Blockade of central vascular endothelial growth factor-A pathway attenuates inflammatory orofacial pain in rats
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The present study investigated the role of the vascular endothelial growth factor (VEGF)-A pathway in inflammatory pain transmission in the orofacial region of rats. Complete Freund’s adjuvant (CFA; 40 μL) or formalin (5%; 50 μL) was administered subcutaneously in the vibrissa pad of male Sprague-Dawley rats (weight: 230–280 g) to induce inflammatory pain. The findings showed that subcutaneous injection of CFA increased thermal hypersensitivity 1 day after injection, while administration of formalin produced a biphasic nociceptive behavioral response. Furthermore, subcutaneous pretreatment with VEGF-A164 antibody did not affect head withdrawal latency time in either treatment group. In contrast, intracisternal injection of VEGF-A164 antibody (1, 5 μg) significantly suppressed thermal hypersensitivity in the CFA group and the number of scratches observed in the second phase in the formalin group. Furthermore, intracisternal administration of VEGF-A type 1 (100 μg) and VEGF-A type 2 (20 μg) receptor inhibitors resulted in attenuation of the number of scratches observed in the second phase in the formalin group. These results suggest that blockade of the central VEGF-A pathway can serve as a potential therapeutic approach for the onset of inflammatory pain in the orofacial region.
Abstract
The present study investigated the role of the vascular endothelial growth factor (VEGF)-A pathway in inflammatory pain transmission in the orofacial region of rats. Complete Freund’s adjuvant (CFA; 40 μL) or formalin (5%; 50 μL) was administered subcutaneously in the vibrissa pad of male Sprague-Dawley rats (weight: 230–280 g) to induce inflammatory pain. The findings showed that subcutaneous injection of CFA increased thermal hypersensitivity 1 day after injection, while administration of formalin produced a biphasic nociceptive behavioral response. Furthermore, subcutaneous pretreatment with VEGF-A164 antibody did not affect head withdrawal latency time in either treatment group. In contrast, intracisternal injection of VEGF-A164 antibody (1, 5 μg) significantly suppressed thermal hypersensitivity in the CFA group and the number of scratches observed in the second phase in the formalin group. Furthermore, intracisternal administration of VEGF-A type 1 (100 μg) and VEGF-A type 2 (20 μg) receptor inhibitors resulted in attenuation of the number of scratches observed in the second phase in the formalin group. These results suggest that blockade of the central VEGF-A pathway can serve as a potential therapeutic approach for the onset of inflammatory pain in the orofacial region.
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