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Role of chloride channels in nitric oxide-induced rat hippocampal neuronal apoptosis in vitro

Neural Regeneration Research 2010年第9期5卷 690-694页

作者： quanzhong chang shuling zhang jinbao yin Department of Physiology Zhuhai Campus of Zunyi Medical College Zhuhai 519041 Guangdong Province China

BACKGROUND：Chloride channels participate in non-neuronal ***,it remains unclear whether chloride channels are involved in ischemic neuronal ***：To explore the effects of 4-acetamido-4＇-isothiocyanatostilbene-2,2＇-disulfonic acid （SITS） and 4,4＇-diisothiocyanostilbene-2,2＇-disulfonic acid （DIDS）,two chloride channel blockers,on the hippocampal neuronal apoptosis induced by 3-morpholinosydnonimine （SIN-1） based on the nitric oxide toxicity theory of neuronal apoptosis following ischemic brain ***,TIME AND SETTING：Comparative observation and in vitro experiments were performed at the laboratory of Zhuhai Campus of Zunyi Medical College from January to May ***：SIN-1,SITS,and DIDS were purchased from Sigma,***：Hippocampal neurons from Sprague-Dawley rats,aged 1 day,were cultured In vitro for 12 days and randomly assigned to control,SIN-1,or chloride channel blocker ***-1 group neurons were induced by SIN-1 for 18 hours to establish a model of ischemic neuronal *** in chloride channel blocker groups were treated with SITS or DIDS plus SIN-1 for 18 *** controls were cultured in DMEM/Ham＇s F12 complete medium *** OUTCOME MEASURES：The apoptotic neurons and nuclear appearance were detected by Hoechst 33258 fluorescence staining; neuronal viability was quantitatively determined by 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide ***-3 activity was analyzed by Western ***：SIN-1 （1 mmol/L） dramatically induced apoptosis （50%-60%）.SITS and DIDS inhibited nitric oxide-induced neuronal injury in a dose-dependent manner,suppressed caspase-3 activation,reduced neuronal apoptosis,and improved neuronal ***：Chloride channel blockers can protect against neuronal injury induced by *** channels might be involved in neuronal apoptosis following cerebral ischemia.

关键词： chloride channel nitric oxide hippocampal neuron rats cerebral ischemia neural regeneration

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Effects of calcium channel on 3-morpholinosydnonimine-induced rat hippocampal neuronal apoptosis

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Neural Regeneration Research 2011年第5期6卷 373-377页

作者： quanzhong chang shuling zhang Yuanyin Zheng Lijuan Xu jinbao yin Shining Cai Department of Physiology Zhuhai Campus of Zunyi Medical College Zhuhai 519041 Guangdong Province China Department of Pediatrics Zh uhai Campus of Zunyi Medical College Zhuhai 519041 Guangdong Pro vince China

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 CdCI2 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＇-diisethiocyanostilbene-2, 2＇-disulfonic acid （DIDS） increased the survival rate of 3-morpholinosydnonimine （SIN-1）-treated neurons and suppressed SIN-l-induced neuronal apoptosis. The calcium channel blocker CdCI2 did not increase the survival rate of neurons and did not affect SIN-l-induced apoptosis or SITS- or DIDS-suppressed neuronal apoptosis. Results demonstrated that calcium channels did not significantly affect neuronal apoptosis.

关键词： calcium channel chloride channel 3-morpholinosydnonimine rats hippocampus

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Chloride channel blocker 4,4-diisothiocyanatostilbene-2,2'-disulfonic acid inhibits nitric oxide-induced apoptosis in cultured rat hippocampal neurons

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Neural Regeneration Research 2013年第2期8卷 121-126页

作者： jinbao yin Lijuan Xu shuling zhang Yuanyin Zheng Zhichao Zhong Hongling Fan XiLi quanzhong chang Department of Physiology Zhuhai Campus of Zunyi Medical College Department of Pathology Dongguan Campus of Guangdong Medical College

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.

关键词： neural regeneration brain injury chloride channel 3-morpholinosydnonimine hippocampus poly(adenosine diphosphate-ribose)polymerase-1 apoptosis inducing factor neuronal apoptosis grants-supported paper photographs-containing paper neuroregeneration

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ClC-3 chloride channel in hippocampal neuronal apoptosis

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Neural Regeneration Research 2013年第32期8卷 3047-3054页

作者： Lijuan Xu shuling zhang Hongling Fan Zhichao Zhong Xi Li Xiaoxiao Jin quanzhong chang Department of Physiology Zhuhai Campus of Zunyi Medical College First Hospital of Putian City Department of Pediatrics Zhuhai Campus of Zunyi Medical College

Over-production of nitric oxide is pathogenic for neuronal apoptosis around the ischemic area fol- lowing ischemic brain injury. In this study, an apoptotic model in rat hippocampal neurons was es- tablished by 0.5 mmol/L 3-morpholinosyndnomine （SIN-l）, 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 immunochemilumi- nescence 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 CIC-3 chloride channel protein and mRNA expression in the apoptotic neurons. DIDS reversed the effect of SIN-I. Our findings indicate that the increased activities of the CIC-3 chloride channel may be involved in hippocampal neuronal apoptosis induced by nitric oxide.

关键词： neural regeneration brain injury nitric oxide CIC-3 chloride channel 3-morpholinosyndnomine 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid hippocampal neurons apoptosis grants-supportedpaper neuroregeneration

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Effects of minocycline on learning and memory of mice following ischemic-hypoxic cerebral injuries

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Neural Regeneration Research 2012年第2期7卷 114-118页

作者： Hongling Fan Yuanyin Zheng Lijuan Xu Zhichao Zhong Shining Cai shuling zhang quanzhong chang Department of Physiology Zhuhai Campus of Zunyi Medical College Zhuhai 519041 Guangdong Province China

An ischemic-hypoxic animal model was established using right common carotid artery occlusions and inhalation of low concentrations of oxygen in mice. At 10 days after the ischemic-hypoxic injuries, saline-treated mice exhibited significantly prolonged escape latencies in water-maze tests and significantly shorter memory latencies and more mistakes in step-down tests. In contrast, mice treated with 5 mg/kg minocycline exhibited significant reversals of each of these effects compared with the saline-treated control mice. Moreover, we found that minocycline can relieve brain water content and morphological changes in mice following ischemic-hypoxic cerebral injuries. Accordingly, our findings indicate that minocycline provides some protections against the deleterious effects of these injuries in mice.

关键词： minocycline ischemic-hypoxic cerebral injury learning and memory cognition

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沉默ClC-3氯通道基因对PC-12细胞凋亡的影响

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郑州大学学报（医学版） 2016年第1期51卷 59-63页

作者：吴琼张淑玲李曦林玲常全忠漯河医学高等专科学校基础部生理学教研室漯河462002 遵义医学院珠海校区生理学教研室珠海519041

目的:观察氯离子通道蛋白3(ClC-3)基因沉默对大鼠肾上腺嗜铬细胞瘤细胞PC-12凋亡的影响。方法:取处于对数生长期的PC-12细胞,随机分为4组:对照组(用正常培养基培养)、H_2O_2组(用300nmol/LH_2O_2诱导12h)、H_2O_2+空质粒组(细胞转染pGPU... 详细信息

目的:观察氯离子通道蛋白3(ClC-3)基因沉默对大鼠肾上腺嗜铬细胞瘤细胞PC-12凋亡的影响。方法:取处于对数生长期的PC-12细胞,随机分为4组:对照组(用正常培养基培养)、H_2O_2组(用300nmol/LH_2O_2诱导12h)、H_2O_2+空质粒组(细胞转染pGPU6/GFP24h后用H_2O_2诱导12h)、H_2O_2+siRNA组(细胞转染pGPU6/GFP-ClC-3-siRNA24h后用H_2O_2诱导12h)。通过CCK-8检测细胞存活率,流式细胞术检测细胞凋亡率,Westernblot法检测Caspase-3以及ClC-3蛋白的表达,实时荧光定量PCR检测ClC-3mRNA的表达。结果:与对照组比较,H_2O_2组、H_2O_2+空质粒组和H_2O_2+siRNA组均表现为细胞存活率下降,细胞凋亡增加,ClC-3mRNA和Caspase-3、ClC-3蛋白表达增加(P0.05);但与H_2O_2组、H_2O_2+空质粒组比较,H_2O_2+siRNA组细胞存活率较高,细胞凋亡率较低,ClC-3mRNA和Caspase-3、ClC-3蛋白表达较弱(P<0.05)。结论:ClC-3氯离子通道参与了H_2O_2诱导的PC-12细胞凋亡。

关键词： siRNA ClC-3 大鼠细胞凋亡

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