[1]唐 铸 李延良 桂 铮 张鹏飞 赵立文 姬文婕 于耀宇.甘草酸二铵对大鼠脑缺血-再灌注损伤的保护作用[J].中国临床神经外科杂志,2016,(05):287-289.[doi:10.13798/j.issn.1009-153X.2016.05.010]
 TANG Zhu,LI Yan-liang,GUI Zheng,et al.Diammonium glycyrrhizinate attenuates cerebral ischemia-reperfusion injury by Akt/caspase-3 pathway in rats[J].,2016,(05):287-289.[doi:10.13798/j.issn.1009-153X.2016.05.010]
点击复制

甘草酸二铵对大鼠脑缺血-再灌注损伤的保护作用()
分享到:

《中国临床神经外科杂志》[ISSN:1009-153X/CN:42-1603/TN]

卷:
期数:
2016年05期
页码:
287-289
栏目:
论著
出版日期:
2016-05-25

文章信息/Info

Title:
Diammonium glycyrrhizinate attenuates cerebral ischemia-reperfusion injury by Akt/caspase-3 pathway in rats
文章编号:
1009-153X(2016)05-0287-03
作者:
唐 铸 李延良 桂 铮 张鹏飞 赵立文 姬文婕 于耀宇
作者单位:063009 河北唐山,华北理工大学研究生院(唐 铸);300162 天津,武警后勤学院附属医院神经外科(李延良、桂 铮、张鹏飞、赵立文、姬文婕、于耀宇)
通讯作者:于耀宇,E-mail:yuyaoyu666@aliyun.com
Author(s):
TANG Zhu1 LI Yan-liang2 GUI Zheng2 ZHANG Peng-fei2 ZHAO Li-wen2 JI Wen-jie2 YU Yao-yu2.
1. Gratuate School, North China University of Science and Technology, Tangshan 063000, China; 2. Department of Neurosurgery, Affiliated Hospital, Logistics University of People's Armed Police Forces, Tianjin 300162, China
关键词:
脑缺血-再灌注损伤细胞凋亡甘草酸二铵脑保护作用大鼠
Keywords:
Cerebral ischemical-reperfusion injury Cell apoptosis Diammonium glycyrrhizinate Cerebral protection Rats
分类号:
R 739.41; R 651.1+1
DOI:
10.13798/j.issn.1009-153X.2016.05.010
文献标志码:
A
摘要:
目的 探讨甘草酸二铵对大鼠脑缺血-再灌注损伤的作用。方法 将30只雄性SD大鼠(体重为250~300 g)随机分为假手术组、甘草酸二铵组、模型组,每组10只。采用可逆性大脑中动脉线栓法制作大鼠局灶性脑缺血-再灌注损伤模型。采用Zea-Longa评分评估大鼠神经功能。运用尼氏体染色检测大鼠海马组织尼氏小体数量,免疫组化法检测大鼠海马组织Akt、caspase-3阳性细胞数量。结果 术后24 h甘草酸二铵组和模型组大鼠Zea-Longa评分明显高于假手术组(P<0.05);造模后3 d,甘草酸二铵组神经功能较模型组明显改善(P<0.05)。甘草酸二铵组海马组织尼氏小体数量和Akt阳性细胞数量较模型组明显增加,而caspase-3阳性细胞数量较模型组明显减少(P<0.05)。结论 甘草酸二铵可通过Akt/caspase-3途径减轻脑缺血-再灌注损伤大鼠细胞凋亡,发挥对大鼠缺血-再灌注损伤的保护作用。
Abstract:
Objective To study the effect of diammonium glycyrrhizinate (DG) on cerebral ischemia-reperfusion injury in rats. Methods Thirty SD rats were randomly divided into 3 groups, i.e. sham operation group (n=10), model group (n=10) and DG treatment group (n=10). The rat model of focal cerebral ischemia-reperfusion injury was made by reversible middle cerebral artery occlusion in rats. The rats in DG traetment group received intraperitoneal injection of DG [20 mg/(kg.d), qd] for 3 days, and the rats in sham operation and model groups received intraperitoneal injection of indentical volume of physiological saline. Zea-longa score was used to assess the neurological function 2 hours and 3 days after the injury. The number of Nissl bodies of neurons was assess by Nissl's staining and the numbers of caspase-3 positive cells and Akt positive cells were detected by immunohistochemistry staining in the hippocampus tissues 3 days after the injury. Results Two hours after injury, the Zea-longa scores in DG treatment group [(2.60±0.51) points] and model group [(2.59±0.54) points] were significantly higher than that (zero point) in sham operation group (P<0.05), and there was no significant difference between DG treatment and model groups (P>0.05). Three days after injury, the Zea-longa score in DG treatment group [(1.90±0.74) points] was still significantly higher than that (zero point) in sham operation group (P<0.05), and significantly lower than that [(2.50±0.48) points] in model group (P<0.05). The numbers of Nissl bodies of neurons and Akt positive cells in DG treatment group were significantly more than that in model group (P<0.05), and the number of caspase-3 positive cells in DG treatment group was significantly fewer than that in model group (P<0.05). Conclusion It is suggested that DG can reduce the level of neuron apoptosis by Akt/caspase-3 pathway, thus protect the cerebral tissues after the cerebral ischemia-reperfusion injury in the rats.

参考文献/References:

[1] Lapi D, Colantuoni A. Remodeling of cerebral microcircu- lation after ischemia-reperfusion [J]. J Vasc Re, 2015, 52 (1): 22-31.
[2] Longa EZ, Weinstein PR, Carlson S, et al. Reversible middle cerebralartery occlusion without craniectomyinrats [J]. Stroke, 1989, 20(1): 84-91.
[3] Zhu Y, Liu F, Zou X, et al. Comparison of unbiased estima- tion of neuronalnumberin the rat hippocampus with different staining methods [J]. J Neurosci Methods, 2015, 30, 254: 73-79.
[4] Mullonkal CJ, Toledo-Pereyra LH. Akt in ischemia and reperfusion [J]. J Invest Surg, 2007, 20(3): 195-203.
[5] Zhou J, Du T, Li B, et al. Crosstalk between MAPK/ERK and PI3K/AKT signal pathways during brain ischemia/reperfu- sion [J]. ASN Neuro, 2015, 7(5): pii: 1759091415602463.

相似文献/References:

[1]冯 驰 郭双毅 程龙海 罗 杰.氯喹通过抑制自噬促进TRAIL诱导的胶质瘤细胞凋亡[J].中国临床神经外科杂志,2016,(04):227.[doi:10.13798/j.issn.1009-153X.2016.04.011]
 FENG Chi,GUO Shuang-yi,CHENG Long-hai,et al.Chloroquine promotes TRAIL-induced apoptosis of glioma cells through inhibition of autophagy[J].,2016,(05):227.[doi:10.13798/j.issn.1009-153X.2016.04.011]
[2]李晓东 徐 军.脊髓慢性压迫性损伤后细胞凋亡和BDNF表达的观察[J].中国临床神经外科杂志,2016,(03):167.[doi:10.13798/j.issn.1009-153X.2016.03.012]
 LI Xiao-dong,XU Jun..Observation of cell apoptosis and BDNF expression in spinal cord injured by chronic compression[J].,2016,(05):167.[doi:10.13798/j.issn.1009-153X.2016.03.012]
[3]陈文彬 曾 贤 综述 唐 瑛 鞠殿文 审校.细胞程序性死亡在脑缺血中的作用与调控机制的研究进展[J].中国临床神经外科杂志,2015,(08):509.[doi:10.13798/j.issn.1009-153X.2015.08.025]
[4]李国亮 邸 方 杨亚东.葛根素对大鼠颅脑损伤的保护作用[J].中国临床神经外科杂志,2016,(08):479.[doi:10.13798/j.issn.1009-153X.2016.08.012]
 LI Guo-liang,DI Fang,YANG Ya-dong..Neuroprotective effects of puerarin on cerebral tissues injured by trauma and its mechanism in rats[J].,2016,(05):479.[doi:10.13798/j.issn.1009-153X.2016.08.012]
[5]李国亮 邸 方 杨亚东.香芹酚对大鼠急性脊髓损伤的保护作用[J].中国临床神经外科杂志,2016,(09):549.[doi:10.13798/j.issn.1009-153X.2016.09.012]
 LI Guo-liang,DI Fang,YANG Ya-dong..Effects of carvacrol on spinal cord edema and oxidative stress reaction after spinal cord injury in rats[J].,2016,(05):549.[doi:10.13798/j.issn.1009-153X.2016.09.012]
[6]卢文婕 杨 李 吕丽辉 综述 徐国政 审校.热休克蛋白70的功能及其临床应用前景[J].中国临床神经外科杂志,2016,(10):649.[doi:10.13798/j.issn.1009-153X.2016.10.031]
[7]王跃飞,李明昌,邹长林,等.血液溶解产物对原代培养的小鼠脑皮层神经元的影响[J].中国临床神经外科杂志,2016,(11):689.[doi:10.13798/j.issn.1009-153X.2016.11.012]
 WANG Yue-fei,LI Ming-chang,ZOU Chang-lin,et al.Effects of hemolysate on primary cultured mouse cortical neurons[J].,2016,(05):689.[doi:10.13798/j.issn.1009-153X.2016.11.012]
[8]冯 驰,罗 杰.自噬对TRAIL诱导的肿瘤细胞凋亡的影响[J].中国临床神经外科杂志,2016,(11):724.[doi:10.13798/j.issn.1009-153X.2016.11.028]
[9]韩铖琛,胡晨浩,杨帆,等.miRNA-145在脑胶质瘤中的作用[J].中国临床神经外科杂志,2017,(07):486.[doi:10.13798/j.issn.1009-153X.2017.07.013]
 HAN Cheng-chen,HU Chen-hao,YANG Fan,et al.Effects of miRNA-145 on proliferation and apoptosis of U251 glioma cells[J].,2017,(05):486.[doi:10.13798/j.issn.1009-153X.2017.07.013]
[10]冯 驰 郭双毅 程龙海 罗 杰.外源性TRAIL基因转染联合氯喹诱导胶质瘤U251细胞凋亡[J].中国临床神经外科杂志,2017,(08):563.[doi:10.13798/j.issn.1009-153X.2017.08.014]
 FENG Chi,GUO Shuang-yi,CHENG Long-hai,et al.Effect of exogenous TRAIL gene transfection combined with chloroquine on glioma U251 cells apoptosis[J].,2017,(05):563.[doi:10.13798/j.issn.1009-153X.2017.08.014]

更新日期/Last Update: 2016-05-30