Protective mechanism of sevoflurane inhalation anesthesia on neurological function in rats with cerebral infarction
10.3760/cma.j.cn121382-20210309-00401
- VernacularTitle:七氟烷吸入麻醉后调节保护脑梗死大鼠神经功能的机制研究
- Author:
Chunlai SHI
1
Author Information
1. 河南新乡公立医院麻醉科 453002
- Keywords:
Sevoflurane;
Postconditioning;
Cerebral infarction;
Neurological function;
Inflammation
- From:
International Journal of Biomedical Engineering
2021;44(4):261-265,271
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the protective mechanism of sevoflurane inhalation anesthesia on neurological function in rats with cerebral infarction.Methods:Sixty SD rats were randomly and equally divided into the sham group, cerebral obstruction group, and sevoflurane post conditioning group (Sevo group). Rats in the cerebral obstruction group and Sevo group were underwent wire embolization to establish permanent focal cerebral ischemia rat model. Rats in the sham group were not treated with wire embolization. Rats in the Sevo group received sevoflurane at a volume fraction of 2.5% immediately after reperfusion and were maintained with oxygen for 30 min with 1 L/min oxygen flow. Rats in the sham and cerebral obstruction group received 30 min of continuous oxygen inhalation with 1 L/min oxygen flow. After 24 h, modified neurological deficit bisection (mNSS) was used to assess the neurological function of the rats in the three groups. After that, blood was taken and the rats were sacrificed, and their brain tissues were collected to determine the level of cerebral infarction volume, apoptosis rate, and the levels of serum inflammatory factors, including interleukin (IL)-6, IL-10, IL-1β and tumor necrosis factor-α (TNF-α), as well as malondialdehyde (MDA) levels, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities in brain tissue. Toll like receptor 4 (TLR4) and nuclear transcription factor κB (NF-κB) p65 protein expression levels in rat brain tissues were determined by Western blot analysis.Results:In the Sevo group, the mNSS score, cerebral infarct volume ratio, apoptosis rate, IL-6 level, IL-1β level, TNF-α level, MDA level as well as the expression levels of TLR4 and NF-κB p65 in the brain tissues were higher than those of the sham group (all P<0.05) and lower than those of the cerebral obstruction group (all P<0.05). In the Sevo group, IL-10 level as well as SOD and GSH-Px activities were lower than those of the sham group (all P<0.05) and higher than those of the cerebral obstruction group (all P<0.05). Conclusions:Sevoflurane has a certain protective effect on the brain tissue and neurological function of rats with cerebral infarction. This protective effect may be achieved by inhibiting the inflammatory response mediated by the TLR4/NF-κB signal channel, reducing the release of inflammatory factors, reducing inflammation and oxidative stress, and inhibiting cell apoptosis.
