Exercise protects against ethanol-induced damage in rat heart and liver through the inhibition of apoptosis and activation of Nrf2/Keap-1/HO-1 pathway.

PROPOSE

Understanding the protective effect of exercise against ethanol-induced toxicity through the oxidative stress signaling pathway, apoptosis, and cholesterol metabolism is important to prevent development of cardiovascular diseases.

METHODS

Thirty-two male Wistar rats were randomly divided into four equal groups as follow: control, exercise training (ET), ethanol (4 g/kg of body weight/day) and ET + ethanol. The ET and ET + Ethanol groups ran on the treadmill at 65% maximum running speed for 60 min for five sessions per week for eight weeks. The ethanol and ET + Ethanol groups received ethanol for eight weeks. At the end of the study, animals were anesthetized and blood and tissues were sampled to examine the biochemical and molecular evaluation.

RESULTS

The results showed that the antioxidant enzymes activity decreased and MDA levels increased in the heart and liver of animals in ethanol group compared to control group. The levels of these oxidative biomarkers improved by ET in ET + Ethanol group compared to ethanol group. It showed that ET could protect the heart and liver against oxidative damage induced by ethanol through up-regulating the expression of the Nrf2/Keap-1/HO-1 pathway. ET could exert a cardioprotective effect on ethanol-induced apoptosis through down-regulating the Bax and the caspase-3 and via up-regulating the Bcl-2 expression in the heart. ET could also improve the impairment of cholesterol metabolism induced by ethanol.

CONCLUSION

Exercise can protect against ethanol-induced toxicity through moderating the expression of genes which are involved in oxidative status, apoptosis and cholesterol metabolism.