大蒜素对6－羟多巴胺所致 PC12细胞损伤的保护作用及机制.pdf

《大蒜素对6－羟多巴胺所致 PC12细胞损伤的保护作用及机制.pdf》由会员上传分享，免费在线阅读，更多相关内容在行业资料-天天文库。

1、·208·中华神经外科疾病研究杂志(ChinJNeurosurgDisRes)2015；14(3文章编号：1671—2897(2015)14—208—05·神经损伤研究·大蒜素对6一羟多巴胺所致PC12细胞损伤的保护作用及机制杨军岭杨侠(解放军323医院药剂科，陕西西安710054；陕西省人民医院医务处，陕西西安710068)摘要目的研究大蒜素对6．羟多巴胺(6-hydroxydopamine，6-OHDA)引起的PC12细胞损害的保护作用和相关机制。方法使用6-OHDA在PC12细胞建立损伤模型，细胞活力、乳酸脱氢酶

2、(1actatedehydrogenase，LDH)释放和细胞凋亡检测被用于观察大蒜素的保护作用，氧自由基(reactiveoxygenspecies，ROS)和内源性抗氧化酶活性被用于检测其抗氧化活性，蛋白免疫印迹用于检测大电导、钙离子激活的钾离子通道(Large—conductanceCa“-activatedKchannels，BK)蛋白表达并研究可能的相关机制。结果①大蒜素显著减轻6-OHDA所致的细胞活力下降和LDH释放，并抑制细胞凋亡。②大蒜素显著抑制6-OHDA所致的ROS产生和丙二醛(malondial

3、dehyde，MDA)升高，并增加内源性抗氧化酶的活性。③大蒜素显著增加BK蛋白表达，使用BK阻滞剂paxilline可部分逆转大蒜素的保护作用。结论大蒜素通过激活BK和抗氧化机制对6-OHDA损伤的PC12细胞发挥保护作用。关键词大蒜素；氧化应激；PC12细胞；6-羟多巴胺；BK通道中国图书资料分类号R446R446．1文献标识码AProteelionofallidnonPC12ceilsuryinducedby5．0HDAinvitroYANGJunling．YANGDepartmentof∞砌，323凰删of蹦，

4、皿锄71(I)54；D／v／s／onofMedicalAfairs，SbaanxiProvincialPeoplesHospital，施710068，ChinaAl~raetObjectiveTheprotectionofallicinonPC12ceUsinjuryinducedby6-hydroxydopamine(6一OHDA)andthepossibleunderlyingmechanismareinvestigated．MethodsTheinjurymodelofPC12ceHswereestablishe

5、dbyusing6-OI-IDAandtheprotectiveefectsofallieinwerea．~sessedbycellviability，lactatedehydrogenase(LDH)releaseandapoptosisanalysis．Theintracellularreactiveoxygenspecies(ROS)generationandendogenousantioxidativeenzymeactivitiesweremeasuredtodetermineitsanti—oxidativ

6、eactivities．Westernblotanalysiswasusedtodetecttheexpressionoflarge—conductanceCa=一activatedKchannels(BK)proteinandtoinvestigateitsroleintheprotectionofallicin．ResultsAlicinsigniticanflyattenuated5．0HDA—induceddecreaseofcelviability，inhibitedLDHreleaseandreduceda

7、poptoticcelldeathinPC12cels．Alicinsignificantlyattenuated6一OHDA-inducedROSandmalondialdehyde(MDA)gener~ion，andpreservedendogenousantioxidativeenzymeactivities．AndallicinalsosignificantlyincreasedtheexpressionofBKchannels，andthepretreatmentwithBKantagonistpaxilin

8、epartiallyreservedtheprotectiveefectsofallicin．ConclusionAllicinprotectsPC12eelsagainst6-OHDA—inducedcytotoxicitythroughtheactivationofBKchannelsanditsanti—oxidativea