动物造模,糖尿病神经痛 z-bio 2022-01-10 601

　　Objective To observe the expression of phosphorylated calcineurin II (p-CaMK II) in the dorsal root ganglion (DRG) of diabetic neuropathic pain model rats at different stages.

　　Method 1) Twenty-one healthy male SD rats were injected with streptozotocin (STZ) at one time to establish a DNP rat model, and the DNP rat models were observed before modeling (Base), 7 days after modeling (Day 7), and 14 days after modeling. Changes of paw withdrawal latency (PWL) after thermal radiation stimulation on d(Day 14), 21 d(Day 21), and 28 d(Day 28); and the rats L4-L6 DRG were collected at the above time points , The expression of p-CaMKII positive cells on L4-L6 DRG was detected by immunofluorescence. (2) 20 rats were randomly divided into normal + normal saline (Control + NS) group, model + normal saline (DNP + NS) group, model + CaMKII inhibitor KN93 group (DNP + KN93); STZ injection for 14 days After treatment, the DNP+KN93 group was injected with KN93 solution on the dorsum of the foot, and the other two groups were injected with the same amount of NS.

　　Results 1) Compared with the normal group, the DNP model group had no significant change in D7 PWL, but the PWL on Day 14, Day 21, and Day 28 decreased significantly. The results of immunofluorescence showed that compared with the normal group, the expression of p-CaMKII positive cells on L4 DRG of DNP rats was significantly increased after 7, 14, 21, and 28 days of STZ injection, and the expression of p-CaMKII on L5 and L6 DRG was significantly increased. The expression of positive cells also increased significantly. (2) Before KN93 intervention, there was no significant difference in PWL between DNP+NS group and DNP+KN93 group.

　　Conclusions The generation and maintenance of diabetic neuropathic pain is related to the up-regulation of p-CaMK II expression in DRG neurons. Dorsal injection of CaMK II inhibitor KN93 can inhibit thermal hyperalgesia.