动物造模,糖尿病神经痛大鼠 z-bio 2021-11-10 788

　　Objective: To observe the expression of phosphorylated calcineurin II (p-CaMKII) in the dorsal root ganglia (DRG) of rats with diabetic neuropathic pain (DNP) at different stages.

　　Method: 1) A DNP rat model was established by injecting a single high dose of streptozotocin (STZ) into 21 healthy male SD rats. After constructing the model (basic), 7 days (day 7) and 14 days (day 14), observe the model. ), 21d (21st day), 28d (28th day) thermal radiation stimulated paw withdrawal response time (pawwithdrawallatency, PWL) changes, and the rat L4-L6DRG was collected at each of the above time points, and immunofluorescence was used Check L4-. p-CaMKII positive cells are expressed in the upper part of L6DRG. (2) Twenty rats were randomly divided into normal saline + normal saline (control group + S) group, model + normal saline (DNP + S) group, model + CaMKII inhibitor KN93 group (DNP + KN93). 14 days after the injection of STZ, in the DNP + KN93 group, KN93 solution was injected into the soles of the feet, and the other two groups were injected with the same amount of NS.

　　Results: 1) Compared with the normal group, the D7PWL of rats in the DNP model group did not change significantly, and the PWL decreased significantly on the 14, 21 and 28 days. The immunofluorescence results showed that at 7, 14, 21, and 28 days after STZ injection, the expression of p-CaMKII positive cells in L4DRG of DNP rats increased significantly, while the expression of p-CaMKII positive cells in L5 was significantly higher than normal increase. The results showed that the expression of positive cells increased significantly. And L6DRG also rose sharply. (2) Before the intervention of KN93, there was no significant difference in PWL between the DNP + S group and the DNP + KN93 group. After 1 hour of intervention, the PWL of the DNP + KN93 group was compared with the DNP + S group.

　　Conclusion: The occurrence and maintenance of diabetic neuropathic pain is related to the up-regulation of p-CaMKII expression in DRG neurons, and injection of the CaMKII inhibitor KN93 into the dorsal of the foot can inhibit thermal hyperalgesia.