钙蛋白酶1在瑞芬太尼诱发大鼠疼痛过敏中的作用

doi:10.3969/j.issn.2095-9400.2019.12.010

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Abstract Objective: To investigate the role of calpain 1 (CANP1) and its related signaling pathway in hyperalgesia induced by remifentanil in rats with incisional pain. Methods: Incisional pain model was established in SD rats qualified for tail vein and sheath tube. The control group, remifentanil group, remifentanil+U0126 group and remifentanil+Calpeptin group were established. Remifentanil induced model incision pain. Pretreatment with MEK kinase inhibitor U0126 inhibited MEK activity in the spinal cord. Calmodulin (CANP)-specific inhibitor Calpeptin pretreatment intervened with CANP activity in the spinal cord. Mechanical contraction threshold (MWT) and heat-shrinking latency (TWL) were measured 24 h before intravenous infusion of saline or remifentanil, 2, 6, 24, and 48 h after intravenous administration (T0-T4). The mechanical contraction threshold (MWT) and heat-shrinking latency (TWL) were measured at 24 h before intravenous administration and 2, 6, 24, 48 h after intravenous administration (T0-T4). The protein expression levels of ERK, Calpain1 and GSK-3β were detected by Western blot. Results: There was no significant change in MWT and TWL in the control group at T0-T4. The MWT of the rats in the remifentanil group gradually decreased, and the TWL gradually shortened. The difference in the time points between the two groups was statistically significant (P<0.01). Compared with the remifentanil group, both the remifentanil+U0126 group and the remifentanil+calpeptin group had higher MWT and TWL at each time point (P<0.05 or P<0.01). Compared with the control group, the expression of p-ERK protein and CANP1 large subunit hydrolyzed protein (Cleaved-CANP1) was significantly up-regulated in the remifentanil group (P<0.01). Compared with the remifentanil group, the expression of p-ERK protein was significantly down-regulated in the remifentanil+U0126 group (P<0.01), and there was no significant change in the remifentanil+Calpeptin group. Compared with the control group, the relative protein expressions of GSK-3β and pGSK-3β/GSK-3β in the remifentanil group were significantly increased (P<0.01). Compared with the remifentanil group, the relative protein expression levels of GSK-3β and pGSK-3β/GSK-3β were significantly decreased in the remifentanil+U0126 group and remifentanil+Calpeptin group (P<0.01). Conclusion: The pain allergic effect induced by remifentanil may be related to the activation of ERK/CANP1/GSK-3β signaling pathway.

Key words： remifentanil calpain 1 spinal cord hyperalgesia mechanism

Received: 16 May 2019

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	HUANG Yan
	ZHOU Nan

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https://xb.wmu.edu.cn/EN/10.3969/j.issn.2095-9400.2019.12.010 OR https://xb.wmu.edu.cn/EN/Y2019/V49/I12/905

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