Amelioration of methamphetamine cardiotoxicity by propofol

Methamphetamine (MET) is a stimulant and one of the most abused drugs in worldwide. MET could cause several organ toxicity such as cardiotoxicity. Oxidative stress has been proposed as the main mechanism for MET toxicity. Propofol as a sedative-hypnotic agent has antioxidant property. In this study, we used propofol for attenuating of MET-induced cardiotoxicity in rats. The groups (six rats in each group) were as follows: control, MET (5 mg/kg IP) and treated groups that were received propofol (5, 10 and 20 mg/kg, IP) and vitamin E, 30 min before MET administration. After 24 hours, animals were killed, and heart tissue and blood were separated. MET cardiotoxicity was assessed by the evaluation of the levels of lactic acid dehydrogenase (LDH) and creatine phosphokinase (CPK) as cardiac marker enzymes. On the other hand, oxidative stress markers such as reactive oxygen species (ROS), lipid peroxidation (LPO), glutathione (GSH) and protein carbonyl were measured in heart tissue. Treatment with propofol significantly decreased the cardiac marker enzymes level which increased in MET-treated group. Propofol significantly inhibited the ROS formation and protected the cardiac tissue against LPO. Propofol also significantly prevented MET induced GSH oxidation in cardiac tissue. Protein carbonyl level was increased after MET exposure, but was significantly decreased with propofol pre-treatment. This study showed that propofol prevented MET-induced cardiotoxicity via inhibition of oxidative stress damage. Therefore, the efficacy of this antioxidant could be evaluated for the treatment of MET toxicity situation.

Amelioration of methamphetamine cardiotoxicity by propofol Keywords:

Methamphetamine , cardiotoxicity , propofol , oxidative stress , cardiac enzyme