Effects of sevoflurane on microglial polarization after traumatic brain injury in rats
10.3760/cma.j.issn.0254-1416.2019.09.030
- VernacularTitle: 七氟醚对大鼠创伤性颅脑损伤时小胶质细胞极化的影响
- Author:
Guodong ZHANG
1
;
Laiguang SUN
;
Jiaqi ZHANG
;
Yuanchao LI
;
Zhenguo CHENG
Author Information
1. Department of Neurosurgery, Xinxiang Central Hospital, Xinxiang 453000, Henan Province, China
- Publication Type:Journal Article
- Keywords:
Anesthetics, inhalation;
Craniocerebral trauma;
Microglia;
Polarization
- From:
Chinese Journal of Anesthesiology
2019;39(9):1143-1146
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To evaluate the effects of sevoflurane on microglial polarization after traumatic brain injury (TBI) in rats.
Methods:Seventy-two healthy adult male Sprague-Dawley rats, weighing 230-250 g, were divided into 3 groups (n=24 each) using a random number table method: sham operation group (group Sham), group TBI, and TBI plus sevoflurane anesthesia group (group TBI+ Sevo). TBI models were established by using Feeney′s method in TBI and TBI+ Sevo groups, 30 min later 2.4% sevoflurane was inhaled for 1 h once a day for 3 consecutive days in TBI+ Sevo group, while pure oxygen was inhaled instead in Sham and TBI groups.At 1, 3, 7 and 14 days after establishing the model, 6 rats were selected, the neurological function was evaluated with the modified neurologic severity score (mNSS), and tail venous blood samples were taken for determination of tumor necrosis factor-a (TNF-α), interleukin-1beta (IL-1β) and IL-6 concentrations by enzyme-linked immunosorbent assay.The rats were then sacrificed, the limbic cortical tissues of brain contusion lesion were taken for determination of cell apoptosis (by TUNEL) and expression of microglial marker Iba-1, microglial M1 phenotypic marker CD86 and microglial M2 phenotypic marker CD206 (by Western blot).
Results:Compared with group Sham, the mNSS score, apoptosis rate of cortical cells, expression of Iba-1, CD86 and CD206, and concentrations of serum TNF-α, IL-1β and IL-6 were significantly increased in TBI and TBI+ Sevo groups (P<0.05). Compared with TBI group, the mNSS score, apoptosis rate of cortical cells, expression of Iba-1 and CD86 and concentrations of serum TNF-α, IL-1β and IL-6 were significantly decreased, and the expression of CD206 was up-regulated in TBI+ Sevo group (P<0.05).
Conclusion:The mechanism by which sevoflurane anesthesia reduces TBI may be related to promoting microglial polarization and inhibiting systemic inflammatory response in rats.
