CAJ | 학술논문

目的探讨细胞红蛋白(eytoglobin,CYGB)在7日龄新生大鼠缺氧缺血性脑损伤(hypoxic-isehemie brain damage,HIBD)脑内的表达变化.方法健康7日龄SD大鼠70只,按简单随机抽样法随机取50只制备HIBD模型作为HIBD组,再随机分为HIBD后0、4、12、24和48 h组,每组10只;假手术组10只,只分离左颈总动脉,不结扎,也不放入缺氧箱;另10只不做任何处理作为对照组.假手术组术后即断头取脑,对照组同时取脑,HIBD组在相应时间点取脑.采用免疫组织化学法和Western印迹法从蛋白水平分析CYGB在脑组织中的分布及表达特点. 结果 (1)免疫组织化学染色显示CYGB主要表达于大脑皮质、丘脑和海马神经元的胞浆,HIBD组CYGB表达数量及染色强度均高于对照组,其中缺氧24、48 h组表达最强.(2)Western印迹结果显示,HIBD后0、4、12、24和48 h CYGB平均吸光度分别为261.5土5.0,263.0土5.4,464.3±6.8,522.8±11.2,512.9±7.9,明显高于假手术组(117.6±7.0)及对照组(116.6±9.0),P<0.01.其中缺氧0和4 h组明显高于对照组(P<0.01);缺氧12 h组的表达明显高于缺氧0、4 h组(P<0.01);缺氧24、48 h组明显高于缺氧12 h组(P<0.01);缺氧0、4 h组间,缺氧24、48 h组间差异无统计学意义(P>0.05). 结论 7日龄新生大鼠HIBD后脑内CYGB表达明显增强,并且随着缺氧缺血发展呈现时相性变化,提示其可能在脑缺氧缺血的适应性调节过程中起重要作用.
목적 탐토세포홍단백(eytoglobin,CYGB)재7일령신생대서결양결혈성뇌손상(hypoxic-isehemie brain damage,HIBD)뇌내적표체변화.방법 건강7일령SD대서70지,안간단수궤추양법수궤취50지제비HIBD모형작위HIBD조,재수궤분위HIBD후0、4、12、24화48 h조,매조10지;가수술조10지,지분리좌경총동맥,불결찰,야불방입결양상;령10지불주임하처리작위대조조.가수술조술후즉단두취뇌,대조조동시취뇌,HIBD조재상응시간점취뇌.채용면역조직화학법화Western인적법종단백수평분석CYGB재뇌조직중적분포급표체특점. 결과 (1)면역조직화학염색현시CYGB주요표체우대뇌피질、구뇌화해마신경원적포장,HIBD조CYGB표체수량급염색강도균고우대조조,기중결양24、48 h조표체최강.(2)Western인적결과현시,HIBD후0、4、12、24화48 h CYGB평균흡광도분별위261.5토5.0,263.0토5.4,464.3±6.8,522.8±11.2,512.9±7.9,명현고우가수술조(117.6±7.0)급대조조(116.6±9.0),P<0.01.기중결양0화4 h조명현고우대조조(P<0.01);결양12 h조적표체명현고우결양0、4 h조(P<0.01);결양24、48 h조명현고우결양12 h조(P<0.01);결양0、4 h조간,결양24、48 h조간차이무통계학의의(P>0.05). 결론 7일령신생대서HIBD후뇌내CYGB표체명현증강,병차수착결양결혈발전정현시상성변화,제시기가능재뇌결양결혈적괄응성조절과정중기중요작용.
Objective To study the expression of cytoglobin (CYGB) in the brain tissues of 7-day-old rats with hypoxic-ischemic brain damage (HIBD). Methods Seventy 7-day-old SD rats were divided into HIBD group(n=50),sham-operated group (n=10) and control group (n=10). HIBD group rats were HIBD models and subdivided into 0 h,4 h,12 h,24 h and 48 h groups after hypoxic-ischemic injury. Brain tissues of rats in sham-operated and control group were collected after operation immediately and brain tissues in HIBD group were collected at different times. Western blot and immunohistochemistry were used to detect the expression of CYGB. Results Immunohistochemistry test showed that CYGB was located in the cortex, thalamencephalon and hippocamp and stronger CYGB expression was found in the HIBD group in comparison with the other two groups. Western blot showed that the expression of CYGB at 0 h,4h,12h, 24 h and 48 h after hypoxic-ischemic injury (261. 5±5. 0,263. 0±5.4,464. 3±6.8,522. 8±11. 2,512. 9±7. 9) were significantly stronger than that in the sham-operated group (117. 6±7.0) and the control group (116. 6±9. 0)(P<0. 01). The expression of CYGB was up-regulated in HIBD 12 h group than in HIBD 0 and 4 h groups, and that in HIBD 24 and 48 h groups was higher than in the HIBD 12 h group. However, no significant difference were found between HIBD 0 and 4 h groups, neither between the 24 and 48 h groups (P>0. 05). Conclusions CYGB may have important role in protecting the brain from hypoxic-ischemic injury.