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β-Eudesmol Alleviates Inflammatory Injury in Septic Cardiomyopathy Through Enhancing GSK3B Activity to Inhibiting
Sihua Jiang1, Zhuoqing Dai1, Tingting Pang2
1Department of Emergency Medicine, The Second Affiliated Hospital of Guizhou University of Traditional Chinese Medicine, No. 83, Feishan Street, Yunyan District, Guiyang, 550001, China.
Biochemical Genetics
|July 13, 2026
Summary
Beta-eudesmol treatment alleviates septic cardiomyopathy (SCM) in rats by reducing inflammation and apoptosis. It enhances GSK3B activity to suppress IL-17-mediated chemokine expression, offering a potential therapeutic strategy for SCM.
Area of Science:
- Biochemistry
- Pharmacology
- Cardiology
Background:
- Septic cardiomyopathy (SCM) is a critical complication of sepsis, characterized by excessive inflammation and cardiac dysfunction.
- Beta-eudesmol, a natural sesquiterpene alcohol, exhibits anti-inflammatory properties, but its role in SCM is not well understood.
Purpose of the Study:
- To investigate the therapeutic effects of beta-eudesmol on SCM.
- To elucidate the underlying molecular mechanisms of beta-eudesmol in mitigating SCM-induced myocardial injury.
Main Methods:
- Established a rat model of SCM using cecal ligation and puncture (CLP).
- Assessed cardiac function markers (BNP, cTnI) via ELISA.
- Evaluated myocardial tissue damage using HE and TUNEL staining.
- Quantified gene and protein expression (RT-qPCR, Western blotting) including inflammatory cytokines and GSK3B pathway components.
Main Results:
- Beta-eudesmol treatment significantly reduced serum BNP and cTnI levels, indicating improved cardiac function.
- It decreased pro-inflammatory cytokines (IL-6, IL-1β, TNF-α, LPS) and IL-17 levels in SCM rats.
- Beta-eudesmol inhibited myocardial apoptosis and inflammatory cell infiltration.
- The compound enhanced GSK3B activity by reducing its phosphorylation, thereby suppressing IL-17A, CXCL1, CXCL2, and CCL20 expression.
Conclusions:
- Beta-eudesmol effectively alleviates myocardial inflammation and apoptosis in a rat model of septic cardiomyopathy.
- The therapeutic effect is mediated by the inhibition of IL-17-driven chemokine expression through enhanced GSK3B activity.
- Beta-eudesmol presents a promising therapeutic candidate for managing septic cardiomyopathy.