天津医药
天津醫藥
천진의약
TIANJIN MEDICAL JOURNAL
2015年
9期
988-991,1092
,共5页
王继权%赵兴长%孙平%李昊天%褚鑫%吕刚%范仲凯
王繼權%趙興長%孫平%李昊天%褚鑫%呂剛%範仲凱
왕계권%조흥장%손평%리호천%저흠%려강%범중개
脊髓损伤%细胞凋亡%半胱氨酸天冬氨酸蛋白酶3%半胱氨酸天冬氨酸蛋白酶12%模型,动物%大鼠, Sprague-Dawley%内质网应激%依达拉奉%转录因子CHOP
脊髓損傷%細胞凋亡%半胱氨痠天鼕氨痠蛋白酶3%半胱氨痠天鼕氨痠蛋白酶12%模型,動物%大鼠, Sprague-Dawley%內質網應激%依達拉奉%轉錄因子CHOP
척수손상%세포조망%반광안산천동안산단백매3%반광안산천동안산단백매12%모형,동물%대서, Sprague-Dawley%내질망응격%의체랍봉%전록인자CHOP
spinal cord injury%apoptosis%caspase 3%caspase 12%models,animal%rats,Sprague-Dawley%endoplasmic reticulum stress%edaravone%transcription factor CHOP
目的:探讨依达拉奉(EDA)对大鼠脊髓损伤(SCI)后内质网应激(ERS)介导的细胞凋亡的影响。方法36只SD大鼠随机分为假手术(sham)组、SCI组、EDA组,每组12只。采用Allen’s法建立SCI模型,sham组仅行椎板切除术。术后Sham组和SCI组给予与EDA组等体积等频次生理盐水处理;EDA组在SCI模型建成以后予以EDA(10 mg/kg),每12 h腹腔注射给药1次。于术后3 d取脊髓,应用Western blot检测C/EBP同源蛋白(CHOP)、Cleaved caspase-12和Cleaved caspase-3的表达水平,免疫荧光技术检测脊髓组织中caspase-12、CHOP阳性细胞的比率,TUNEL法检测脊髓细胞凋亡水平。结果 SCI组较sham组CHOP、Cleaved caspase-12、Cleaved caspase-3的表达升高,Cleaved caspase-12、CHOP阳性细胞比率增加,脊髓组织细胞凋亡比率增加(均P<0.01)。EDA组较SCI组CHOP、Cleaved caspase-12和Cleaved caspase-3的表达降低,Cleaved caspase-12、CHOP阳性细胞比率减少,脊髓组织细胞凋亡比率减少(均P<0.01)。结论 EDA对脊髓损伤有保护作用,机制可能与其抑制SCI后脊髓细胞的ERS和脊髓细胞的凋亡有关。
目的:探討依達拉奉(EDA)對大鼠脊髓損傷(SCI)後內質網應激(ERS)介導的細胞凋亡的影響。方法36隻SD大鼠隨機分為假手術(sham)組、SCI組、EDA組,每組12隻。採用Allen’s法建立SCI模型,sham組僅行椎闆切除術。術後Sham組和SCI組給予與EDA組等體積等頻次生理鹽水處理;EDA組在SCI模型建成以後予以EDA(10 mg/kg),每12 h腹腔註射給藥1次。于術後3 d取脊髓,應用Western blot檢測C/EBP同源蛋白(CHOP)、Cleaved caspase-12和Cleaved caspase-3的錶達水平,免疫熒光技術檢測脊髓組織中caspase-12、CHOP暘性細胞的比率,TUNEL法檢測脊髓細胞凋亡水平。結果 SCI組較sham組CHOP、Cleaved caspase-12、Cleaved caspase-3的錶達升高,Cleaved caspase-12、CHOP暘性細胞比率增加,脊髓組織細胞凋亡比率增加(均P<0.01)。EDA組較SCI組CHOP、Cleaved caspase-12和Cleaved caspase-3的錶達降低,Cleaved caspase-12、CHOP暘性細胞比率減少,脊髓組織細胞凋亡比率減少(均P<0.01)。結論 EDA對脊髓損傷有保護作用,機製可能與其抑製SCI後脊髓細胞的ERS和脊髓細胞的凋亡有關。
목적:탐토의체랍봉(EDA)대대서척수손상(SCI)후내질망응격(ERS)개도적세포조망적영향。방법36지SD대서수궤분위가수술(sham)조、SCI조、EDA조,매조12지。채용Allen’s법건립SCI모형,sham조부행추판절제술。술후Sham조화SCI조급여여EDA조등체적등빈차생리염수처리;EDA조재SCI모형건성이후여이EDA(10 mg/kg),매12 h복강주사급약1차。우술후3 d취척수,응용Western blot검측C/EBP동원단백(CHOP)、Cleaved caspase-12화Cleaved caspase-3적표체수평,면역형광기술검측척수조직중caspase-12、CHOP양성세포적비솔,TUNEL법검측척수세포조망수평。결과 SCI조교sham조CHOP、Cleaved caspase-12、Cleaved caspase-3적표체승고,Cleaved caspase-12、CHOP양성세포비솔증가,척수조직세포조망비솔증가(균P<0.01)。EDA조교SCI조CHOP、Cleaved caspase-12화Cleaved caspase-3적표체강저,Cleaved caspase-12、CHOP양성세포비솔감소,척수조직세포조망비솔감소(균P<0.01)。결론 EDA대척수손상유보호작용,궤제가능여기억제SCI후척수세포적ERS화척수세포적조망유관。
Objective To investigate the effects of edaravone (EDA) on cell apoptosis induced by endoplasmic reticu?lum stress (ESR) after spinal cord injury (SCI) in rats. Methods Thirty-six healthy adult SD rats were randomly divided in?to three groups (12 rats for each group):Sham group, SCI group and EDA group. The rat model of SCI was made by Allen’s method and the sham group was only received laminectomy and kept the spinal cord intact. Rats in sham group and SCI group accepted the same volume and frequency of saline injection as EDA group. The EDA group was given 10 mg/kg EDA once every 12 h intraperitoneally. Three days after injuring, the spinal cords were harvested, and the protein levels of C/EBP homologous protein (CHOP), Cleaved caspase-12 and Cleaved caspase-3 were detected by Western blot assay. Immunofluo?rescence staining was used to analyze the positive ratio of caspase-12 and CHOP in spinal cord of three groups. Meanwhile, TUNEL staining was used to identify cell apoptosis of spinal cord. Results Compared with sham group, the protein levels of CHOP, Cleaved caspase-12 and Cleaved caspase-3 were obviously higher in SCI group (P<0.01);the proportion of Cas?pase-12 and CHOP positive cells was significantly increased (P<0.01), and the apoptotic rates were also significantly in?creased in spinal cord (P<0.01). However, compared with SCI group, the protein levels of CHOP , Cleaved caspase-12 and Cleaved caspase-3 were significantly decreased in EDA group (P<0.01);the proportion of Caspase-12 and CHOP positive cells was significantly reduced (P<0.01), and the apoptotic rates were also significantly decreased in spinal cord (P<0.01). Conclusion EDA has neuroprotective potential to spinal cord injury. The mechanism of its neuroprotective effect may asso?ciate with its inhibitory effect to the cell apoptosis induced by endoplasmic reticulum stress after SCI.