Abstract
BackgroundPeripheral nerve injury results in chronic neuropathic pain characterized by allodynia and/or spontaneous pain. It has been suggested that activation of mitogen-activated protein kinases such as extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) contribute to the neuropathic pain. ObjectivesWe investigated if curcumin could prevent the development of neuropathic pain in rats with chronic constriction injury (CCI) of the sciatic nerve. MethodsThe animals were divided into 3 groups. In the curcumin treatment group (n = 10), curcumin (50 mg/kg/d PO) was administered once daily from 1 day before CCI to 7 days after CCI. The rats in the sham group (n = 10) and CCI group (n = 10) received a control vehicle. The mechanical allodynia was assessed using von Frey at 1, 3, 5, and 7 days after nerve injury. Western blots were used to evaluate the levels of p-ERK, p-JNK, and phosphorylation of NR1 (p-NR1) subunits of N-methyl-D-aspartate in the spinal dorsal root ganglion. ResultsIn the CCI group, mechanical allodynia was observed during 7 days after nerve injury. However, curcumin treatment reversed the mechanical allodynia 7 days after nerve ligation. There were no differences in the expression of p-ERK, p-JNK, and p-NR1 between the sham and curcumin groups. However, the expression of p-ERK, p-JNK, and p-NR1 in the CCI group were higher than the sham group and curcumin group, respectively (P < 0.05). ConclusionsTreatment with curcumin during the early stages of peripheral neuropathy can prevent the development of chronic neuropathic pain.
Highlights
Peripheral nerve injury often results in chronic neuropathic pain that is characterized by allodynia and/or spontaneous pain
The expression of phosphorylated extracellular signal-regulated kinase (ERK) (p-ERK) in the spinal dorsal ganglion (DRG) has been implicated in the induction of neuropathic pain behavior in rat models of chronic constriction injury (CCI) and its normalization after decompression of CCI reflects the reversal of the pain behaviors.[5]
In the CCI group, this mechanical allodynia was observed during the 7 days following nerve injury
Summary
Peripheral nerve injury often results in chronic neuropathic pain that is characterized by allodynia and/or spontaneous pain. Peripheral nerve injury results in chronic neuropathic pain characterized by allodynia and/ or spontaneous pain. It has been suggested that activation of mitogen-activated protein kinases such as extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) contribute to the neuropathic pain. Objectives: We investigated if curcumin could prevent the development of neuropathic pain in rats with chronic constriction injury (CCI) of the sciatic nerve. Results: In the CCI group, mechanical allodynia was observed during 7 days after nerve injury. There were no differences in the expression of p-ERK, p-JNK, and p-NR1 between the sham and curcumin groups. Conclusions: Treatment with curcumin during the early stages of peripheral neuropathy can prevent the development of chronic neuropathic pain
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