| 锂剂抑制脊髓损伤后大鼠细胞凋亡的机制研究 |
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投稿时间：2017-12-21
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| 作者 | Author | 单位 | Address | E-Mail |
| 王放 |
WANG Fang |
西安交通大学第二附属医院骨二科, 陕西 西安, 710004 |
The Second Department of Orthopaedics, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, Shaanxi, China |
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| 周超 |
ZHOU Chao |
西安交通大学理学院, 陕西 西安 710004 |
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| 高正超 |
GAO Zheng-chao |
西安交通大学第二附属医院骨二科, 陕西 西安, 710004 |
The Second Department of Orthopaedics, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, Shaanxi, China |
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| 李宇欢 |
LI Yu-huan |
西安交通大学第二附属医院骨二科, 陕西 西安, 710004 |
The Second Department of Orthopaedics, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, Shaanxi, China |
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| 杨文龙 |
YANG Wen-long |
西安交通大学第二附属医院骨二科, 陕西 西安, 710004 |
The Second Department of Orthopaedics, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, Shaanxi, China |
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| 王栋 |
WANG Dong |
西安交通大学第二附属医院骨二科, 陕西 西安, 710004 |
The Second Department of Orthopaedics, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, Shaanxi, China |
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| 李浩鹏 |
LI Hao-peng |
西安交通大学第二附属医院骨二科, 陕西 西安, 710004 |
The Second Department of Orthopaedics, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, Shaanxi, China |
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| 贺西京 |
HE Xi-jing |
西安交通大学第二附属医院骨二科, 陕西 西安, 710004 |
The Second Department of Orthopaedics, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, Shaanxi, China |
xijing_h@vip.tom.com |
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| 期刊信息：《中国骨伤》2018年，第31卷，第4期，第379-385页 |
| DOI：10.3969/j.issn.1003-0034.2018.04.016 |
| 基金项目:国家自然科学基金（编号：81701223）；陕西省自然科学基金（编号：2017JQ8019）；中央高校基本科研业务费专项资金资助（编号：1191329737） |
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中文摘要:
目的：研究锂剂是否通过抑制脊髓损伤（spinal cord injury，SCI）后大鼠神经细胞的凋亡产生神经保护作用。
方法：将42只SD雄性大鼠，体重为200~250 g，按随机数字法分成3组：空白对照组（6只）不做手术；生理盐水（NS）组（18只）经腹腔注射NS（40 mg/kg）；氯化锂（Licl）组（18只）经腹腔注射Licl（40 mg/kg）。按照Allen法对大鼠建模后，Licl组于脊髓损伤术后15 min内开始腹腔注射Licl溶液（40 mg·kg-1·d-1）2周，NS组在同时间内注入等量的NS作为对照。分别于术后3、7、14 d进行BBB评分，利用免疫组化染色观察Bcl-2和Bax的表达，并采用TUNEL染色观察神经细胞凋亡。
结果：BBB评分：空白对照组大鼠为21±0，Licl组与NS组比较，术后7、14 d时Licl组大于NS组（P<0.05）。Bcl-2蛋白表达：空白对照组大鼠为0.081±0.003，术后7、14 d两个时间点Bcl-2蛋白表达Licl组分别为0.151±0.003和0.163±0.003，NS组为0.143±0.003和0.154±0.002，Licl组能明显升高其表达（P<0.05）。Bax蛋白的表达：空白对照组大鼠为0.071±0.003，术后7、14 d两个时间点Bax蛋白的表达Licl组分别为0.121±0.002和0.106±0.002，NS组为0.126±0.001和0.120±0.002，Licl组可以明显降低其表达（P<0.05）。神经细胞凋亡：TUNEL染色显示，空白对照组阳性细胞较少，凋亡指数（AI）为1.98±0.19，术后7、14 d两个时间Licl组分别为13.12±0.69和4.29±1.00，NS组为18.26±0.87和5.48±0.70，Licl组能显著抑制细胞凋亡（P<0.05）。
结论：锂剂能够促进SCI后大鼠的神经元细胞内Bcl-2蛋白的表达，抑制神经元内Bax蛋白的表达，从而起到了抑制神经细胞凋亡的作用，这可能是锂剂促进大鼠运动功能恢复的机制之一。 |
| 【关键词】脊髓损伤 锂剂 神经元 细胞凋亡 |
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| Depressant effect of Lithium on apoptosis of nerve cells of adult rats after spinal cord injury |
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ABSTRACT
Objective: To study whether lithium agent produces neuroprotective effect by inhibiting the nerve cell apoptosis of rats after spinal cord injury.
Methods: Forty-two male SD rats weighing 200 to 250 g were randomly divided into 3 groups:blank control group(n=6) without surgery,normal saline(NS) group(n=18) with intraperitoneal injection of NS (40 mg/kg); and Lithium chloride (Licl) group (n=18) with intraperitoneal injection of Licl (40 mg/kg). After Allen method modeling,Licl group started intraperitoneal injection of Licl solution (40 mg·kg-1·d-1) within 15 min after operation to the second week. NS group,during the same interval,was injected with a same amount of NS. Postoperative 3,7,14 d,BBB scores in each group were measured;the expression of Bcl-2 and Bax protein were observed by immunohistochemisty staining;TUNEL staining was used to observe the nerve cell apoptosis.
Results: The BBB scores in blank control group were 21. Postoperative 7,14 d,BBB scores of Licl group were higher than that of NS group(P<0.05). As for the Bcl-2 protein expression,black control group has a level of 0.081±0.003;7 d and 14 d postoperatively,the level in Licl group was 0.151±0.003,0.163±0.003 and in NS group,0.143±0.003,0.154±0.002,respectively. Licl group showed significantly increased Bcl-2 protein expression(P<0.05). As for the Bax protein expression,black control group showed a level of 0.071±0.003; 7 d and 14 d postoperatively,the level in Licl group was 0.121±0.002,0.106±0.002 and in NS group was 0.126±0.001,0.120±0.002,respectively. The Bax protein expression is significantly inhibited in the Licl group(P<0.05). In nerve cell apoptosis by TUNEL staining,the positive cells were fewer in the black control group with apoptosis index (AI) of 1.98±0.19;while 7d and 14d postoperatively,the AI of Licl group was 13.12±0.69,4.29±1.00 and of NS group,18.26±0.87,5.48±0.70,respectively. Licl group showed significant inhibition of the cell apoptosis(P<0.05).
Conclusion: Licl can promote the Bcl-2 protein expression and inhibit the Bax proteins expression in nerve cells of rat after SCI,thereby playing a role in the inhibition of nerve cell apoptosis. This may be one of the mechanisms that Licl can promote the recovery of motor function of rats after SCI. |
| KEY WORDS Spinal cord injury Lithium Neurons Apoptosis |
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| 引用本文，请按以下格式著录参考文献： |
| 中文格式: | 王放,周超,高正超,李宇欢,杨文龙,王栋,李浩鹏,贺西京.锂剂抑制脊髓损伤后大鼠细胞凋亡的机制研究[J].中国骨伤,2018,31(4):379~385 |
| 英文格式: | WANG Fang,ZHOU Chao,GAO Zheng-chao,LI Yu-huan,YANG Wen-long,WANG Dong,LI Hao-peng,HE Xi-jing.Depressant effect of Lithium on apoptosis of nerve cells of adult rats after spinal cord injury[J].zhongguo gu shang / China J Orthop Trauma ,2018,31(4):379~385 |
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