关键词: 右美托咪定, 氧化应激, 腺苷酸活化蛋白激酶(AMPK)

Abstract: Objective To study the effect of dexmedetomidine (DEX) on TNF-α-induced injury of human neuroblastoma cell line SH-SY5Y and its mechanism. Methods CCK8 assay was used to detect cell activity and determine the optimal dose of DEX and TNF-α. The cells were divided into control group, model group, DEX intervention model group, and the intervention group of DEX plus compound C. Western blot was used to detect the expression of p-AMPK, SNHP, KIF5B, Drp1 and OPA1, and ELISA was used to detect the level of IL-1β and IL-6. Mitochondrial membrane potential (Δψm), respiratory chain complex enzyme activity (complex Ⅰ-Ⅳ), ATP, MDA, SOD, GSH, ROS were determined with commercially available kits. Results Compared with control group, level of p-AMPK,OPA1 and SNPH l in model group significantly decreased, while the level of Drp1 and KIF5B significantly increased (P＜0.01). The level of complex Ⅰ~Ⅳ, Δψm, ATP, GSH and SOD in DEX group significantly increased as compared with model group. The level of MDA, IL-1β and IL-6 significantly decreased(P＜0.01). Compared with DEX group, the level of Complex Ⅰ-Ⅳ, Δψm, ATP, GSH and SOD in DEX+CC group significantly decreased, while the level of MDA, IL-1β and IL-6 significantly increased(P＜0.01). Conclusions DEX improves mitochondrial function, alleviates oxidative stress and inflammatory response as well as TNF-α-induced cell damage with an AMPK dependent mechanism.

Key words: dexmedetomidine, oxidative stress, adenylate activates protein kinase (AMPK)