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隐丹参酮对脑缺血再灌注损伤神经元细胞凋亡的作用
引用本文:郝红,李方,王志,赵宪文,田继新,朱雪萍,王晓丽,赵宁民. 隐丹参酮对脑缺血再灌注损伤神经元细胞凋亡的作用[J]. 中国临床药理学杂志, 2021, 0(3): 250-254
作者姓名:郝红  李方  王志  赵宪文  田继新  朱雪萍  王晓丽  赵宁民
作者单位:郑州第九人民医院药学部
基金项目:河南省科学技术厅基金资助项目(162102310287)。
摘    要:目的 探讨隐丹参酮(CTs)抑制c-Jun氨基末端激酶/p38丝裂原活化蛋白激酶(JNK/p38 MAPK)信号通路对脑缺血再灌注损伤(CIRI)神经元细胞凋亡的作用.方法 将30只SD大鼠随机分为假手术组、模型组和实验组,每组10只,模型组和实验组参照改良Longa法制备CIRI模型.造模成功后,实验组腹腔注射CTs...

关 键 词:隐丹参酮  脑缺血再灌注  氧糖剥夺/复氧糖损伤  c-Jun氨基末端激酶/p38丝裂原活化蛋白激酶

Effects of cryptotanshinone on the apoptosis of neurons after cerebral ischemia reperfusion injury
HAO Hong,LI Fang,WANG Zhi,ZHAO Xian-wen,TIAN Ji-xin,ZHU Xue-ping,WANG Xiao-li,ZHAO Ning-min. Effects of cryptotanshinone on the apoptosis of neurons after cerebral ischemia reperfusion injury[J]. The Chinese Journal of Clinical Pharmacology, 2021, 0(3): 250-254
Authors:HAO Hong  LI Fang  WANG Zhi  ZHAO Xian-wen  TIAN Ji-xin  ZHU Xue-ping  WANG Xiao-li  ZHAO Ning-min
Affiliation:(Department of Pharmacy,Ninth People's Hospital of Zhengzhou,Zhengzhou 450000,Henan Province,China)
Abstract:Objective To explore the effects of cryptotanshinone(CTs)on the apoptosis of neurons after cerebral ischemia reperfusion injury(CIRI)by inhibiting the c-Jun N-terminal kinase/p38 mitogen-activated protein kinase(JNK/p38 MAPK)signaling pathway.Methods Thirty SD rats were randomly divided into sham-operation group,model group and experimental group,with 10 rats in each group.Animal model of CIRI was prepared by modified Longa method in model group and experimental group.The experimental group was intraperitoneally administered with CTs solution(20 mg·kg-1).The model group and sham-operation group received intraperitoneal injection of 0.9%NaCl,once a day for 2 weeks.After 2 weeks of treatment,the neurological deficit score was measured.Neonatal rats were collected and cerebral cortical neurons cells were isolated,and then they were divided into normal group,model group and experimental group.The experimental group was pretreated with complete medium containing 5μmol·L-1CTs.The model group and normal group were pretreated with complete medium without CTs.After 24 h of culture,the model group and the experimental group were established OGD/R model.The methyl thiazolyl tetrazolium method was used to determine the cell survival rate in each group.The apoptosis results of each group were detected by TUNEL method,and the phosphorylation levels of JNK/p38 MAPK signaling pathway were detected by Western Blot.Results Compared with model group,the neurological deficit score in sham-operation group and experimental group was significantly decreased[(0.37±0.07),(1.62±0.15)vs(2.63±0.23),all P<0.05].Compared with model group,the survival rates of neurons in normal group and experimental group significantly increased[(99.94±7.95)%,(72.37±6.42)%vs(48.57±4.63)%,all P<0.05],and the apoptosis rates significantly decreased[(6.37±1.22)%,(13.65±2.71)%vs(26.75±4.82)%,all P<0.05],the level of p-JNK significantly decreased[0.39±0.03,0.45±0.05 vs 0.82±0.08,all P<0.05],and the level of p-38 significantly decreased[0.48±0.04,0.63±0.06 vs 1.25±0.12,all P<0.05].Conclusion CTs may inhibit the apoptosis of neuronal cells and improve neurological function in CIRI rats by inhibiting the phosphorylation of JNK/p38 MAPK.
Keywords:cryptotanshinone  cerebral ischemia-reperfusion  oxygen glucose deprivation/reoxygenation injury  c-Jun N-terminal kinase/p38 mitogen-activated protein kinase
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