Preventive effects of Pentoxifylline and Pregabalin on neuropathic pain induced by Vincristine in mice

Abstract

Introduction: In the process of neuropathy induced by anticancer drugs, several mechanisms have been mentioned such as activation of the oxidative stress system, increasing the activity of NMDA receptors, and serotonin receptors. Neuropathic pain is a result of various mechanisms operating at the peripheral, spinal cord and supra-spinal levels, which cause alterations in the pain conduction pathway. This may also develop secondary to some other pathological conditions such as diabetes mellitus, cancer, herpes infection, autoimmune diseases and HIV infection etc. Goal: The aim of the current study was to evaluate the preventive effects of pentoxifylline and pregabalin on vincristine-induced neuropathic pain that was the result of vincristine in the (spurious) mice. Materials and methods: 81 male mice in a weight range of 25 to 35 grams were randomly divided into 9 equal groups and underwent pentoxifylline and pregabalin for 25 days. Different doses of pentoxifylline and pregabalin were injected three days before injection of vincristine (1 mg/kg,IP ) at 4th day. Then injection of pentoxifylline and pregabalin continued for 3 days. After that we have 3 days for rest. Finally we performed hot plate test. This 7 day cycle repeated 3 times for all groups. At day 25, blood samples were collected for MDA and TAC estimation. Result: The results showed a meaningful increase in reaction to the pain injection of these doses (25, 50, 100 mg/kg, IP) of pentoxifylline and pregabalin (5,10,20 mg/kg, IP) and also the meaningful impact of pentoxifylline in these doses (25, 50, 100 mg/kg, IP) can decrease MDA level. Also, injecting low doses of these two drugs together had a better effect than injecting these two drugs alone. Conclusion: It is probable that a part of the inhibitory effects of pentoxifylline is mediated by the control of oxidavtive stress. At the same time, we suggest further studies to obtain precise mechanisms.