The present study investigates the involvement of the l-arginine-Nitric Oxide-cGMP-K+ ATP pathways responsible for the action of anti-allodynic and antihyperalgesic activities of zerumbone in chronic constriction injury (CCI) induced neuropathic pain in mice. The role of l-arginine-NO-cGMP-K+ was assessed by the von Frey and the Randall-Selitto tests. Both allodynia and hyperalgesia assessments were carried out on the 14th day post CCI, 30 min after treatments were given for each respective pathway. Anti-allodynic and antihyperalgesic effects of zerumbone (10 mg/kg, i.p) were significantly reversed by the pre-treatment of l-arginine (10 mg/kg), 1H [1,2,4]Oxadiazole[4,3a]quinoxalin-1-one (ODQ), a soluble guanosyl cyclase blocker (2 mg/kg i.p.) and glibenclamide (ATP-sensitive potassium channel blocker) (10 mg/kg i.p.) (p < 0.05). Taken together, these results indicate that systemic administration of zerumbone produces significant anti-allodynic and antihyperalgesic activities in neuropathic pain in mice possibly due to involvement of the l-arginine-NO-cGMP-PKG-K+ ATP channel pathways in CCI model.
Traumatic brain injury (TBI) is one of the leading causes of death and morbidity worldwide especially in industrialized countries. 1 TBI has become a major public health concern with a global prevalence that has escalated to almost 27.08 million people in 2016 as reported by the Global Burden of Diseases, Injuries, and Risk Factors (GBD) study. 2 The study also stated that about 8.1 million people were living with long-term disability caused by TBI, mainly due to falls and motor vehicle accidents. Traumatic brain injury has also been alarmingly related to a number of adverse long-term effects, including elevated risk toward long-term complications such as Parkinson's disease, Alzheimer's disease, Dementia Pugilistica, and posttraumatic epilepsy. 3 TBI is comprised of two phases which are the primary and secondary injury phase. The primary injury phase is the initial impact encountered from the external mechanical force that results in blood vessel damage, axonal tearing, 4 cell death at the injury site, blood-brain barrier disruption, presence of edema, and generation of damage-associated molecular patterns (DAMPs). 5
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