黄蜀葵花总黄酮对海马神经元缺氧复氧损伤的保护作用  被引量:1

Protective effect of total flavones of abelmoschl manihot on hippocampal neurons subjected to anoxia-reoxygenation injury

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作  者:文继月[1] 陈志武[1] WEN Jiyue CHEN Zhiwu(Department of Pharmacology, Anhui Medical University, Hefei 230032, Anhui, Chin)

机构地区:[1]安徽医科大学,基础医学院药理学教研室,安徽合肥230032

出  处:《中国临床药理学与治疗学》2017年第4期367-372,共6页Chinese Journal of Clinical Pharmacology and Therapeutics

基  金:国家自然科学基金(81173596)

摘  要:目的:研究黄蜀葵花总黄酮(total flavones of abelmoschl manihot,TFA)对海马神经元缺氧复氧损伤的保护作用以及可能的内皮衍生超级化因子(endothelium-dependent hyperpolarizing factor,EDHF)相关机制。方法:采用原代培养的海马神经元建立缺氧4 h/复氧24 h损伤模型,预先在细胞培养上清内加入大鼠脑基底环动脉(basilar artery,BA)环,分别给予乙酰胆碱(acetylcholine,Ach)联合一氧化氮(nitric oxide,NO)合酶抑制剂Nω-nitro-L-arginine-methyl-ester(L-NAME)和前列环素(prostacyclin,PGI2)抑制剂indomethacin(Indo);TFA联合L-NAME和Indo预处理。检测缺氧/复氧损伤后海马神经元存活率、培养上清液中乳酸脱氢酶(lactate dehydrogenase,LDH)活力的变化;另外,用激光共聚焦法检测细胞内游离Ca^(2+)浓度。结果:与单独应用Ach或者TFA预处理比较,Ach或者TFA联合脑基底动脉环均能明显改善缺氧/复氧后海马神经元存活率的降低,培养上清中LDH活力降低。此外,TFA联合脑基底动脉环抑制海马神经元细胞内游离Ca^(2+)的增高,L-NAME及Indo对此结果并无显著影响。结论:TFA对缺氧/复氧致海马神经元损伤有明显的保护作用,其机制可能与促进EDHF释放,抑制细胞内Ca^(2+)超载有关。AIM: To study the protective effect of total flavones of abelmoschl manihot (TFA) on hippocampal neurons subjected to the injury of anox- ia/re-oxygenation (A/R) and its endothelium-de- pendent hyperpolarizing factor (EDHF) mechanism. METHODS: The injury of primarily cultured hipp- ocampal neurons plus with cerebral basilar artery ring was induced by hypoxia for 4 hours and re-oxy- genation for 24 hours, pretreated with TFA, acetyl- choline ( Ach ) , dehydrogenase ( served as the ce etc. Cell viability and the lactate LDH) activity in 11 damage index. supernatant were The level of free calcium fluorescence intensity in the neurons was detected by laser scanning confocal microscope. RE- SULTS: Pretreated with TFA and cerebral artery could increase the cell viability, reduce the activity of LDH in culture medium significantly, pretreated with Ach had a similiar effect. The N -nitro-L-argi- nine-methyl-ester ( L-NAME ) and indomethacin (Indo) didn -t influence the effect of Ach or TFA. Moreover, pretreated with TFA plus with cerebral artery lowered the calcium concentration in neuron (compared with model group ). CONCLUSION: TFA has remarkably neuroprotective effect induced by A/R, the mechanism is partially concerned with the calcium overload inhibited by EDHF released from cerebral basilar artery ring.

关 键 词:黄蜀葵花总黄酮 内皮衍生超级化因子 缺氧/复氧损伤 乳酸脱氢酶 钙超载 

分 类 号:R965.2[医药卫生—药理学]

 

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