The effects of aerobic exercise training with octopamine supplementation on cardiomyocyte apoptosis induced by deep-frying oil: The role of caspase and procaspase 3.

BACKGROUND AND AIM

Clinicians who understand how the body responds to exercise, how aerobic training enhances cardiovascular fitness and the benefits and essentials of prescribing aerobic exercise can effectively encourage patients to be active. Deep-frying is a standard cooking method accompanied by the production of carcinogenesis substances such as acrolein. Acrolein is a toxic byproduct of lipid peroxidation involved in the development of pulmonary, cardiac, and neurodegenerative diseases. This study aimed to explore the effect of aerobic exercise (E.X.E.), and octopamine (OCT) on caspase three expression levels in the heart tissue of rats were fed deep-frying oil (D.F.O.).

METHODS

30 male Wistar rats were divided into 5 groups (n = 6 in each) including (1) control (CO), (2) deep-frying oil (DFO), (3) deep-frying oil + exercise (DFO + EXE), (4) deep-frying oil + octopamine (DFO + OCT), and (5) deep-frying oil + exercise + octopamine (DFO + EXE + OCT). The apoptotic effects of D.F.O. in heart tissue were examined by TUNEL assay. Masson's trichrome stain was used to study cardiomyocytic fibers. Moreover, caspase three gene expression in all groups was evaluated using quantitative real-time PCR and the Western blot method.

RESULTS

Data showed a significant increase in apoptotic cells in the D.F.O. group (P < 0.05). In Masson's Trichrome stain analysis, more cardiomyocytic fibers degradation and lymphocytic aggregation cells in the DFO + EXE + OCT group significantly improve this degradation. Also, the expression level of caspase 3 was significantly decreased in the DFO + EXE + OCT group (P < 0.05).

CONCLUSION

According to the result of the current study, it can be assumed that D.F.O. can lead to programmed cell death via the activation of caspases in heart tissue. However, it seems that aerobic exercise with octopamine supplementation improves heart tissue function by inhibiting the expression of caspase 3 and pro-caspase 3, leading to a significantly decreased apoptosis in cardiomyocytes of DFO-treated models.