Research on the function and mechanism of survivin in heart failure mice model

To observe the role of survivin in the heart failure mice model and to study its mechanism.

20 male C57BL/ 6J mice were selected and randomly divided into two groups: normal group (n=10) and heart failure group (n=10). After continuous modeling, the cardiac functions of mice in the two groups were detected via ultrasonic cardiogram equipment. The pathological conditions of hearts in the two groups were detected via hematoxylin and eosin (HE) staining. The expressions of survivin in heart tissues in both groups were detected via immunofluorescence method. The mRNA expressions of tumor necrosis factor-α (TNF-α), factor associated suicide (Fas) and factor associated suicide ligand (FasL) were detected via reverse transcription polymerase chain reaction (RT-PCR). The expressions of survivin in heart tissues of two groups were detected via Western blotting.

Ultrasonic cardiogram showed that the myocardial motion amplitude of mice in heart failure group was significantly decreased compared with that in normal group. HE staining further revealed the pathological conditions in heart failure group. RT-PCR showed that the mRNA expressions of TNF-α, Fas and FasL in heart failure group were significantly higher than those in normal group. Immunofluorescence and Western blotting showed that the expression of survivin in heart failure group was significantly higher than that in normal group.

Survivin expression is closely related to the occurrence and development of heart failure, indicating that survivin has an important value in the research on heart failure and the mechanism is related to inflammation and apoptosis.