Myocardial infarction (MI) is a serious
heart disease in which cardiomyocytes are damaged, caused by
hypoxia. This study explored the possible protective activity of
Skullcapflavone I (SF I), a
flavonoid isolated from the root of Scutellaria baicalensis Georgi, on
hypoxia-stimulated cardiomyocytes cell injury in vitro. Viability and apoptosis of H9c2 cells and primary cardiomyocytes were tested using cell counting kit-8 (CCK-8) assay and Guava Nexin
Reagent, respectively. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to measure the
long non-coding RNA regulator of reprogramming (
lincRNA-ROR) expression. si-ROR was transfected to knockdown
lincRNA-ROR. Western blotting was conducted to assess the
protein levels of key molecules related to cell proliferation, apoptosis, and
mitogen-activated protein kinase/
extracellular signal-regulated kinase (MEK/ERK) pathway. We discovered that
hypoxia stimulation obviously reduced H9c2 cell and primary cardiomyocytes' viability and proliferation, but promoted cell apoptosis. SF I treatment mitigated the cell viability and proliferation inhibition, as well as cell apoptosis caused by
hypoxia. Moreover, SF I promoted the
hypoxia-caused up-regulation of
lincRNA-ROR in H9c2 cells and primary cardiomyocytes. Knockdown of
lincRNA-ROR reversed the influence of SF I on
hypoxia-stimulated H9c2 cells and primary cardiomyocytes. Besides, SF I activated MEK/ERK pathway in H9c2 cells and primary cardiomyocytes via up-regulating
lincRNA-ROR. To sum up, our research verified the beneficial activity of SF I on
hypoxia-caused cardiomyocytes injury. SF I protected cardiomyocytes from
hypoxia-caused injury through up-regulation of
lincRNA-ROR and activation of MEK/ERK pathway.