Abstract

Curcumin (diferuloylmethane) is a major component of turmeric, which is isolated from the rhizomes of Curcuma longa L. from the family Zingiberaceae. It is used as a dietary pigment for curry and in traditional Indian medicine for its anti-inflammatory and attenuating pain effects. This study aimed to evaluate the beneficial effects of curcumin in a rat model of diabetic neuropathic pain. Additionally, we investigated the involvement of the phosphorylated form of c-Jun N-terminal kinase (pJNK) located in the neurons and astrocytes of the dorsal root ganglion (DRG). To induce diabetic neuropathic pain in rats, 50 mg/kg of streptozotocin (STZ) was intraperitoneally injected. After 4 weeks, rats were administered the vehicle, 10 mg/kg/day curcumin, or 50 mg/kg/day curcumin orally for 4 consecutive weeks. One day after the final drug administration, we performed behavioral tests to measure responses of rats to mechanical, heat, cold, and acetone-induced cold stimuli. After behavioral tests, pJNK expression in the DRG was evaluated using western blot assay and immunohistochemistry. Curcumin treatment for 4 consecutive weeks in STZ-induced diabetic neuropathic pain rats improved behavioral responses to mechanical, cold, and thermal stimuli. Increased pJNK expression in the astrocytes and neurons of the DRG in STZ-induced diabetic neuropathic pain rats was reduced by curcumin treatment for 4 consecutive weeks. We suggest that curcumin can be an option for the treatment of diabetes-related neuropathic pain, and one of the mechanisms that underlie the action of curcumin may involve pJNK expression in the astrocytes and neurons of the DRG.

Highlights

  • Neuropathic pain is one of the most common complications of diabetes mellitus (DM) and an estimated one-third of patients with DM have painful diabetic neuropathy [1]

  • In the immunohistochemical analysis to determine dorsal root ganglion (DRG) cells that expressed phosphorylated form of c-Jun N-terminal kinase (pJNK), we found that pJNK was activated in the neurons and in the astrocytes of the DRG in STZ-induced diabetic neuropathic pain rats. e present study demonstrated that curcumin normalized pJNK expression in the astrocytes and neurons of the DRG in STZ-induced diabetic neuropathic pain rats. is suggests that curcumin administration decreases diabetic neuropathic pain responses by normalizing functional Jun N-terminal kinase (JNK) activation in DRG cells in STZ-induced diabetic neuropathic pain rats

  • We demonstrated the effect of curcumin in a rat model of diabetic pain induced by STZ

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Summary

Introduction

Neuropathic pain is one of the most common complications of diabetes mellitus (DM) and an estimated one-third of patients with DM have painful diabetic neuropathy [1]. It is characterized by hyperalgesia (increased sensitivity to pain), allodynia (pain sensation to nonpainful stimulation), dysesthesia (an unpleasant sense of touch), and paresthesia (abnormal sensation without a cause) and is caused by either peripheral nerve damage or changed neuronal signaling. Curcumin (diferuloylmethane) is a natural product from the Curcuma longa L. from the family Zingiberaceae. It is a member of the curcuminoid family and used as a dietary pigment in curry and an ancient medicine for many purposes including asthma, allergy, anorexia, coryza, cough, hepatic disease, and sinusitis. There are other analgesic mechanisms involved in curcumin such as activation of

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