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MiR141. 3p levels in obese rats' cardiomyocytes are markedly elevated after a high-fat diet, according to it. The role of miR1413p in lipotoxic injury of H9c2 cells caused by palmitic acid and its potential mechanisms was investigated in the current study. Moreover, blocking the Notch1/AKT signaling pathway by its inhibitor could help to prevent miR141+3p's effect on mitochondrial-mediated apoptosis induced by PA. MiR141/3p controls saturated fatty acid-induced cardiomyocyte apoptosis in the Notch1/PTEN/AKT pathway, giving the presenter a new insight into the causes of myocardial lipotoxic injury.
The leading cause of cardiovascular mortality in cardiovascular disease is cardiac myocyte apoptosis, which is correlated to cardiac myocyte apoptosis. Butorphanol is a opioid receptor agonist with a potential cardioprotective role. cardiomyocyte apoptosis stimulated by oxygen and glucose deprivation/reperfusion. The aim of this research is to investigate butorphanol's function and mechanism in oxygen and glucose deprivation/reperfusion. The human cardiomyocyte AC16 cells were incubated with butorphanol and then stimulated with OGD/R and OGD/R. Cell injury was investigated by Cell Counting Kit, lactate dehydrogenase assay kit, TUNEL staining, caspase 3 activity assay kit, and Western blotting. A total of 93 overlapping targets of ischemic heart disease and butorphanol were discovered. Butorphanol alone had no cytotoxicity to cardiomyocytes, and it shielded against OGD/Rinduced viability inhibition, LDH release, cell apoptosis, and an increase of caspase3 activity and expression levels of cleaved caspases 3 and Bim.
Source link: https://onlinelibrary.wiley.com/doi/10.1002/jat.4260
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