军事医学
軍事醫學
군사의학
BULLETIN OF THE ACADEMY OF MILITARY MEDICAL SCIENCES
2014年
12期
952-956
,共5页
李泽君%呼丹%熊克朝%刘悦%樊星%吴纯启%丁日高%王茜莎%王全军
李澤君%呼丹%熊剋朝%劉悅%樊星%吳純啟%丁日高%王茜莎%王全軍
리택군%호단%웅극조%류열%번성%오순계%정일고%왕천사%왕전군
白藜芦醇%曲格列酮%活性氧%抗氧化%抗氧化物酶
白藜蘆醇%麯格列酮%活性氧%抗氧化%抗氧化物酶
백려호순%곡격렬동%활성양%항양화%항양화물매
resveratrol%troglitazone%reactive oxygen species%antioxidant%antioxidant enzymes
目的:探讨白藜芦醇对曲格列酮诱发HepaRG细胞氧化损伤的影响及可能作用机制。方法实验分组包括:正常对照组(含有0.1%DMSO的RPMI 1640培养基)、50μmol/L曲格列酮组、白藜芦醇3种浓度(3.75,7.5,15μmol/L)与50μmol/L曲格列酮的共处理组。 MTT法检测曲格列酮、白藜芦醇以及白藜芦醇与50μmol/L曲格列酮共同作用对HepaRG细胞的增殖抑制作用。以上各组作用48 h后检测各组细胞内活性氧( reactive oxygen spe-cies, ROS)的含量,脂质过氧化( lipid peroxidation )和细胞凋亡程度,细胞的总抗氧化能力,以及细胞内过氧化氢酶(catalase, CAT)、谷胱甘肽过氧化物酶(glutathione peroxidase, GSH-px)、超氧化物歧化酶(superoxide dismutase, SOD)的活性。结果曲格列酮能明显导致HepaRG细胞产生氧化应激现象。与正常对照组相比,曲格列酮处理组ROS和脂质过氧化产物丙二醛(malondialdehyde,MDA)水平以及细胞凋亡和坏死率均显著升高(P<0.05),总抗氧化能力大幅降低(P<0.05),CAT、GSH-px、SOD的活性均降低(P<0.05)。加入不同浓度白藜芦醇共同作用后, ROS和MDA生成量有所下降(P<0.05),细胞凋亡和坏死率也相应下降(P<0.05),细胞总抗氧化能力以及以上3种抗氧化物酶的活性均有所提高(P<0.05),且有一定的剂量依赖关系。结论曲格列酮能引起HepaRG细胞产生明显的氧化应激作用,白藜芦醇能够显著改善由曲格列酮对 HepaRG细胞所造成的氧化损伤。
目的:探討白藜蘆醇對麯格列酮誘髮HepaRG細胞氧化損傷的影響及可能作用機製。方法實驗分組包括:正常對照組(含有0.1%DMSO的RPMI 1640培養基)、50μmol/L麯格列酮組、白藜蘆醇3種濃度(3.75,7.5,15μmol/L)與50μmol/L麯格列酮的共處理組。 MTT法檢測麯格列酮、白藜蘆醇以及白藜蘆醇與50μmol/L麯格列酮共同作用對HepaRG細胞的增殖抑製作用。以上各組作用48 h後檢測各組細胞內活性氧( reactive oxygen spe-cies, ROS)的含量,脂質過氧化( lipid peroxidation )和細胞凋亡程度,細胞的總抗氧化能力,以及細胞內過氧化氫酶(catalase, CAT)、穀胱甘肽過氧化物酶(glutathione peroxidase, GSH-px)、超氧化物歧化酶(superoxide dismutase, SOD)的活性。結果麯格列酮能明顯導緻HepaRG細胞產生氧化應激現象。與正常對照組相比,麯格列酮處理組ROS和脂質過氧化產物丙二醛(malondialdehyde,MDA)水平以及細胞凋亡和壞死率均顯著升高(P<0.05),總抗氧化能力大幅降低(P<0.05),CAT、GSH-px、SOD的活性均降低(P<0.05)。加入不同濃度白藜蘆醇共同作用後, ROS和MDA生成量有所下降(P<0.05),細胞凋亡和壞死率也相應下降(P<0.05),細胞總抗氧化能力以及以上3種抗氧化物酶的活性均有所提高(P<0.05),且有一定的劑量依賴關繫。結論麯格列酮能引起HepaRG細胞產生明顯的氧化應激作用,白藜蘆醇能夠顯著改善由麯格列酮對 HepaRG細胞所造成的氧化損傷。
목적:탐토백려호순대곡격렬동유발HepaRG세포양화손상적영향급가능작용궤제。방법실험분조포괄:정상대조조(함유0.1%DMSO적RPMI 1640배양기)、50μmol/L곡격렬동조、백려호순3충농도(3.75,7.5,15μmol/L)여50μmol/L곡격렬동적공처리조。 MTT법검측곡격렬동、백려호순이급백려호순여50μmol/L곡격렬동공동작용대HepaRG세포적증식억제작용。이상각조작용48 h후검측각조세포내활성양( reactive oxygen spe-cies, ROS)적함량,지질과양화( lipid peroxidation )화세포조망정도,세포적총항양화능력,이급세포내과양화경매(catalase, CAT)、곡광감태과양화물매(glutathione peroxidase, GSH-px)、초양화물기화매(superoxide dismutase, SOD)적활성。결과곡격렬동능명현도치HepaRG세포산생양화응격현상。여정상대조조상비,곡격렬동처리조ROS화지질과양화산물병이철(malondialdehyde,MDA)수평이급세포조망화배사솔균현저승고(P<0.05),총항양화능력대폭강저(P<0.05),CAT、GSH-px、SOD적활성균강저(P<0.05)。가입불동농도백려호순공동작용후, ROS화MDA생성량유소하강(P<0.05),세포조망화배사솔야상응하강(P<0.05),세포총항양화능력이급이상3충항양화물매적활성균유소제고(P<0.05),차유일정적제량의뢰관계。결론곡격렬동능인기HepaRG세포산생명현적양화응격작용,백려호순능구현저개선유곡격렬동대 HepaRG세포소조성적양화손상。
Objective To explore the effect of resveratrol ( Rev) as an antioxidant on oxidative damage to HepaRG cells induced by troglitazone ( Tro).Methods Cells were divided into five groups: control ( RPMI 1640 only with 0.1%DMSO), Tro(50 μmol/L), Tro(50 μmol/L) +Rev(15 μmol/L), Tro(50 μmol/L) +Rev(7.5 μmol/L) and Tro (50 μmol/L)+Rev(3.75 μmol/L) groups.MTT assay was performed to detect the viability of Rev-treated, Tro-treated and Rev with 50 μmol/L Tro-treated HepaRG cells.After 48 hours, the level of reactive oxygen species (ROS) and lipid oxidation ( malondialdehyde , MDA ) , degree of apoptosis , total antioxidant capacity , activity of hydrogenperoxidase (catalase, CAT), glutathione peroxidase (GSH-px) and superoxide dismutase(SOD)of these groups were identified. Results Tro could obviously cause HepaRG cells to produce oxidative stress .Compared with control group ,ROS and lipid peroxidation ( MDA) levels and the rate of apoptosis and necrosis in Tro-treated group were significantly increased ( P<0.05),total antioxidant capacity greatly reduced (P<0.05),and the activity of CAT,GSH-px and SOD was decreased (P<0.05).After adding various concentrations of Rev interaction , ROS and MDA production volume decreased (P < 0.05), and the apoptosis and necrosis rate correspondingly declined (P<0.05).Total antioxidant capacity of the cells and the activity of the three antioxidant enzymes were increased (P<0.05), and there was a dose-dependent relationship. Conclusion Tro can cause HepaRG cells to produce significant oxidative stress while Rev can significantly improve the oxidative damage of Tro to HepaRG cells .