Abstract
Neuropathic pain is caused by the peripheral or central nervous system structure damage or dysfunction. VEGF is involved in nociception and inflammation. VEGF may target VEGF receptor-2 (VEGFR-2) on the surface of neurons. P2X(2/3) receptors play a crucial role in facilitating pain transmission at the spinal sites. Chronic constriction injury (CCI) rats were used as neuropathic pain model. Sprague-Dawley male rats were randomly divided into sham group, anti-recombinant VEGF antibody group with phosphate-buffer saline (anti-rVEGF+PBS group), CCI rats treated with phosphate-buffer saline group (CCI+PBS group) and CCI rats treated with anti-recombinant VEGF antibody group (CCI+anti-rVEGF group). The expressions of VEGFR-2, P2X(2) and P2X(3) protein in spinal dorsal horn (SDH) were detected by immunohistochemistry, double-label immunofluorescence and western blotting. The protein levels of VEGFR-2, P2X(2) and P2X(3) in L4/5 SDH of CCI+PBS group were higher than those in sham group. VEGFR-2 and P2X(2) or P2X(3) receptors were co-expressed in the cytoplasm and surface membranes of SDH. Anti-rVEGF treatment in CCI rats reduced the expression of VEGFR-2 and P2X(2/3) receptors in L4/5 SDH compared with those in CCI+PBS group. Therefore, VEGF may activate VEGFR-2 to participate the process of neuropathic pain. Anti-rVEGF treatment in CCI rats reduced the expression of VEGFR-2 and inhibited the transmission of neuropathic pain in L4/5 SDH via decreasing the expression of P2X(2/3). There is a cross-potentiation between VEGFR-2 and P2X(2/3) receptors in neuropathic pain state.
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