Drunkenness increases the expressions of inflammatory factors and brain edema after traumatic brain injury in rats
10.16571/j.cnki.1008-8199.2018.02.006
- VernacularTitle:乙醇对大鼠颅脑创伤后炎症因子以及水通道蛋白-4的表达影响
- Author:
Ye ZHANG
1
;
Xiao-Mei ZHENG
;
Ji-Min HE
;
Hao HUANG
;
Xue-Liang LIU
;
Bin XU
;
Chong ZHOU
;
Li-Gang CHEN
;
Yong JIANG
;
Liang LIU
Author Information
1. 西南医科大学附属医院神经外科
- Keywords:
traumatic brain injury;
inflammation factor;
ethanol;
tumor necrosis factor;
interleukin-6;
aquaporin-4
- From:
Journal of Medical Postgraduates
2018;31(2):142-145
- CountryChina
- Language:Chinese
-
Abstract:
Objective The expressions of inflammatory factors and brain edema after traumatic brain injury (TBI) are the main factors for deterioration of the condition.TBI after drunkenness is even more difficult to be managed than simple TBI.This study was to discuss the effects of drunkenness on the inflammatory factors TNF-o and IL-6 and the aquaporin-4 (AQP-4) protein in rats after TBI.Methods Forty-eight male adult SD rats were randomly divided into a TBI and an ethanol (ETH) pretreatment group.TBI was induced using the Feeney's method after intraperitoneal injection of 3％ chloral hydrate at 30 mg/kg (the TBI group) or following gavage of ETH (the ETH group).At 1,3 and 5 days after modeling,modified neurological function scores (mNSS) were obtained,the expressions of TNF-α,IL-6 and AQP-4 protein determined by Western blot,and the levels of TNF-α.IL-6 and AOP-4 mRNA measured by RT-PCR at 6,24 and 72 hours.Results Compared with the TBI group,the ETH group showed significantly decreased mNSS at 1 day (9.00±0.63 vs 7.17±1.72,P＜0.05),3 days (7.00±1.10 vs 4.83±1.47,P＜0.05) and 5 days after modeling (5.50±1.05 vs 3.83± 0.75,P＜ 0.05),but remarkably up-regulated expressions of TNF-α (0.068± 0.008 vs 0.257 ± 0.008,P＜ 0.01),IL-6 (0.102 ±0.013 vs 0.320±0.016,P＜0.01) and APQ4 (0.054±0.007 vs 0.212±0.015,P＜0.01) at 6 hours,as well as at 24 and 72 hours (P＜0.01).Conclusion Drunkenness may increase the expressions of inflammatory factors and brain edema after traumatic brain injury and consequently aggravate secondary brain injury.
