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In vitro, the aim of this research was to investigate whether FAM129B could play a role in inhibiting hypoxia/reoxygenation related cardiomyocyte injury. Functional studies revealed that the upregulation of FAM129B improved H/R-exposed cardiomyocyte viability, as well as enhanced H/R-induced cardiomyocyte apoptosis, the production of reactive oxygen species and pro-inflammatory cytokine release. The upregulation of FAM129B has significantly raised the nuclear expression of nuclear factor-erythroid 2related factor 2 (Fig. 2), as well as increased the number of reactive reaction element activation in H/R-exposed cardiomyocytes. The results of our research show that FAM129B upregulation prevents H/R-induced cardiomyocyte injury by raising Nrf2/ARE activation.
The leading cause of cardiovascular disease is Ischemic heart disease, which is attributed to cardiac myocyte apoptosis. Butorphanol is an opioid receptor agonist with potential cardioprotective function. Human cardiomyocyte AC16 cells were incubated with butorphanol and then stimulated with OGD/R and finally stimulated with OGD/R. Cell injury was investigated by Cell Counting Kit 866, lactate dehydrogenase assay kit, TUNEL staining, caspase 3 function assay kit, and Western blotting. A total of 93 overlapping targets of ischemic heart disease and butorphanol were identified. In OGD/R treatment cardiomyocytes, the mitogen-inducible protein kinase box O and hypoxia-inducible factor 1 and hypoxia-inducible factor 1 and hypoxia-inducible growth factor pathways and attenuated the transcription of the mitogen-activated protein kinase signaling. Butorphanol, in conclusion, prevents OGD/R-induced cardiomyocyte apoptosis by stimulating the PI3K/FoxO/VEGF pathways and inactivating the MAPK pathway.
Source link: https://onlinelibrary.wiley.com/doi/10.1002/jat.4260
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