Figure 1

The specific CXCR4 antagonist, AMD3100, reversed neuropathic pain in type II diabetic mice. A. Experimental animals: (1) wild type (wt) mice on Regular Diet (RD) injected with saline (n = 8), (2) wt on RD injected with CXCR4 antagonist, AMD3100 (n = 8), (3) Diabetic wt mice on High Fat Diet (HFD) injected with saline (n = 8); (4) Diabetic wt on HFD injected with AMD3100 (n = 8). Pain behavior was assessed using Von Frey test prior (0), 2hrs (2) and 24 hrs (24) after antagonist or saline injection. In diabetic wt mice on HFD (3) prior to antagonist injection the withdrawal threshold was significantly reduced compared with wt on RD (1) demonstrating neuropathic pain in HFD induced diabetes. Following CXCR4 antagonist injection in wt HFD (4) at 2hrs after injection (2) paw withdrawal threshold increases significantly demonstrating that blocking CXCR4 receptors reversed neuropathic pain in HFD induced diabetic mice. At 24hrs (24) this effect was absent. Wt mice on HFD injected with saline (3) did not show any change. B. Experimental animal: (5) Control db-db heterozygous (db het) mice injected with AMD3100 (n = 6), (6) Diabetic db-db homozygous (db/db) mice injected with saline (n = 8) (7) Diabetic db/db mice injected with AMD3100 (n = 8). In diabetic db/db mice (6) prior to antagonist injection the withdrawal threshold was significantly reduced compared with control db het mice, demonstrating neuropathic pain in the db/db model of type II diabetes. Following CXCR4 antagonist injection in diabetic db/db mice (7) at 2hrs after injection (2) paw withdrawal threshold increases significantly, demonstrating that blocking CXCR4 receptor reverse neuropathic pain in db-db model of type II diabetes. Db het control mice injected with AMD3100 (5) did not show any change. Values are expressed as mean+/− S.E. (p < 0.001).