中华神经医学杂志
中華神經醫學雜誌
중화신경의학잡지
CHINESE JOURNAL OF NEUROMEDICINE
2010年
11期
1090-1094
,共5页
叶昇%胡海燕%孟伟%郭洪波
葉昇%鬍海燕%孟偉%郭洪波
협승%호해연%맹위%곽홍파
肝细胞%辐射损伤%细胞修复
肝細胞%輻射損傷%細胞脩複
간세포%복사손상%세포수복
Stem cell%Radiation injury%Cytothesis
目的 研究胚胎肝细胞对脑组织辐射损伤的修复作用.方法 24只雌性SD大鼠按随机数字表法分为对照组、模型组和治疗组,每组8只.后2组大鼠行一次性全脑照射20GyX线制备脑辐射损伤模型,造模后1、7、14、21 d治疗组大鼠后尾静脉注射雄性大鼠胚胎肝细胞1 mL(3×106个/mL),模型组大鼠尾静脉注射等量生理盐水.于每次输注后12h取各组大鼠血清,分光光度计测定丙二醛(MDA)、超氧化物歧化酶(SOD)的水平,ELISA法测定肿瘤坏死因子α(TNFα)、白介素-1(IL-1)和白介素-6(IL-6)的含量.造模28 d后处死大鼠,RT-PCR检测治疗组大鼠脑组织Y染色体mRNA的表达,HE染色观察海马区脑组织的病理变化.结果 造模后1、7、14、21、28 d,与对照组比较,模型组和治疗组大鼠血清SOD水平较低,而MDA、TNFα、IL-1和IL6水平较高,差异有统计学意义(P<0.05);与模型组比较,治疗组大鼠血清SOD水平较高,而MDA、TNFα、IL-1和IL6水平较低,差异有统计学意义(P<0.05);RT-PCR结果显示治疗组大鼠脑组织有Y染色体mRNA表达;HE染色显示治疗组大鼠海马区虽可见凋亡状态的尼氏小体,但大脑皮质较模型组大鼠明显增厚,可见再生的海马神经元.结论 胚胎肝细胞能够修复脑组织的辐射损伤.
目的 研究胚胎肝細胞對腦組織輻射損傷的脩複作用.方法 24隻雌性SD大鼠按隨機數字錶法分為對照組、模型組和治療組,每組8隻.後2組大鼠行一次性全腦照射20GyX線製備腦輻射損傷模型,造模後1、7、14、21 d治療組大鼠後尾靜脈註射雄性大鼠胚胎肝細胞1 mL(3×106箇/mL),模型組大鼠尾靜脈註射等量生理鹽水.于每次輸註後12h取各組大鼠血清,分光光度計測定丙二醛(MDA)、超氧化物歧化酶(SOD)的水平,ELISA法測定腫瘤壞死因子α(TNFα)、白介素-1(IL-1)和白介素-6(IL-6)的含量.造模28 d後處死大鼠,RT-PCR檢測治療組大鼠腦組織Y染色體mRNA的錶達,HE染色觀察海馬區腦組織的病理變化.結果 造模後1、7、14、21、28 d,與對照組比較,模型組和治療組大鼠血清SOD水平較低,而MDA、TNFα、IL-1和IL6水平較高,差異有統計學意義(P<0.05);與模型組比較,治療組大鼠血清SOD水平較高,而MDA、TNFα、IL-1和IL6水平較低,差異有統計學意義(P<0.05);RT-PCR結果顯示治療組大鼠腦組織有Y染色體mRNA錶達;HE染色顯示治療組大鼠海馬區雖可見凋亡狀態的尼氏小體,但大腦皮質較模型組大鼠明顯增厚,可見再生的海馬神經元.結論 胚胎肝細胞能夠脩複腦組織的輻射損傷.
목적 연구배태간세포대뇌조직복사손상적수복작용.방법 24지자성SD대서안수궤수자표법분위대조조、모형조화치료조,매조8지.후2조대서행일차성전뇌조사20GyX선제비뇌복사손상모형,조모후1、7、14、21 d치료조대서후미정맥주사웅성대서배태간세포1 mL(3×106개/mL),모형조대서미정맥주사등량생리염수.우매차수주후12h취각조대서혈청,분광광도계측정병이철(MDA)、초양화물기화매(SOD)적수평,ELISA법측정종류배사인자α(TNFα)、백개소-1(IL-1)화백개소-6(IL-6)적함량.조모28 d후처사대서,RT-PCR검측치료조대서뇌조직Y염색체mRNA적표체,HE염색관찰해마구뇌조직적병리변화.결과 조모후1、7、14、21、28 d,여대조조비교,모형조화치료조대서혈청SOD수평교저,이MDA、TNFα、IL-1화IL6수평교고,차이유통계학의의(P<0.05);여모형조비교,치료조대서혈청SOD수평교고,이MDA、TNFα、IL-1화IL6수평교저,차이유통계학의의(P<0.05);RT-PCR결과현시치료조대서뇌조직유Y염색체mRNA표체;HE염색현시치료조대서해마구수가견조망상태적니씨소체,단대뇌피질교모형조대서명현증후,가견재생적해마신경원.결론 배태간세포능구수복뇌조직적복사손상.
Objective To study the cytothesis effects of haemopoietic stem cells (HSCs) from rat fetal liver on brain injury induced by radiation. Methods Twenty-four female SD rats were randomly divided into normal control group, model group and treatment group (n=8). Total brain irradiation with 20 Gy X-ray was performed in the model group and the treatment group. Rats in the treatment group received infusion of HSCs from fetal liver (3×106 cells) 24 h, and 7, 14 and 21 d after irradiation, while rats in the model group and controls received infusion of saline at the same dosage. The serum of the rats was collected 12 h after infusion of HSCs each time; spectrophotometry was employed to detect the levels of malonaldehyde (MDA) and superoxide dismutase (SOD); the contents of tumor necrosis factor α (TNFα), interleukin (IL-1 and IL6) were measured by ELISA. Rats were sacrificed on the 28th d for assessing the pathological changes in brain tissue by HE staining and the mRNA level of Y chromosome by RT-PCR. Results Compared with that in the model group, the level of SOD in the treatment group was significantly higher, but the levels ofMDA, TNFα, IL-1 and IL6 were significantly lower in the treatment group 24 h, and 7, 14 and 21 d after the irradiation (P<0.05). The mRNA expression of Y chromosome was noted and apoptosis of Nissl bodies was also observed in the treatment group; the cerebral cortex in the treatment group was significantly thicker as compared with that in the model group (P<0.05); regenerative hippocampal neurons were observed in the treatment group. Conclusion HSCs from fetal liver can effectively repair the radiation brain injury.