ArticleCytoJournal2024
A mechanism study of tripartite motif 10 modulating septic cardiomyopathy.
Article in CytoJournal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objective: Septic cardiomyopathy (SCM), as a complication of the septic process, severely affects the myocardial function of patients, but its pathogenesis remains unclear. The article aims to explore the mechanism of tripartite motif 10 (TRIM10) in rats with SCM and provide animal experimental basis for the treatment and prevention of SCM. Material and Methods: An SCM rat model was constructed by intraperitoneal injection of lipopolysaccharide (LPS). Sh-NC and sh-TRIM10 groups were injected with sh-NC and sh-TRIM10 in the tail vein for 3 consecutive days before SCM modeling. The expression of TRIM10 was detected by Western blot and reverse transcription-polymerase chain reaction analyses. Hematoxylin-eosin staining was performed to observe pathological changes in myocardium. Cardiomyocyte apoptosis was detected by flow cytometry. Serum levels of cardiac troponin I, myohemoglobin, creatine kinase-MB, interleukin-18 (IL-18), interleukin-1 β (IL-1β), tumor necrosis factor-α (TNF-α), superoxide dismutase, and glutathione peroxidase (GSH-Px) were detected by enzyme-linked immunosorbent assay. Apoptosis-related proteins and toll-like receptor 4 (TLR4)/nuclear transcription factor-κB (NF-κB) pathway-related proteins were explored by Western blot assay. Results: TRIM10 expression increased in the LPS group ( Conclusion: TRIM10 knockdown can reduce inflammation, oxidative stress, and apoptosis in SCM rats and has a protective effect on cardiomyocytes, which may be attributed to the regulation of the TLR4/NF-κB pathway.
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