Open AccessEffect of dexmedetomidine on oxidative stress response and expression of intracellular adhesion factor-1 (ICAM-1) and S100B in patients
Author(s) -
Mingxin Ji,
Peng Zhao,
Cui Y,
Xinyu Li
Publication year - 2021
Language(s) - English
DOI - 10.32592/ircmj.2021.23.10.270
Subject(s) - malondialdehyde , dexmedetomidine , medicine , oxidative stress , lipid peroxidation , superoxide dismutase , glasgow coma scale , anesthesia , neuroprotection , pharmacology , gastroenterology , sedation
[Abstract] Objective: To study the effect of dexmedetomidine on oxidative stress response and the expression of intracellular adhesion factor-1 (ICAM-1) and S100B in patients with traumatic brain injury (TBI). Method: TBI patients treated in our hospital from May 2017 to April 2019 were enrolled in the study and divided into control group and treatment group by random number table method. The treatment group was administered with dexmedetomidine injection via intravenous pump on the basis of conventional treatment in the control group. Glasgow coma scale (GCS) and Glasgow outcome scale (GOS) were used to evaluate patients’ injury, recovery and prognosis. ELISA method was taken to detect 4 oxidative stress index levels including serum superoxide dismutase (SOD), lipid peroxidation (LPO), malondialdehyde (MDA) and total antioxidant capacity (TAC), as well as ICAM-1 and S100B levels at admission and at different time points after operation. Results: At 3d and 14 d after operation, the treatment group had higher GCS score than the control group (P<0.05).At 30 d, 90 d and 180 d after discharge, the treatment group had higher GOS score than the control group (P<0.05). At 3d, 5d, and 14d after operation, the treatment group had higher SOD activity than the control group (P<0.05). Immediately after operation, at 3d, 5d, and 14d after operation, the treatment group had higher LPO level than the control group (P<0.05); at 3d, 5d, and 14d after operation, blood MDA level gradually decreased in both groups, which was lower in the treatment group than in the control group (P<0.05); at 3d, 5d and 14d after operation, the treatment group had higher TAC activity in the blood than the control group (P<0.05). At 3d, 5d and 14d after operation, the treatment group had lower S100B level than the control group (P<0.05). Conclusion: Dexmedetomidine can relieve TBI-induced oxidative stress state and reduce the levels of brain injury markers (ICAM-1, S100B), which has a protective effect on the brain tissue with TBI.