RESUMO
AIM:ToexplorewhetherMCP-1-JAK2/STAT3signaltransductioninthespinaldorsalhornin-volves the formation and development of rat type 2 diabetic neuropathic pain (DNP).METHODS: The male Sprague-Dawley rats were fed with a high-fat and fructose diet for 8 weeks,and then received a single intraperitoneal streptozocin in-jection to prepare the type 2 DNP model.The type 2 DNP rats were randomly divided into 4 groups (n=16):DNP group, MCP-1 neutralizing (DM) group, DNP+AG490 (DA) group and solvent control (SC) group.A catheter of PE-10 was placed into the subarachnoid space of the rats in groups DM , DA and SC.After 3 d, the rats in DM,DA and SC groups were injected with MCP-1 inhibitor 10μL at 0.1 mg/L, AG490 10μL at 1 mmol/L and DMSO 10μL at 3.5%once a day for 14 days, respectively.Another 16 normal rats were selected as control (C) group and were fed with common forage. The mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) were measured at 1, 3, 7 and 14 d after subarachnoid injection .The lumbar segments 4-6 of the spinal cord were removed at the same time for determination of the expressions of p-JAK2 and p-STAT3 by Western blot .RESULTS:Compared with C group , MWT was significantly de-creased, TWL was shortened and the expression of p-JAK2 and p-STAT3 in the spinal dorsal horn was up-regulated at 1, 3, 7 and 14 d in DNP and SC groups (P0.05).CONCLUSION:The MCP-1-JAK2/STAT3 signal transduction in the spinal dorsal horn involves the formation and development of DNP in rats .