Ghrelin may attenuate proinflammatory cytokine-mediated neuropathic pain.

Nerve damage that affects peripheral or central nerve systems leads to abnormal pain states referred to as neuropathic pain. The precise mechanisms in neuropathic pain are very complex, since they are thought to originate through multiple pathophysiological processes. There is quite evidence implicating the proinflammatory cytokines in the induction and facilitation of neuropathic pain. This pain syndrome is usually poorly controlled by available medications. Ghrelin, a peptide hormone predominantly secreted from the stomach, is an endogenous ligand to the growth hormone secretagogue receptor. Previous studies showed that ghrelin has potent anti-inflammatory effect; inhibiting proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta) and interleukin-6 (IL-6). Furthermore, there are recent studies which prove the interaction between ghrelin and the systems that play role in pain modulation. Therefore, we hypothesize that ghrelin might ameliorate neuropathic pain by diminishing the proinflammatory cytokines and also regulating pain system.