The effect of L-carnitine on authophagy in infarcted heart in wistar male rats
Abstract
Introduction: Autophagy is a physiological catabolic process that, through lysosomes, destroys inefficient cell components. It has been shown that impairment of genes associated with autophagy can exacerbate heart failure following myocardial infarction. Carnitine supplementation is a factor that has a well-known effect on cellular metabolism processes and ATP production. It is an important component of energy production and plays an important role in aerobic respiration.
Eating meat can obtain 75% of body needs carnitine. Although body can prepare carnitine by using lysine and methionine amino acids it is negligible.
Objective of Study: In this study, we investigated the effect of L carnitine on cardiac structural changes including hemodynamic and autophagy factors in myocardial infarction in rats.
Methods and Materials: In this study, male Wistar rats weighing 270-300 g were kept at 25-27 ° C and the dark- brightness cycle for 12 hours. Water and food were supplied to them. For induction of myocardial infarction, isoproterenol, via saline solution, was injected subcutaneously for 24 hours within two days. Injectable L carnitine received half an hour after induction in several doses for 24 hours for 4 days.
Results: With receiving the injection of L carnitine supplement, hemodynamic parameters have been improved somewhat better than the isoproterenol group. The increase in the ratio of LC3-II/LC-I and the BECLIN1 the P62protein represent the induction of autophagy. With the intake of L carnitine, this ratio of protein was slightly increased compared to the isoproterenol group and Moreover, P62 protein was increased compared to the isoproterenol group.
Discussion: According to the results of this study, L carnitine supplementation has a protective effect against infraction caused by isoproterenol, this protective effect is associated with an antiirritant effect on heart muscles. It seems that strengthening autophagia can protect the heart from damage of myocardial infarction.