氯化锂对脊髓挫伤大鼠模型中脑源性神经营养因子（BDNF）、神经营养因子3（NT3）及其受体mRNA水平的影响。
The effect of lithium chloride on BDNF, NT3, and their receptor mRNA levels in the spinal contusion rat models.
作者信息
Abdanipour Alireza, Moradi Fatemeh, Fakheri Farzaneh, Ghorbanlou Mehrdad, Nejatbakhsh Reza
机构信息
a Department of Anatomy , School of Medicine, Zanjan University of Medical Sciences (ZUMS) , Zanjan , Iran.
b Department of Biology , Science and Research Branch, Islamic Azad University , Tehran , Iran.
出版信息
Neurol Res. 2019 Jun;41(6):577-583. doi: 10.1080/01616412.2019.1588507. Epub 2019 Mar 17.
OBJECTIVE
Nowadays, there seems to be no decisive way for treatment of spinal cord injury (SCI).Extensive cell death (apoptosis and necrosis) occurring in SCI can cause considerable progressive sensorimotor disabilities. Preventing cell death by improving endogenous regenerative capability could an effective strategy for the treatment of SCI. This study was designed to evaluate the effects of lithium chloride (LiCl) on the cell survival through overexpression of BDNF and NT3 mRNA level and their receptors in the contusion rat models.
METHODS
Rats were randomly divided into four experimental groups (eight rats/group) including: contused animals (the non-treatment group); contused animals (the control group) which received laminectomy; contused animals received normal saline (vehicle)and contused animals received intraperitoneal injection of 20 mg/kg LiCl three days after surgery. Injection continued for 14 days as treatment. Basso, Beattie, Bresnahan (BBB) rating scale was used to assess the motor function of the rats. To evaluate the histopathological and gene expression analysis, rats were sacrificed 28 days after surgery. Real-time reverse transcriptase polymerase chain reaction (RT-PCR) was performed to obtain the relative levels of mRNA for BDNF, NT3 and their receptors.
RESULTS
The results showed LiCl ameliorates BBB scores via up-regulation of BDNF and TrkB receptors. Also, histological analysis showed that the numerical density per area of TUNEL- positive cells and the percentage of cavity significantly decreased in the LiCl-treated group.
CONCLUSION
Our findings suggest that LiCl protects neural cells and effectively enhances locomotor function, which was done through up-regulation of endogenous BDNF expression in rats with SCI.
ABBREVIATIONS
SCI: spinal cord injury; LiCl: lithium chloride; BDNF: Brain-derived neurotrophic factor; NT3: Neurotrophin-3; BBB: Basso, Beattie, Bresnahan; TrkB: Tropomyosin receptor kinase B; TUNEL: Terminal deoxynucleotidyl transferase dUTP nick end labeling.
目的
目前，对于脊髓损伤（SCI）的治疗似乎尚无决定性方法。SCI中发生的广泛细胞死亡（凋亡和坏死）可导致严重的进行性感觉运动功能障碍。通过提高内源性再生能力来预防细胞死亡可能是治疗SCI的有效策略。本研究旨在评估氯化锂（LiCl）对挫伤大鼠模型中细胞存活的影响，通过过表达脑源性神经营养因子（BDNF）和神经营养因子3（NT3）的mRNA水平及其受体。
方法
将大鼠随机分为四个实验组（每组8只大鼠），包括：挫伤动物（未治疗组）；接受椎板切除术的挫伤动物（对照组）；挫伤动物接受生理盐水（溶剂），以及挫伤动物在手术后三天接受腹腔注射20mg/kg LiCl。注射持续14天作为治疗。使用Basso、Beattie、Bresnahan（BBB）评分量表评估大鼠的运动功能。为了评估组织病理学和基因表达分析，在手术后28天处死大鼠。进行实时逆转录聚合酶链反应（RT-PCR）以获得BDNF、NT3及其受体的mRNA相对水平。
结果
结果显示，LiCl通过上调BDNF和酪氨酸激酶受体B（TrkB）受体改善BBB评分。此外，组织学分析表明，LiCl治疗组中每单位面积TUNEL阳性细胞的数量密度和空洞百分比显著降低。
结论
我们的研究结果表明，LiCl可保护神经细胞并有效增强运动功能，这是通过上调SCI大鼠内源性BDNF表达实现的。
缩写
SCI：脊髓损伤；LiCl：氯化锂；BDNF：脑源性神经营养因子；NT3：神经营养因子3；BBB：Basso、Beattie、Bresnahan；TrkB：原肌球蛋白受体激酶B；TUNEL：末端脱氧核苷酸转移酶介导的dUTP缺口末端标记
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