myc participates in lipopolysaccharide-induced sepsis via promoting cell proliferation and inhibiting apoptosis

Objective: this study aimed to explore the potential mechanism of myc proto-oncogene, bhlh transcription factor (myc) gene, on sepsis. materials and methods: in this experimental study, rat-derived h9c2 cardiomyocyte cells were cultured in vitro, followed by lipopolysaccharide (lps) treatment with different concentration gradients. the cholecystokinin octapeptide (cck-8) assay, enzyme-linked immunoassay (elisa) assay, quantitative reverse transcription polymerase chain reaction (qrt-pcr), cell transfection, western blot and flow cytometry were used to observe the cellular apoptosis and proliferation of cells in both treated lps groups and normal control group. results: the result of cck-8 assay showed that silencing myc inhibited cellular proliferation of sepsis in absence or presence of lps treatment. elisa assay showed that the expressions of tumor necrosis factor-α (tnf-α) and interleukin-6 (il-6) were decreased in myc silenced group, but they were increased after lps treatment. moreover, flow cytometry assay showed that myc silencing contributed to the apoptosis of sepsis cells. furthermore, the expression of inflammatory factors showed that myc silencing elevated the expression of inflammation factors. conclusion: myc might take part in the process of lps induced sepsis through suppressing apoptosis and inducing cell proliferation. moreover, myc might reduce inflammation during the progression of lps induced sepsis.