AIM To elucidate the potential function and molecular mechanism of lipocalin 2 (Lcn 2) in acute myocardial injury associated with infrasound through a rat model.

METHODS  Ninety SD rats aged 6-8 weeks were randomly divided into control group and two experimental groups with different exposure doses to establish infrasound injury model. Cardiac function was evaluated by echocardiography; Paraffin sections were prepared and stained with HE and TUNEL; The mRNA expression levels of IL-6, CD3 and CD45 in myocardial tissue were detected by qRT-PCR; The content of LCN 2 in plasma and myocardial tissue was detected by ELISA; The expressions of p-NF-κB and P-I кB were detected by Western blot. In vitro, H9C2 cells or H9C2 cells co-cultured with neutrophils were exposed to infrasound. Some cells were added with Lcn 2 inhibitor zinc00640089 0.5 hours before exposure, and then the degree of cell injury and the expression of Lcn 2, p-NF-κB and P-IкB were detected.

RESUITS  Infrasound caused myocardial injury in a frequency and time-dependent manner. The closer to the heart’s natural frequency and the longer the exposure, the more severe the injury. (P<0.05, P<0.01) . Infrasound exposure significantly increased the number of TUNEL positive cells and the mRNA expressions of IL-6, CD3 and CD45 (P<0.01) , and increased the content of Lcn 2 (P<0.01) , activating NF-κB pathway (P<0.01) . The results of in vitro experiments showed that after co-culture with neutrophils, infrasound reduced the activity of H9C2 cells (P<0.05, P<0.01) , increased the activity of caspase 3 (P<0.05, P<0.01) , and activated NF-κB pathway (P<0.01) , while Lcn 2 inhibitor significantly improved infrasound induced cell injury (P<0.01) and inhibited the activation of NF-κB pathway (P<0.01) .

CONCLUSION  Lcn 2 released by neutrophils is an important cytokine in infrasound induced myocardial injury.