ArticleBioscience reports2025
Hydrogen sulfide attenuates sepsis-induced cardiac dysfunction in infant rats by inhibiting the expression of cold-inducible RNA-binding protein.
Article in Bioscience reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Endogenous H₂S promotes HSPA8 sulfhydration to downregulate HIF1α and prevent ferroptosis in septic myocardial injury.Redox report : communications in free radical research · 2026Article
- The Role of Cold-Inducible RNA-Binding Protein (CIRP) in Neurological Disorders.Brain sciences · 2026Review
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13 authors.
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Abstract
Sepsis-induced cardiac dysfunction is one of the most common complications of sepsis. It is also a major cause of death in pediatric intensive care units. The underlying mechanism of sepsis-induced cardiac dysfunction remains elusive. Cold-inducible RNA-binding protein (CIRP) is a damage-associated molecular pattern that is up-regulated during sepsis. Hydrogen sulfide (H2S) has been shown to play a protective role in sepsis-induced cardiac dysfunction in adult animals. The present study aimed to determine whether H2S ameliorates the cardiac function in infant rats by inhibiting CIRP-mediated sepsis-induced cardiac dysfunction. Rat pups aged 17-18 days were subjected to cecal ligation and puncture (CLP) to induce sepsis. Six hours after CLP, hemodynamic results demonstrated that there was a significant decrease in +dP/dtmax, -dP/dtmax, left ventricular ejection fraction, and left ventricular shortening fraction, indicating cardiac dysfunction. The plasma levels of myocardial injury markers such as creatine kinase-myocardial band and cardiac troponin I were significantly increased at 6 h after CLP. The inhibition of CIRP with C23 improved the cardiac function of the rats with CLP-induced sepsis, accompanied by a significant decrease in endoplasmic reticulum stress (ERS) activation. Moreover, treatment with sodium 4-phenylbutyrate (an inhibitor of ERS) ameliorated myocardial injury and dysfunction, accompanied by a significant decrease in ERS activation. Sodium hydrosulfide, a H2S donor, ameliorated CLP-induced cardiac dysfunction and decreased CIRP levels and ERS. In contrast, the inhibition of endogenous H2S production by propargylglycine (a cystathionine-γ-lyase inhibitor) aggravated CLP-induced cardiac dysfunction and increased CIRP levels. In conclusion, the present study demonstrated that H2S exerted cardioprotective effects by inhibiting the CIRP/ERS pathway in infant rats with sepsis. These findings might indicate a novel target in the treatment of sepsis in infants.
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