摘要
目的观察不同剂量牛肉水煮液对局灶性脑缺血大鼠血清白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)水平的影响。方法将60只雄性SD大鼠随机分成假手术组、模型组及低剂量〔200mg/(kg·d)〕、中剂量〔400mg/(kg·d)〕和高剂量〔600mg/(kg·d)〕牛肉水煮液组,每组12只。采用线栓法复制局灶性大脑中动脉缺血模型,造模后2h用Longa法对大鼠进行神经功能评分,造模后7d,再次进行神经功能评分;用2,3,5-氯化三苯四氮唑(TTC)染色法测定脑梗死体积;用酶联免疫吸附测定(ELISA)法测定血清IL-6、TNF-α水平。结果造模2h和7d后,各剂量牛肉水煮液组Longa评分和模型组相比无统计学差异(P>0.05);和模型组相比,中、高剂量牛肉水煮液组大鼠脑梗死体积分数明显减小(P<0.01);与假手术组相比,模型组血清IL-6、TNF-α水平明显升高(P<0.01),给予高剂量牛肉水煮液组可明显降低其水平(P<0.01,P<0.05)。结论高剂量牛肉水煮液可显著改善脑缺血大鼠的脑梗死体积,降低血清IL-6、TNF-α水平,这可能是牛肉水煮液对脑缺血神经损伤的保护作用机制之一。
Objective To investigate the neuroprotective effect of beef decoction(BD)on the serum levels of interleukin-6(IL-6)and tumor necrosis factor-α(TNF-α)in middle cerebral artery occlusion model(MCAO)rats.Methods Sixty SD rats were randomly divided into five groups:sham-operated group,model group,low dosage BD-treated group[200mg/(kg·d)],middle dosage BD-treated group[400mg/(kg·d)]and high dosage BD-treated group [600 mg/(kg·d)],there were 12 rats in each group.Intraluminal thread methods were applied to establish the MCAO in the model group and the three BD treated groups.The neurological function was scored with Longa 5-point scale at 2hand 7days after modeling,the cerebral infract volume was revealed by 2,3,5-triphenyltetrazolium chloride(TTC)stain,and the serum levels of IL-6and TNF-αwere detected by enzyme-linked immunosorbent assay(ELISA)methods.Results Both 2hand 7days after MCAO,compared with the model group,the neurological function scores of the BD-treated groups were not significantly different(P〉0.05).The infarction volumes of the BD-treated groups were smaller than those of the model group,and statistically significantly reduced in the high and middle dosage groups(P〈0.01).The levels of IL-6and TNF-αin the model group were much higher than those in the sham-operated group(P〈0.01),while the levels of IL-6and TNF-αin the high dosage BD group were lower than those in the model group(P〈0.01,P〈0.05).Conclusions High dosage BD is effective to reduce infract volume and restrain IL-6and TNF-αexpression,this may be its protective mechanism of BD on cerebral ischemia.
出处
《中国神经免疫学和神经病学杂志》
CAS
2015年第1期62-66,共5页
Chinese Journal of Neuroimmunology and Neurology
基金
江苏省青蓝工程项目资助
江苏省优势学科项目资助项目(编号:YSHL0201-26)