摘要
目的颅脑创伤后炎症因子的表达及脑水肿均是导致病情恶化的主要因素,酒后颅脑创伤较单纯颅脑创伤更难救治。文中旨在探讨乙醇大鼠颅脑创伤后炎症因子(TNF-α、IL-6)以及脑组织水通道蛋白-4(APQ-4)的表达。方法选取成年雄性SD大鼠48只,随机分为对照组(予以3%水合氯醛30 mg/kg腹腔注射,高处落下打击垫片,建立颅脑创伤模型)、醉酒组(打击前予以乙醇3 g/kg灌胃,随后建立颅脑创伤模型),每组24只。大鼠造模成功后,分别于1、3、5 d行改良神经功能评分(m NSS)比较,Western blot检测6、24、72h TNF-α、IL-6及APQ-4蛋白的表达,RT-PCR检测TNF-α、IL-6及APQ-4 mRNA水平。结果对照组1、3、5d m NSS评分[(7.17±1.72、4.83±1.47、3.83±0.75)分]均明显低于醉酒组[(9.00±0.63、7.00±1.10、5.50±1.05)分],差异有统计学意义(P<0.05)。6 h,醉酒组TNF-α、IL-6、APQ-4表达(0.257±0.008、0.320±0.016、0.212±0.015)较对照组(0.068±0.008、0.102±0.013、0.054±0.007)明显升高(P<0.001),24、72 h时亦升高(P<0.001)。结论醉酒加重颅脑创伤过程中炎症反应、脑水肿发生,进而进一步加重继发性脑损伤。
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-a and IL-6 and the aquaporin-4 （AQP-4） protein in rats af- ter 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 garage 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 AQP-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-oL （ 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） /rod 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.
出处
《医学研究生学报》
CAS
北大核心
2018年第2期142-145,共4页
Journal of Medical Postgraduates
基金
四川省教育厅重点项目(12ZA075)
