ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University2024
[HTD4010 attenuates myocardial injury in mice with septic cardiomyopathy by promoting autophagy
Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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5 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
objectiveTo investigate the protective effects of HTD4010 against lipopolysaccharide (LPS)-induced septic cardiomyopathy (SCM) in mice and explore the mechanisms mediating its effect.
methodsForty-five male ICR mice were randomized equally into control group, LPS (10 mg/kg) group, and LPS+HTD4010 group (in which 2.5 mg/kg HTD4010 was injected subcutaneously at 1 h and 6 h after LPS injection). Cardiac function of the mice was evaluated by ultrasound, and pathological changes in the myocardial tissues were observed with HE staining. The levels of IL-6 and TNF-α in serum and myocardial tissues were detected using ELISA, and apoptosis of the cardiomyocytes was detected with TUNEL staining. The expression levels of the key proteins associated with apoptosis, autophagy and the AMPK/mTOR pathway in the myocardial tissues were detected using Western blotting. The ultrastructural changes of cardiac myocardial mitochondria was observed with transmission electron microscopy.
resultsLPS exposure caused severe myocardial damage in mice, characterized by myocardial fiber rupture, structural disorder, inflammatory cell infiltration, and mitochondrial damage. The LPS-treated mice exhibited significantly decreased cardiac LVEF and FS values, elevated IL-6 and TNF-αlevels in serum and myocardial tissue, and an increased myocardial cell apoptosis rate with enhanced expressions of Bax, p-62 and p-mTOR and lowered expressions of Bcl-2, LC3 II/I, Beclin-1 and p-AMPK (
conclusionHTD4010 can attenuate myocardial injury in SCM mice possibly by promoting autophagy via modulating the AMPK/mTOR signaling pathway.
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