Objective To investigate the effects of etomidate on lipopolysaccharide (LPS)‑induced inflammation and apoptosis of cardiomyocytes and its possible mechanism. Methods According to the random number table method, rat cardiomyocytes H9c2 cultured in vitro were divided into five groups (n=3, and each experiment was repeated three times): a normal control (Con) group, a LPS group, a LPS+20 μmol/L etomidate (E‑L) group, a LPS+50 μmol/L etomidate (E‑M) group, and a LPS+100 μmol/L etomidate (E‑H) group. The Con group was normally cultivated; the LPS group was cultured in dulbecco's modified eagle medium (DMEM) medium containing 1 mg/L LPS for 24 h; and the E‑L group, E‑M group, and E‑H group were treated with different concentrations (20, 50 μmol/L, and 100 μmol/L) etomidate and 1 mg/L LPS in DMEM medium for 24 h. According to the random number table method, normal cultured cardiomyocytes were divided into two groups (n=3, and each experiment was repeated three times): a LPS+100 μmol/L etomidate+anti‑microRNA (microRNA, miR)‑NC (anti‑miR‑NC) group and a LPS+100 μmol/L etomidate+anti‑miR‑214‑3p (anti‑miR‑214‑3p) group. The anti‑miR‑NC group and anti‑miR‑214‑3p group were transfected with anti‑miR‑NC or anti‑miR‑214‑3p to cardiomyocytes, respectively, before cultivation with DMEM medium containing 100 μmol/L etomidate and 1 mg/L LPS for 24 h. The enzyme‑linked immunosorbent assay (ELISA) method was used to detect the levels of tumor necrosis factor‑α (TNF‑α), interleukin (IL)‑6, and IL‑1β, while flow cytometry was used to detect cell apoptosis rate. The quantitative real‑time polymerase chain reaction (qRT‑PCR) was used to detect the expression of miR‑214‑3p and transducin β‑like 1X related protein 1 (TBL1XR1). The dual luciferase report test was used to verify the targeted regulation relationship between miR‑214‑3p and TBL1XR1. The expression of TBL1XR1 and B‑cell lymphoma‑2 (Bcl‑2)‑associated X protein (Bax), Bcl‑2 was measured by Western blot. Results Compared with the Con group, the LPS group presented remarkable increases in the levels of TNF‑α, IL‑6, IL‑1β and Bax protein, apoptosis rate and the amount of TBL1XR1 mRNA (P<0.05), and decreases in the level of Bcl‑2 and miR‑214‑3p protein (P<0.05). Compared with the LPS group, the levels of TNF‑α, IL‑6, IL‑1β, and Bax, apoptosis rate and the amount of TBL1XR1 mRNA in the E‑L, E‑M, and E‑H group decreased in a dose‑dependent manner (P<0.05), while the level of Bcl‑2 and miR‑214‑3p increased in a dose‑dependent manner (P<0.05), and statistical differences were found among the E‑L, E‑M, and E‑H groups (P<0.05). MiR‑214‑3p negatively regulated the expression of TBL1XR1 (P<0.05). Compared with the anti‑miR‑NC group, the levels of TNF‑α, IL‑6, IL‑1β, and Bax, apoptosis rate in the anti‑miR‑214‑3p group increased (P<0.05), while the level of Bcl‑2 decreased (P<0.05). Conclusions Etomidate inhibits LPS‑induced inflammation and apoptosis in cardiomyocytes through regulating the miR‑214‑3p/TBL1XR1 molecular axis.