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| 1 | 新生大鼠离体海马神经元原代培养方法及鉴定显示文摘目的:建立一种稳定的生后大鼠离体海马神经元的培养方法。方法:无菌环境下将出生24 h内SD大鼠断头取脑分离海马,经消化后差速贴壁,采用无血清培养基进行培养,倒置显微镜下观察不同时间段细胞生长形态变化:采用Hoechst33258与NeuN抗体双染方法鉴定神经元。结果:采用差速贴壁后,使用无血清培养基培养的神经元生长良好,纯度较高,12 d时经鉴定神经元纯度可以达到92%以上。结论:差速离心法后可以采用无血清培养神经元,培养的神经元具有纯度高,结果稳定的优点,该方法为以后进行相关的研究奠定了基础。 | 尹金宝 常全忠 韩宇东 | 2012 | 神经解剖学杂志2012，28，6： | 9 |
| 2 | ClC-3 chloride channel in hippocampal neuronal apoptosis显示文摘Over-production of nitric oxide is pathogenic for neuronal apoptosis around the ischemic area following ischemic brain injury.In this study,an apoptotic model in rat hippocampal neurons was established by 0.5 mmol/L 3-morpholinosyndnomine(SIN-1),a nitric oxide donor.The models were then cultured with 0.1 mmol/L of 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid(DIDS;the chloride channel blocker) for 18 hours.Neuronal survival was detected using the 3-(4,5-dimethylthiazol- 2-yl)-2,5-diphenyltetrazolium bromide(MTT) assay,and apoptosis was assayed by Hoechst 33342-labeled neuronal DNA fluorescence staining.Western blot analysis and immunochemiluminescence staining were applied to determine the changes of activated caspase-3 and CIC-3 channel proteins.Real-time PCR was used to detect the mRNA expression of CIC-3.The results showed that SIN-1 reduced the neuronal survival rate,induced neuronal apoptosis,and promoted ClC-3 chloride channel protein and mRNA expression in the apoptotic neurons.DIDS reversed the effect of SIN-1.Our findings indicate that the increased activities of the ClC-3 chloride channel may be involved in hippocampal neuronal apoptosis induced by nitric oxide. | Lijuan Xu Shuling Zhang Hongling Fan Zhichao Zhong Xi Li Xiaoxiao Jin Quanzhong Chang | 2013 | Neural Regeneration Research2013，8，32： | 3 |
| 3 | DIDS对SIN-1诱导大鼠海马神经元凋亡及PARP-1/AIF表达的影响显示文摘目的观察氯通道阻断剂4,4'-二异硫氰基芪-2,2'-二磺酸(DIDS)对NO诱导的大鼠离体海马神经元凋亡的保护作用。方法离体培养12 d的SD大鼠海马神经元,随机分为正常对照组、3-吗啡斯德酮亚胺(3-morpholinosyndnomine,SIN-1)处理组、SIN-1+DIDS组。对各组神经元分别在相应的时间点用MTT法测定细胞生存率、Hoechst 33258测定凋亡百分数、免疫化学荧光分析检测凋亡信号蛋白PARP-1/AIF的变化、Western blot分析凋亡蛋白Caspase-3的变化。结果 DIDS呈剂量依赖性地抑制SIN-1诱导的神经元损伤,减少凋亡发生数目,并能抑制损伤所引起的Caspase-3的激活、削弱PARP-1/AIF的表达。结论氯通道可能参与了NO诱导的海马神经元损伤,氯通道阻断剂DIDS的保护作用可能与削弱PARP-1/AIF的表达有关。 | 李曦 尹金宝 钟志超 范洪领 许黎娟 郑原印 蔡仕宁 常全忠 | 2012 | 中国药理学通报2012，28，11： | 3 |
| 4 | 氯通道阻断剂DIDS对过氧化氢诱导PC12细胞凋亡的影响显示文摘目的:探讨氯通道阻断剂DIDS抗PC12细胞凋亡的作用机制。方法:取处于对数生长期的PC12细胞,随机分为对照组、模型组(用400 nmol/L H2O2诱导细胞凋亡)和DIDS组(H2O2+DIDS),培养12 h后,用MTT法测定各组细胞的存活率,Western blot法观察凋亡相关蛋白Caspase-3和Bcl-2蛋白的表达情况,用流式细胞仪检测细胞凋亡率。结果:400 nmol/L H2O2可以明显诱导PC12细胞损伤,细胞存活率为(35.07±1.23)%;DIDS组细胞存活率明显高于模型组,且具有一定浓度依赖性(F=640.420,P<0.001)。与对照组比较,模型组细胞凋亡率和Caspase-3蛋白表达增加,Bcl-2蛋白表达降低(P<0.05);与模型组相比,DIDS组Caspase-3表达降低,Bcl-2蛋白表达增加,细胞凋亡率降低(P<0.05)。结论:DIDS可能通过抑制Caspase-3依赖性凋亡信号通路发挥抗凋亡作用。 | 任京力 林玲 王雁梅 王福青 李超彦 蔡智慧 常全忠 | 2015 | 郑州大学学报(医学版)2015，50，1： | 3 |
| 5 | Chloride channel blocker 4,4-diisothiocyanatostilbene-2,2'-disulfonic acid inhibits nitric oxide-induced apoptosis in cultured rat hippocampal neurons显示文摘Apoptosis in cultured rat hippocampal neurons was induced using the nitric oxide donor 3-morpholinosydnonimine, and cells were treated with the chloride channel blocker, 4,4-diisothiocyanatostilbene-2,2'-disulfonic acid. Results showed that the survival rate of neurons was significantly increased after treatment with 4,4-diisothiocyanatostilbene-2,2'-disulfonic acid, and the rate of apoptosis decreased. In addition, the expression of the apoptosis-related proteins poly(adenosine diphosphate-ribose)polymerase-1 and apoptosis-inducing factor were significantly reduced. Our experimental findings indicate that the chloride channel blocker 4,4- diisothiocyanatostilbene-2,2'-disulfonic acid can antagonize apoptotic cell death of hippocampal neurons by inhibiting the expression of the apoptosis-related proteins poly(adenosine diphosphate-ribose)polymerase-1 and apoptosis-inducing factor. | Jinbao Yin Lijuan Xu Shuling Zhang Yuanyin Zheng Zhichao Zhong Hongling Fan XiLi Quanzhong Chang | 2013 | Neural Regeneration Research2013，8，2： | 2 |
| 6 | 侧脑室注射DIDS对缺血再灌注脑损伤大鼠神经元凋亡的拮抗作用显示文摘目的:观察侧脑室注射氯通道阻断剂DIDS对在体神经元凋亡的影响。方法:72只雄性SD大鼠随机分为假手术组、缺血再灌注(I/R)组、生理盐水组和DIDS组。除假手术组,余3组用线栓法建立大鼠局灶性缺血再灌注脑损伤模型。模型制备成功后生理盐水组和DIDS组分别立即通过侧脑室注射生理盐水和有效剂量的DIDS。72 h后TTC染色观察脑梗死灶面积,用HE染色观察脑组织形态学的变化,Western blot法观察海马CA1区活性Caspase-3的表达。结果:假手术组无脑梗死灶出现,海马CA1区神经元排列较好,胞体饱满,折光性较好;余3组脑梗死灶面积差异有统计学意义(F=4.778,P=0.025);I/R组和生理盐水组有明显的梗死灶出现,海马CA1区神经元排列错乱,水肿,间隙增宽;与I/R组和生理盐水组相比,DIDS组脑梗死面积缩小(P<0.05),组织形态明显改善。4组海马CA1区活性Caspase-3表达差异有统计学意义(F=166.700,P<0.001);假手术组有少量活性Caspase-3表达;I/R组和生理盐水组活性Caspase-3表达下降(P<0.05);与I/R组和生理盐水组相比,DIDS组活性Caspase-3表达降低(P<0.05)。结论:DIDS对在体神经元的凋亡有拮抗作用,对大鼠缺血再灌注脑损伤有保护作用。 | 任京力 吴琼 王兴红 李超彦 常全忠 | 2015 | 郑州大学学报(医学版)2015，50，2： | 2 |
| 7 | 银杏叶内酯N对PC12细胞凋亡的保护作用显示文摘目的探讨银杏内酯N对过氧化氢(H2O2)诱导的PC12细胞凋亡的保护作用。方法用H2O2诱导PC12细胞损伤,刺激其凋亡,给予不同剂量的受试药物干预。用MTT法检测细胞存活率;用吖啶橙染色检测银杏内酯N对PC12细胞凋亡的作用;用流式细胞术检测银杏内酯N对PC12细胞活性氧(ROS)的影响,荧光定量RT-PCR法、Western印迹法分别检测Bcl-2、Bax mRNA和相应蛋白的表达。结果银杏内酯N可对抗H2O2诱导的PC12损伤,提高存活率和抑制凋亡,降低PC12细胞ROS水平,与模型组比较均有显著差异(P<0.05);Bcl-2蛋白及mRNA表达量升高,而Bax mRNA和Bax蛋白及表达量降低,与模型组比较均有显著差异(P<0.05),且呈一定的量效关系。结论银杏内酯N可对抗H2O2的神经毒性,其机制与调节凋亡相关基因及蛋白的表达有关。 | 赵珍东 夏黎 张现涛 方春生 马建荣 汪小根 | 2017 | 中国老年学杂志2017，37，15： | 1 |
| 8 | 胚胎大鼠皮质神经元原代培养及神经元鉴定显示文摘目的对原有的胚胎大鼠神经细胞原代培养进行改进,建立一种高效、稳定的的原代培养方法。方法自精确控制胎龄的大鼠胚胎大脑中分离出皮质,采用胰酶二次消化法制备神经细胞悬液。并选用神经元特异性烯醇化酶免疫荧光化学法对神经细胞进行鉴定。结果与单次消化法分离细胞及运用DMEM+10%胎牛血清重悬细胞进行种板的原方法相比,方法改进以后,细胞提取数量明显增加,且纯度较高。种板后细胞形态正常且能长期存活。结论该方法结果理想,简易高效,值得借鉴和推广。 | 黄清霞 卢靖 张冬梅 王佳雯 王健 | 2016 | 中国实验诊断学2016，20，1： | 1 |
| 9 | Effects of calcium channel on 3-morpholinosydnonimine-induced rat hippocampal neuronal apoptosis显示文摘Previous studies have demonstrated that increased chloride channel activity plays a role in nitric oxide-induced neuronal apoptosis in the rat hippocampus. The present study investigated the effects of the broad-spectrum calcium channel blocker CdCl2 on survival rate, percentage of apoptosis, and morphological changes in hippocampal neurons cultured in vitro, as well as the effects of calcium channels on neuronal apoptosis. The chloride channel blockers 4-acetamido-4'-isothiocyanatostilbene-2, 2'-disulfonic acid (SITS) or 4, 4'-diisothiocyanostilbene-2, 2'-disulfonic acid (DIDS) increased the survival rate of 3-morpholinosydnonimine (SIN-1)-treated neurons and suppressed SIN-1-induced neuronal apoptosis. The calcium channel blocker CdCl2 did not increase the survival rate of neurons and did not affect SIN-1-induced apoptosis or SITS- or DIDS-suppressed neuronal apoptosis. Results demonstrated that calcium channels did not significantly affect neuronal apoptosis. | Quanzhong Chang Shuling Zhang Yuanyin Zheng Lijuan Xu Jinbao Yin Shining Cai | 2011 | Neural Regeneration Research2011，6，5： | 1 |
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