CAJ | 학술논문

目的：探讨半胱氨酸蛋白酶（ caspase ）-3抑制剂z-DEVD-fmk对大鼠颅脑创伤后神经细胞凋亡及血浆血管内皮素（ ET）、降钙素基因相关肽（ CGRP）水平的影响。方法将24只SD大鼠随机分为正常对照组、创伤组、治疗组。每组8只。创伤组、治疗组制作改进的Feeney自由落体大鼠颅脑损伤模型。治疗组通过脑立体定位仪经脑室注射z-DEVD-fmk 10μl（1μg／μl ），创伤组仅注射生理盐水。用TUNEL法观察神经细胞凋亡情况，用放射免疫法检测ET、CGRP含量。结果创伤组和治疗组的血ET水平在创伤后24 h时达高峰，后逐步下降，创伤后各时间点均显著高于正常对照组（P＜0.05～0．01）。与正常对照组相比，创伤组和治疗组的血CGRP水平在创伤后24 h、48 h时明显降低（P＜0.05～0．01），后上升，72 h时差异无统计学意义。创伤组与治疗组相比的差异无统计学意义。根据免疫组化图像分析，正常对照组凋亡细胞率为（1．8±0．3）％，创伤组为（86．3±8．5）％，治疗组为（67．5±7．8）％。治疗组较创伤组神经细胞凋亡率减少，但与正常对照组相比凋亡率增加（ P＜0.05）。结论 z-DEVD-fmk能抑制创伤后神经细胞凋亡，与ET、CGRP变化没有相关性。
목적：탐토반광안산단백매（ caspase ）-3억제제z-DEVD-fmk대대서로뇌창상후신경세포조망급혈장혈관내피소（ ET）、강개소기인상관태（ CGRP）수평적영향。방법장24지SD대서수궤분위정상대조조、창상조、치료조。매조8지。창상조、치료조제작개진적Feeney자유락체대서로뇌손상모형。치료조통과뇌입체정위의경뇌실주사z-DEVD-fmk 10μl（1μg／μl ），창상조부주사생리염수。용TUNEL법관찰신경세포조망정황，용방사면역법검측ET、CGRP함량。결과창상조화치료조적혈ET수평재창상후24 h시체고봉，후축보하강，창상후각시간점균현저고우정상대조조（P＜0.05～0．01）。여정상대조조상비，창상조화치료조적혈CGRP수평재창상후24 h、48 h시명현강저（P＜0.05～0．01），후상승，72 h시차이무통계학의의。창상조여치료조상비적차이무통계학의의。근거면역조화도상분석，정상대조조조망세포솔위（1．8±0．3）％，창상조위（86．3±8．5）％，치료조위（67．5±7．8）％。치료조교창상조신경세포조망솔감소，단여정상대조조상비조망솔증가（ P＜0.05）。결론 z-DEVD-fmk능억제창상후신경세포조망，여ET、CGRP변화몰유상관성。
Objective To study the effects of caspase-3 inhibitor ( z-DEVD-fmk) on neuronal apoptosis and plasma levels of endothelium ( ET ) , calcitonin gene-related peptide ( CGRP ) in rats with traumatic brain injury . Methods Twenty-two SD rats were randomly divided into normal control group ,traumatic group and therapy group , 8 rats per group.The traumatic and therapy group were made improved Feeney free-fall model;z-DEVD-fmk 10 μl (1μg/μl ) was injected into ventricles by Stereotaxic instrument in therapy group while normal saline was injected into in traumatic group .Neuronal apoptosis was detected by TUNEL staining;while ET and CGRP were detected by radioimmunoassay.Results ET in traumatic group and therapy group reached the peek at 24 h after intrauma,then dropped gradually , and were significantly higher than that in normal control group at each time point after intrauma (P<0.05-0.01).Compared with normal control group , CGRP in traumatic group and therapy group reduced at 24 h and 48 h after intrauma(P<0.05-0.01), then it rised, there was no satistically significant difference at 72 h. The difference was no satistically significance between traumatic group and therapy group . With the immunocytochemical method and image analysis , the rate of apoptosis in normal control group is (1.8 ±0.3)%, rate in traumatic group is (86.3 ±8.5)%, rate in theraphy group is (67.5 ±7.8)%.The rate of apoptosis in therapy group decreased significantly compared with traumatic group but increased dramatically compared with control group ( P<0.05 ) .Conclusions z-DEVD-fmk can inhibit apoptosis of neurons after trauma .There is no significant correlation between z-DEVD-fmk and ET, CGRP.