CAJ | 학술논문

目的探讨小鼠创伤性脑损伤(TBI)后海马区Toll样受体4(TLR4)的表达及其与神经干细胞(NPCs)变化的关系.方法采用Mamarou自由落体打击法制备小鼠TBI模型,5-溴脱氧尿嘧啶核苷(BrdU)标记NPCs,免疫荧光染色、Western blot检测海马TLR4表达变化规律及NPCs时程变化特征.结果伤后1d海马区NPCs数量增多,3d达到高峰,7、14、21 d逐渐减少(P＜0.05).TLR4表达于海马区NPCs的胞膜和胞质,于伤后1d表达显著上调,高峰出现在伤后3d,于7、14、21 d表达逐渐下调(P＜0.05).结论 TBI后海马区TLR4表达与NPCs变化趋势在时程上一致,TLR4可能是激活NPCs修复神经损伤的重要因素.
목적 탐토소서창상성뇌손상(TBI)후해마구Toll양수체4(TLR4)적표체급기여신경간세포(NPCs)변화적관계.방법 채용Mamarou자유락체타격법제비소서TBI모형,5-추탈양뇨밀정핵감(BrdU)표기NPCs,면역형광염색、Western blot검측해마TLR4표체변화규률급NPCs시정변화특정.결과 상후1d해마구NPCs수량증다,3d체도고봉,7、14、21 d축점감소(P＜0.05).TLR4표체우해마구NPCs적포막화포질,우상후1d표체현저상조,고봉출현재상후3d,우7、14、21 d표체축점하조(P＜0.05).결론 TBI후해마구TLR4표체여NPCs변화추세재시정상일치,TLR4가능시격활NPCs수복신경손상적중요인소.
Objective To investigate the expression of hippocampal toll-like receptors 4 (TLR4) and the proliferation of neural progenitor cells (NPCs) in mouse model of traumatic brain injury (TBI).Methods Adult male Balb/c mice were randomly divided into the sham groups and the 1st,3rd,7th,14th,21st days post-traumatic groups.The TBI mouse model was induced by Mamarou weight-drop device.NPCs were labeled with thymidine analog 5-Bromo-2-deoxyUridine (BrdU).The expression and distribution of BrdU and TLR4 in hippocampus were observed by inmmunofluorescence.The expression of TLR4 in protein level was detected by Western-blot.Results It was observed that TLR4 expressed on the NPCs in hippocampus by double-labeling inmmunofluorescence,and the expression of TLR4 protein in hippocampus raised at the 1st day,got to the peak around the 3rd day,then decreased over the 7th day,14th day,and 21st day to a lower value but still higher than the sham group(P ＜ 0.05).NPCs increased at the 1st post-traumatic day,reached the peak at the 3rd day,followed by a gradual reduction from the 3rd day to the 21st day when maintained a higher number than that of the sham group (P ＜ 0.05).Conclusions TLR4 expressed on the NPCs in hippocampus,and the expression of hippocampal TLR4 varied in a similar temporal pattern with the proliferation of NPCs after injury.It suggested that hippocampal TLR4 might play a potential role in the endogenous neurogenesis after TBI.