摘要
目的探讨莱菔硫烷协同氯化锂对创伤性脑损伤大鼠神经保护作用。方法参照feeney法自由落体致伤法制作创伤性脑损伤模型,大鼠分为对照组、模型组、SFN组及协同组,每组各15只,对照组不进行撞击实验,SFN组术后每日给予莱菔硫烷腹腔注射,协同组给予莱菔硫烷与氯化锂腹腔注射,模型组每日腹腔注射等量生理盐水,比较术后1 d、3 d、5 d、7 d各组大鼠神经功能缺失程度评分(m NSS)及术后7 d各组大鼠脑组织含水量、脑组织HE染色结果以及脑组织中SOD活性、IL-6、TNF-α、MDA水平。结果模型组、SFN组、协同组与对照组比较,各时间点m NSS评分均显著升高(P<0.05);术后5 d、术后7 d,SFN组及协同组大鼠m NSS评分显著低于模型组(P<0.05),且协同组m NSS评分显著低于SFN组(P<0.05);术后7 d,对照组大鼠脑组织含水量为(69.29±2.06)%,模型组为(75.40±1.73)%,SFN组为(73.08±1.06)%,协同组为(71.27±1.52)%。各组大鼠脑组织HE染色结果显示,SFN组及协同组其神经细胞的损伤较模型组明显减轻,细胞坏死有所减少,且以协同组神经细胞损伤减轻最为显著。模型组、SFN组、协同组与对照组比较,SOD活性显著下降(P<0.05),IL-6、TNF-α、MDA水平显著上升(P<0.05);SFN、协同组与模型组比较,SOD活性显著上升(P<0.05),IL-6、TNF-α、MDA水平显著下降(P<0.05),且协同组IL-6、TNF-α水平显著低于SFN组(P<0.05)。结论莱菔硫烷协同氯化锂对创伤性脑损伤大鼠具有显著的神经保护作用,其作用机制可能与减轻大鼠脑水肿、神经细胞损伤、抑制氧化应激以及炎症因子的释放有关。
Objective To investigate the effect of sulforaphane synergistic with lithium chloride on neuroprotective of rats with traumatic brain injury. Methods According to feeney method free fall production models of traumatic brain injury induced injury models, and rats were divided into control group, model group, SFN group and collaborative group, each group 15 rats, control group without impact experiment, after operation the SFN group received daily intraperitoneal injection of sulforaphane, collaborative group were given sulforaphane and chloride lithium intraperitoneal injection, the model group received daily intraperitoneal injection of saline, the degree of nerve function impairment score （mNSS） in rats of each group postoperative 1 d, 3 d, 5 d and 7 d, and brain tissue of rats, the water content of brain tissue, HE staining of brain tissue and activity of SOD, IL-6, TNF-alpha, the level of MDA in each group postoperative 7 d were compared. Results Compared with the control group, mNSS scores in the model group, SFN group, collaborative group at each time point were significantly increased （P〈0.05）; After 5 d, 7 d of operation, synergy scores in SFN group and mNSS group rats were significantly lower than those in the model group （P〈0.05）, and mNSS score in collaborative group was significantly lower than that of SFN group（P〈0.05）; After 7 d of operation, the brain tissue water content in control group of rats was （69.29±2.06）%, the model group was（75.40±1.73）%, SFN group was （73.08±1.06）%, collaborative group was （71.27±1.52）%; Brain tissue HE staining results showed that the nerve cell injury of rats in SFN group and cooperative group was obviously alleviated than those in the model group, necrotic cells decreased, and the collaborative group relieve neuronal injury was the most remarkable; The SOD in model group, SFN group, collaborative group decreased significantly compared with the control group （P〈0.05）, IL-6, TNF-alpha, MDA levels increased significantly（P〈0.05）;The activity of SOD in SFN group and collaborative group increased significantlynbsp;compared with the model group（P〈0.05）, IL-6, TNF-alpha, MDA levels decreased significantly （P〈0.05）, and collaborative TNF-alpha and IL-6 levels were significantly lower than that of SFN group （P〈0.05）. Conclusion Sulforaphane in combination with lithium chloride have remarkable neuroprotection on traumatic brain injury in rats, its mechanism may be related with the reduction of brain edema in rats, nerve cell damage, inhibition of oxidative stress and related to the release of inflammatory factors.
出处
《中国现代医生》
2015年第19期26-29,32,共5页
China Modern Doctor
基金
浙江省温州市科学技术第二期科技计划项目(Y20140360)
关键词
莱菔硫烷
氯化锂
创伤性脑损伤
神经保护
Sulforaphane
Lithium chloride
Traumatic brain injury
Neural protection
