动物实验,糖尿病神经痛 z-bo 2020-09-14 406

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

　　Method: 1) A large dose of streptozotocin (STZ) was injected into 21 healthy male SD rats to establish a DNP rat model. Observe before model creation (basic), 7 days (7th day) and 14 days after model creation. The 14th day, the 21st day (the 21st day), the 28th day (the 28th day) heat radiation stimulated foot retraction response time (foot retraction waiting time, PWL) changes, and at each of the above time points, large Rats collect L4-L6DRG, and use the immunofluorescence expression of the upper p-CaMKII positive cells to detect L4-L6DRG.

　　(2) Randomly divide 20 rats into a physiological + normal saline (control group + S) group, a model + normal saline (DNP + S) group, and a model + CaMKII inhibitor KN93 group (DNP + KN93) group. 14 days after STZ injection, they were divided into DNP + KN93 group, KN93 solution was injected into the soles, and the other two groups were injected with the same amount of NS.

　　Results: 1) Compared with the normal group, the D7 PWL of the rats in the DNP model group did not change significantly, and the PWL of the 14th, 21st and 28th days were significantly reduced. Immunofluorescence results showed that, compared with the normal group, the expression of p-CaMKII positive cells on L4DRG of DNP rats increased significantly after STZ injection, while the expression of p-CaMKII positive cells on L5 and L6DRG increased significantly. The results showed that the expression of p-CaMKII positive cells increased. It also rose significantly.

　　(2) Before the intervention of KN93, there was no significant difference in PWL between the DNP + S group and the DNP + KN93 group, and after 1 hour of intervention, compared with the DNP + S group, the PWL of the DNP + KN93 group increased significantly .

　　Conclusion: The development and maintenance of diabetic neuropathic pain is related to the up-regulation of p-CaMKII expression in DRG neurons. Injection of the CaMKII inhibitor KN93 on the dorsal side of the foot can inhibit thermal pain hypersensitivity.