Abstract：Objective To observe the analgesic effect of intraperitoneal injection of Dexmedetomidine on central pain (CPSP) after stroke in rats through TLR4/NF-κB signaling pathway. Methods Thirty SD rats were selected randomly from 90 SD rats for sham operation group, and the remaining 60 rats were modeled by injecting type Ⅳ collagenase into ventralis posterolateral nucleus (VPL). The thermal withdrawal latency (TWL) was measured three days after modeling. The rats with reduced TWL were divided into model group and intervention group by random number table method, with 30 rats in each group. The intervention group was intraperitoneal injected Dexmedetomidine 50 μg/kg for seven consecutive days and the model group was injected with the same amount of narmal saline. TWL values of rats were measured one day before modeling (T0), 10 d after modeling (T1), 17 d after modeling (T2), and 31 d after modeling (T3). Western blot was used to detect protein expression in VPL at T3. The changes of VPL microglia and neurons were observed by immunofluorescence. The release of inflammatory mediators in VPL was detected by enzyme-linked immunosorbent assay. Results In model group and intervention group, TWL at T1-T3 was lower than T0, TWL at T2-T3 was lower than T1, and TWL at T3 was lower than T2 (P ＜ 0.05). The TWL at T1-T3 in the model group was lower than that in the sham operation group, and the TWL at T1-T3 in the intervention group was higher than that in the sham operation group (P ＜ 0.05). Compared with sham operation group, the expression of TLR4 and pNF-κB in VPL of model group was significantly increased (P ＜ 0.05). Compared with model group, the expression of TLR4 and pNF-κB in VPL of intervention group was decreased (P ＜ 0.05). There was no significant difference in NF-κB expression in VPL among the three groups (P ＞ 0.05). Compared with sham operation group, the number of VPL neurons in model group decreased (P ＜ 0.05); compared with model group, there was no significant difference in the number of VPL neurons in the intervention group (P ＞ 0.05). The levels of IbA-1, tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6 in VPL of model group were increased compared with that of sham operation group (P ＜ 0.05), while the levels of IBA-1 and inflammatory factors TNF-α, IL-1β, and IL-6 in VPL of intervention group were decreased compared with that in model group (P ＜ 0.05). Conclusion Dexmedetomidine treat the CPSP may inhibit the proliferation and activation of microglial cells and the progression of neuroinflammation through the TLR4/NF-κB signaling pathway.
黄鼎力 邹宛芸 张英 刘庆. 基于TLR4/NF-κB信号通路研究右美托咪定对脑卒中后中枢痛大鼠的镇痛机制[J]. 中国医药导报, 2022, 19(22): 30-33,38.
HUANG Dingli ZOU Wanyun ZHANG Ying LIU Qing. Based on TLR4/NF-κB signaling pathway study the pain mechanism of Dexmedetomidine on central pain in rats after stroke. 中国医药导报, 2022, 19(22): 30-33,38.
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