In this study, forty rats were divided randomly into the incision surgery (n= 32) and sham surgery (n= 8) groups

In this study, forty rats were divided randomly into the incision surgery (n= 32) and sham surgery (n= 8) groups. surgery group received anesthesia, but not an incision. Von Frey test results showed that, compared with the sham surgery group, incision surgery decreased the withdrawal threshold of rats at 0.5, 3, 6 and 24 hours after incision. Immunofluorescence staining in the dorsal root ganglia of the spinal cord (L35) showed that interleukin-10 and brain-derived neurotrophic factor were expressed mainly on small- and medium-sized neurons (diameter < 20 m and 2040 m) and satellite cells in the dorsal root ganglia of the spinal cord (L35) in the sham surgery group. By contrast, in the surgery group, high expression of Peramivir trihydrate interleukin-10 and brain-derived neurotrophic factor appeared in large-sized neurons (diameter > 40 Peramivir trihydrate m) at 6 and 24 hours after incision surgery, which corresponded to the decreased mechanical withdrawal threshold of rats in the surgery group. These experimental findings suggest that expression pattern shift of interleukin-10 and brain-derived neurotrophic factor induced by incision surgery in dorsal root ganglia of rats was closely involved in lowering the threshold to mechanical stimulus in the hind paw following incision surgery. Pain-related mediators induced by incision surgery in dorsal root ganglia of rats possibly underlie mechanical nociception in ipsilateral hind paws. == INTRODUCTION == Postoperative incision pain is a unique form of acute pain, which is obviously different from antigen-induced inflammatory pain, neuropathic pain and cancer-induced pain[1,2,3,4,5,6,7,8,9]. Postoperative incision pain includes evoked and non-evoked pain. Non-evoked pain is short lasting, moderate and ongoing pain at rest in patients. Evoked pain is severe, long lasting, and movement-related pain, which is usually induced by coughing, mobilization and ambulation[1]. Previous studies showed Rabbit Polyclonal to IRF-3 (phospho-Ser385) that incision surgery induced obvious changes at many parts in the nervous system[10,11,12,13]. Some scholars found that response threshold of primary afferent fibers to mechanical and thermal stimulus decreased after incision of the hind paw[1,14,15,16,17,18,19]. By contrast, Peramivir trihydrate the response magnitude to suprathreshold stimuli, and spontaneous activity receptive field size increased[1,14,15,16,17,18,19]. In the spinal cord, hind paw surgical incision dramatically up-regulated the expression of brain-derived neurotrophic factor (BDNF)[20] and extracellular signal-regulated kinase 1/2[21], and induced activation of glial cells[22,23]. Recently, Pogatzki-Zahnet al[24] detected changes in human brains after incision of the right forearm using functional MRI analysis. They found that incision increased activity of the somatosensory cortex, frontal cortex and limbic system. This evidence suggests that incision pain is a symptom involved in highly complex neural circuitries. However, the mechanism underlying incision pain is still unclear[25,26,27]. In addition, analgesics including anti-inflammatory agents[28,29,30], N-methyl-D-aspartate (NMDA) receptor antagonists[31,32,33], spinal non-NMDA receptor antagonists[31,34] and ionotropic purine receptor antagonists[35] exhibited poor treatment efficacy for incision-induced pain[36,37]. Even after ample pain treatment with these drugs and improved analgesic techniques, about 5070% of patients experienced moderate to severe postoperative incision pain[36,37]. Thus, further investigation into postoperative incision pain is necessary. Pain-related mediators play important roles in the pain process[11,38,39,40]. These mediators include cytokines and chemokines [e.g., CXCL5, interleukin-10 (IL-10)][41,42,43], growth factors (e.g., BDNF, nerve growth factor)[44,45,46], purines/ATP (e.g., ATP)[47], protons (e.g., H+)[48], neuropeptides and peptide hormones (e.g., neurokinin-1, substance P)[49,50], metalloproteinases (e.g., MMP9)[51], and lipid mediators (e.g., prostanoids)[52,53]. Previous studies showed that BDNF was closely involved in all types of pain, including incision pain, inflammatory pain, and neuropathic pain[54,55,56]. For example, Liet al[22] found that hind paw incision increased BDNF expression in the ipsilateral lumbar dorsal root ganglia and spinal cord. And intrathecal injection of BDNF antibody significantly inhibited the mechanical allodynia induced by incision. In visceral pain induced by intraperitoneal injection of acetic acid into Sprague-Dawley rats, pretreatment with anti-BDNF antibody obviously exacerbated the nocifensive response in males, but Peramivir trihydrate attenuated it in females[40]. IL-10 is also an important modulator of neuropathic and inflammatory pain[38,57,58]..