Abstract

BackgroundChemotherapy induced neuropathic pain is a very common adverse effect seen with cancer chemotherapeutic drugs. The activation of BK channels leads to reduced neuronal excitability and suggests its role in the clinical management of pain. The present study investigates the effect of non-selective BK channel activator, Cilostazol (CZ) against vincristine (VC) induced neuropathic pain in mice. MethodsNeuropathic pain was induced in the animals by a single vincristine administration (100 μg/kg, i.v) to all the group of animals. Mice were randomly divided into four groups comprising of a control, two test groups with Cilostazol (20 mg/kg & 40 mg/kg) and a standard group with Gabapentin (GBP, 100 mg/kg). Peripheral neuropathy in animals was verified by mechanical hyperalgesia and mechanical allodynia. Results and discussionControl group did not have any significant effect on mechanical hyperalgesia and mechanical allodynia. Results shows that Cilostazol at both tested dose levels of 5 days administration attenuated mechanical hyperalgesia and mechanical allodynia after the vincristine administration and were comparable with that of Gabapentin. ConclusionThe attenuating effect of Cilostazol in vincristine model suggests that pharmacological activation of BK channel may be potentially useful for managing neuropathic pain.

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