-containing serum enhanced cardiomyocyte viability and significantly upregulated SIRT3 expression. It inhibited the expression of PANoptosis-related molecules (AIM2, ZBP1, RIPK1, RIPK3, FADD, and caspase-8) and promoted the expression of CMA-related proteins HSC70 and LAMP2A. SIRT3 knockdown reversed these effects and increased the release of biochemical markers of myocardial injury (LDH, CK-MB) and inflammatory cytokines (TNF-α, IL-1β, IL-18). Co-IP confirmed that AIM2 interacts with HSC70, indicating lysosomal degradation via CMA.
Conclusion: CTLZC-containing serum attenuates inflammatory and cell death responses in septic cardiomyopathy, likely through a SIRT3-associated modulation of chaperone-mediated autophagy and PANoptosis. These findings highlight the biochemical regulatory role of SIRT3 in mediating autophagic and inflammatory pathways during SCM, offering new insights into potential therapeutic targets.
Keywords: compound tinglizi decoction, cardiomyocytes, SIRT3, chaperone-mediated autophagy, PANoptosis