Document Type : Research articles
Authors
Department of Anesthesiology, Second Hospital of Jilin University, Changchun, China
Abstract
Background: 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).
Objectives: This study aimed to discusses the effects of dexmedetomidine on oxidative stress response and ICAM-1 and S100B expression in patients with TBI to investigate its protective effect on oxidative stress and brain damage in patients with TBI.
Methods: The TBI patients treated in our hospital from May 2017 to April 2020 were enrolled in the study and divided into control and treatment groups by the random number table method. The treatment group was administered with dexmedetomidine injection via an intravenous pump based on the conventional treatment in the control group. Glasgow coma scale (GCS) and Glasgow outcome scale (GOS) were used to evaluate the patients injury, recovery, and prognosis. ELISA method was employed to detect four 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 upon admission and at different time points after the operation.
Results: On the 3rd and 14th day after the operation, the treatment group had a higher GCS score, compared to the control group (P<0.05). Furthermore, on the 30th, 90th, and 180th days after discharge, the treatment group had a higher GOS score than the control group (P<0.05). On the 3rd, 5th, and 14th days after operation, the treatment group had higher SOD activity than the control group (P<0.05). Immediately after the operation, on the 3rd, 5th, and 14th after the operation, the treatment group had higher LPO levels than the control group (P<0.05). Moreover, on the 3rd, 5th, and 14th days after the operation, blood MDA levels gradually decreased in both groups, which was lower in the treatment group than that in the control group (P<0.05). On the 3rd, 5th, and 14th after the operation, the treatment group had higher TAC activity in the blood, compared to that in the control group (P<0.05). On the 3rd, 5th, and 14th days after the operation, the treatment group had lower S100B levels than that in 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.
Keywords
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