CAJ | 학술논문

目的探讨创伤性脑损伤(TBI)大鼠脑组织抵抗素rstn基因表达的变化特征. 方法选择SD大鼠90只,按随机数字表法分成正常对照组(5只),假手术组(10只),轻、中和重度损伤组(每组25只).应用液压冲击法制作大鼠颅脑损伤模型,并应用RT-PGR方法检测各组大鼠伤后3,6,24,72 h和1,2,4周脑组织rstn基因表达的变化,同时监测损伤中度组大鼠外周血糖浓度变化,观察两者之间的关系. 结果重度损伤组大鼠于伤后24 h,中度损伤组大鼠于伤后72 h,轻度损伤组大鼠于伤后4周rstn基因的表达开始明显上升(P＜0.05).伤后4周时,所有损伤组海马、丘脑及皮质区域rstn基因表达均升高(P＜0.05),其中海马区域最高,丘脑区域最低(P＜0.05).不同区域均存在损伤侧rstn基因表达较高,对侧较低的现象(P＜0.05).重度损伤组大鼠rstn基因表达升高最明显(P＜0.05).脑组织rstn基因表达变化与外周血糖浓度呈线性正相关(R=5.32,P=0.03). 结论 TBI后rstn基因表达明显增加,rstn基因表达的时程变化可能与脑损伤严重程度相关.TBI后rstn基因存在同侧海马区域表达明显升高的组织分布特征.创伤后脑组织rstn基因表达变化与血糖代谢之间存在一定关系.
목적 탐토창상성뇌손상(TBI)대서뇌조직저항소rstn기인표체적변화특정. 방법선택SD대서90지,안수궤수자표법분성정상대조조(5지),가수술조(10지),경、중화중도손상조(매조25지).응용액압충격법제작대서로뇌손상모형,병응용RT-PGR방법검측각조대서상후3,6,24,72 h화1,2,4주뇌조직rstn기인표체적변화,동시감측손상중도조대서외주혈당농도변화,관찰량자지간적관계. 결과중도손상조대서우상후24 h,중도손상조대서우상후72 h,경도손상조대서우상후4주rstn기인적표체개시명현상승(P＜0.05).상후4주시,소유손상조해마、구뇌급피질구역rstn기인표체균승고(P＜0.05),기중해마구역최고,구뇌구역최저(P＜0.05).불동구역균존재손상측rstn기인표체교고,대측교저적현상(P＜0.05).중도손상조대서rstn기인표체승고최명현(P＜0.05).뇌조직rstn기인표체변화여외주혈당농도정선성정상관(R=5.32,P=0.03). 결론 TBI후rstn기인표체명현증가,rstn기인표체적시정변화가능여뇌손상엄중정도상관.TBI후rstn기인존재동측해마구역표체명현승고적조직분포특정.창상후뇌조직rstn기인표체변화여혈당대사지간존재일정관계.
Objective To investigate the change of gene rstn expression in brain tissues following traumatic brain injury (TBI). Methods A total 90 SD rats were involved in the study and divided into normal control group (5 rats), sham operation group (10 rats), mild, moderate and severe trauma groups (25 rats per group). Rat model was made with sap pressure clash method and RT-PCR assay was employed to detect expression change of gene rstn at 3, 6, 24, 72 h and 1, 2, 4 weeks after TBI. The change of peripheral blood glucose concentration was measured in moderate trauma group to observe its relationship with gene rstn expression in brain tissue. Results Postoperative expression of gene rstn was increased in severe trauma group at 24 hours, in moderate trauma group at 72 hours and in mild trauma group at four weeks (P＜0.05). The expression of gene rstn was increased in hippocampus, thalamus and cortex of all trauma groups at four weeks postoperatively, when the hippocampus showed the highest expression while the thalamus showed the least (P＜ 0.05). Moreover, the expression of gene rstn showed high level in injury side but low level in contralateral side in different districts (P ＜ 0.05). The expression of gene rstn was increased the most obviously in severe trauma group (P ＜0.05). Peripheral blood glucose concentration showed a linearity positive correlation with gene rstn expression in brain tissue (R=5.32,P＜0.05). Conclusions Expression of gene rstn shows obvious increase after TBI, and the time course correlates with the injury severity. The gene rstn expresses the most in the ipsilateral hippocampus. There shows a certain correlation between gene rstn expression and peripheral blood glucose concentration in brain tissues after TBI.