右美托咪定对脑缺血再灌注损伤小鼠糖萼的影响

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Abstract Objective To investigate the effect of Dexmedetomidine on glycocalyx in mice with cerebral ischemia-reperfusion injury. Methods Forty-five C57BL6/J male adult mice were randomly divided into sham operation group, normal saline group and Dexmedetomidine group, with 15 mice in each group. In sham operation group, only the skin of the right neck was cut and the right common carotid artery was exposed. In Dexmedetomidine group, 40 μg/kg Dexmedetomidine was injected intraperitoneally 30 minutes before the establishment of the model. The mice in normal saline group were injected with equal volume of normal saline 30 minutes before modeling, and then acute cerebral ischemia-reperfusion injury model was established 24 hours after 60 minutes of ischemia-reperfusion. The percentage of infarct volume was calculated by TTC staining, the expression of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were detected by enzyme-linked immunosorbent assay (ELISA), and the expression of oxidative stress-related proteins (malondialdehyde [MDA], superoxide dismutase [SOD]) were detected by ELISA. Results Compared with normal saline group, the infarct volume and neurological deficit score of Dexmedetomidine group were significantly reduced, the differences were statistically significant (P < 0.05). Compared with normal saline group, the activity time and distance of Dexmedetomidine group were significantly lengthened, the differences were statistically significant (P < 0.05 or P < 0.01). Compared with normal saline group, the levels of HPSE/β-actin, TNF-α/β-actin and NF-κB/β-actin in Dexmedetomidine group were significantly decreased, and the levels of SDC-1/β-actin and Tie-2/β-actin in Dexmedetomidine group were significantly increased, the differences were highly statistically significant (P < 0.01). Compared with normal saline group, the levels of TNF-α and IL-6 in Dexmedetomidine group were significantly reduced, the differences were highly statistically significant (P < 0.01). Compared with normal saline group, MDA level of Dexmedetomidine group was significantly decreased, and SOD level of Dexmedetomidine group was significantly increased, the differences were highly statistically significant (P < 0.01). Conclusion Dexmedetomidine can protect glycocalyx from cerebral ischemia-reperfusion injury, reduce inflammation and stress response.

Key words： Dexmedetomidine Cerebral ischemia-reperfusion injury Glycocalyx Inflammatory factors Oxidative stress

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	MA Haibo1 YANG Yingchun2 LIU Jingjing3 MU Dongliang4 XIA Rui5▲

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MA Haibo1 YANG Yingchun2 LIU Jingjing3 MU Dongliang4 XIA Rui5▲. Effect of Dexmedetomidine on glycocalyx in mice with cerebral ischemia-reperfusion injury[J]. 中国医药导报, 2020, 17(13): 8-12,26.

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http://www.yiyaodaobao.com.cn/EN/ OR http://www.yiyaodaobao.com.cn/EN/Y2020/V17/I13/8

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