CAJ | 학술논문

目的探讨17-β雌二醇治疗脊髓损伤的分子机制,为临床应用雌激素治疗脊髓损伤提供理论依据.方法成年雄性SD大鼠180只,采用改良的Allen法构建大鼠急性脊髓挫伤模型后经17-β雌二醇治疗,采用化学比色法测定脊髓组织中丙二醛(MDA)和内源性巯醇抗氧化物(酶):还原型谷胱甘肽(GSH)、超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)含量;免疫组织化学分析凋亡相关因子Caspase-3、Bcl-2和Bax蛋白的表达变化. 结果　 17-β雌二醇治疗组与脊髓损伤组比较,BBB评分明显增加;在多个时间点MDA含量明显降低;巯醇抗氧化物(酶)GSH、SOD和GSH-Px含量显著增加;Caspase-3和Bax表达的阳性细胞数明显减少;Bcl-2表达的阳性细胞数明显增加(P<0.05). 结论大剂量的17-β雌二醇治疗可能通过调控内源性巯醇抗氧化物(酶),提高肢体运动功能,抑制细胞凋亡,从而减轻脊髓损伤程度.
목적 탐토17-β자이순치료척수손상적분자궤제,위림상응용자격소치료척수손상제공이론의거.방법 성년웅성SD대서180지,채용개량적Allen법구건대서급성척수좌상모형후경17-β자이순치료,채용화학비색법측정척수조직중병이철(MDA)화내원성구순항양화물(매):환원형곡광감태(GSH)、초양화물기화매(SOD)화곡광감태과양화물매(GSH-Px)함량;면역조직화학분석조망상관인자Caspase-3、Bcl-2화Bax단백적표체변화. 결과　 17-β자이순치료조여척수손상조비교,BBB평분명현증가;재다개시간점MDA함량명현강저;구순항양화물(매)GSH、SOD화GSH-Px함량현저증가;Caspase-3화Bax표체적양성세포수명현감소;Bcl-2표체적양성세포수명현증가(P<0.05). 결론 대제량적17-β자이순치료가능통과조공내원성구순항양화물(매),제고지체운동공능,억제세포조망,종이감경척수손상정도.
Objective To examine the protective effects of 17-β estradiol on the experimental model of spinal cord injury (SCI) rats. Methods One hundred and eighty male Sprague Dawley (SD) rats, after Allen' s model, SD rats were divided into three groups: the sham group, the acute spinal cord injury (control groups) and the acute spinal cord injury supplying with 17-β estradiol treatment group. SCI was made by Allen's weight dropping, impacting on the posteriors of spinal cord T10. The content of malonyldialdehyed (MDA), glutathione (GSH), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were determined by chromatometry. The expressions of Caspase-3 and Bcl-2 family in the injured spinal cord were detected by immunohistochemical staining. Results The BBB scores at each time point in 17-β estradiol treatment group were significantly higher than that in SCI group (P<0.05). The contents of GSH, SOD, GSH-Px and the expression of Bcl-2 protein at the majority of time point in 17-β estradiol treatment group were significantly higher than that in SCI group(P<0.05), however, the MDA, Caspase-3 and Bax were markedly decreased (P<0.05). Conclusions This study suggests that 17-β estradiol administration might prevent the cells from SCI-induced apoptosis by triggering to reduce the oxidative stress.