Evaluation of the effects of aerial organ hydroalcoholic extract of Tanacetum Kotschyi and Dextromethorphan on morphine withdrawal symptoms

Abstract

Introduction: There are various mechanisms (increased activity of the glutaminergic system, oxidative stress, etc.) in dependence and tolerance to opioids. Dextromethorphan is a non-competitive antagonist of NMDA receptor and Tanacetum kotschyi plant is rich in sesqui terpene lactones and flavonoids, etc., which have been reported to have antioxidant properties. Aim: The inhibitory effect of Tanastom Kotschyi extract and dextromethorphan on the incidence of morphine dependence in male mice. Methods: 81 mice in 9 groups of 9 in the weight range of 20-30 g were randomly selected and received the following drug regimens once a day for two weeks. Different doses of dextromethorphan and extract of Tanacetum kotschyi (T.K) or two drugs were injected into mice every day for half an hour before the daily injection of morphine, then on the fourteenth day, for two hours, after morphine injection in animals, naloxone (4 mg / kg, ip) was injected and withdrawal symptoms (number of jumps and standing on two legs) were measured within half an hour. The animals were then anesthetized and blood samples were taken from the heart to measure serum MDA and TAC levels (tests for oxidative stress biomarkers) in different groups. Results: injection of morphine (25 mg / kg, ip) once daily in animals for fourteen days caused dependence. Use of doses of dextromethorphan (15,30,60 mg / kg, ip) and extract of Tanacetum Kotschyi (25,50,100 mg /kg, ip) caused a significant reduction in the symptoms of animal dependence. In co-injection of dextromethorphan with Tanacetum Kotschyi extract compared to injection of Tanacetum alone, withdrawal symptoms were significant reduced. Different doses of Dextromethorphan and Tanacetum extract caused a significant decrease in MDA level. Conclusion: Based on these findings, Tanacetum extract and dextromethorphan extract improve the symptoms of morphine withdrawal dependence in mice. Probably part of these effects is due to the inhibition of oxidative stress