Abstract:

BACKGROUND: Cold stimulation can result in cardiovascular disease or aggravate cardiovascular disease. It is significant to research the occurrence patterns and molecular mechanism for preventing and treating cardiovascular diseases. 
OBJECTIVE: To explore the effect of hypothermia on the cardiomyoctyes apoptosis and the level of lactate dehydrogenase (LDH) activity, as well as the role of pro- apoptosis protein Bim and PI3K/Akt signal-transduction pathway.
METHODS: Cardiomyoctyes were exposed to 4℃ cold environment for 1 hour, then cultivating in 37 ℃ CO2 incubator for 0, 4, 8, 12, 16, and 24 hours. The degree of apoptosis was measured by flow cytometer by Annexin V-FITC/PI; LDH activity was determined with automatic biochemistry analyzer. Expressions of Bim were determined by Western blotting. All the changes were observed in the nutrient medium after adding PI3K inhibator LY294002.
RESULTS AND CONCLUSION: After hypothermia treatment, the cell apoptosis was significantly increased, the survival rate decreased, and the LDH activity and Bim expression increased (P < 0.05), which reached the peak at 24 hours. After adding LY29004, cell apoptosis increased notably, the LDH activity and Bim expression increased, but p-PI3K expression were declined (P < 0.05). It suggested that hypothermia can induce cardiomyoctyes apoptosis. The PI3K/Aktsignal-transduction pathway is likely to participate in Bim expressions.