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时间:2020-06-03
《灯盏花素调控MICA基因表达对人肾小管上皮细胞缺氧再给氧损伤的保护作用.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、免疫学杂志2014年8月第30卷第8期IMMUN0L0GICALJOURNALVo1.30No.8Aug.2014·691··论著·【文章~]1000-8861(2014)08-0691-04;[DOI]10.13431/j.enki.immuno1.j.20140151灯盏花素调控MICA基因表达对人肾小管上皮细胞缺氧再给氧损伤的保护作用罗蕾,李震宇△,罗光恒,夏曼,盛长城,胡誉怀,方茜【摘要】目的观察灯盏花素提取液对人肾小管细胞(HK一2)缺氧再给氧(hypoxia/re—oxygenation
2、,H/R)损伤的保护作用,探讨其可能的治疗作用及保护机理。方法建立HK一2体外H/R损伤模型。随机分为3组:对照组、缺氧组、灯盏花素组(灯盏花素预处理+缺氧)。在缺氧16h后设立4个时间点:复氧0、4、8、16h。倒置显微镜下观察细胞的形态学改变,荧光定量和流式检测各组HK一2MICA分子和蛋白水平的表达,乳酸脱氢酶释放法测定NK细胞对HK一2的杀伤能力。结果与对照组相比,缺氧组HK一2细胞MICA转录水平和蛋白表达水平在缺氧16h后显著升高,于复氧8h达峰值后逐渐下降,并于复氧16h后恢复正常。N
3、K细胞对H/R处理的HK一2细胞的杀伤活性与MICA的表达变化呈正相关。与缺氧组相比,灯盏花素组显著降低H/R处理的HK一2细胞MICA的表达和NK细胞对其的杀伤活性。结论在IRI过程中,下调H/R处理的HK一2细胞的MICA,从而抑制NK细胞对其的杀伤活性,可能是灯盏花素抗氧化应激和增强抗氧化防御功能的有效机制之一。[关键词】人肾小管上皮细胞;缺氧再给氧;灯盏花素;NK细胞毒实验[中图分类号】R392.5[文献标识码】A.Theprotectiveeffectsofbreviscapineonhu
4、manrenalproximaltubularepithelialcellsduringhypoxia/re-oxygenationinjuryviaregulatingMICAexpressionLUOLei,LIZhengyu,LUOGuangheng,XIAMin,SHENGChangcheng,HUYuhuai,FANGQianDivisionofScienceandEducation,People’SHospitalofGuizhouProvince,Guiyang550002,China
5、CorrespondingAuthor:FANGQian,E-mail:969824080@qq.conATheseauthorscontributedequallytothisworkandsharefirstauthorship[Abstract]Thisstudydesignedtoinvestigatetheprotectiveroleofbreviscapineonhumanrenalproximaltubularepithelialcells(HK-2)anditsrelativemec
6、hanismduringhypoxia/re-oxygenation(H/R).Firstly,ischemia/reperfusion(I/R)injury(IRI)wasmimickedthroughestablishingaHRmodelofHK-2cellsinvitro.HK一2cellswererandomlydividedintothreegroups:control,H/Rgroupandbreviscapinetreatedgroup(breviscapinepretreatmen
7、t+H/R).Sixteenhoursafterhypoxia,HK一2cellswerereoxygenatedfor0,4,8,16hrespectivelyundernormalcondition.QuantitativerealtimePCRandflowcytometryindicatedthatH/RsignificantlyincreasedthelevelsofMICAmRNAandproteinlevelsonHK-2,whilelactatedehydrogenase(LDH)r
8、eleaseassaydemonstratedthatH/RenhancedNKcellcytotoxicactivitytowardsHK-2.AdministrationofbreviscapinesignificantlyreducedthemRNAandproteinlevelsofMICAinI/RHK-2,andthensignificantlydecreasetheNKcellcytotoxicityactivity.Thus,weconcludedth
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