基础医学与临床
基礎醫學與臨床
기출의학여림상
Basic & Clinical Medicine
2015年
9期
1171-1175
,共5页
李开济%郝晓方%章广玲%魏洁%林雅军%魏静波%甄永占
李開濟%郝曉方%章廣玲%魏潔%林雅軍%魏靜波%甄永佔
리개제%학효방%장엄령%위길%림아군%위정파%견영점
赖氨大黄酸%百草枯%心脏损伤%活性氧自由基
賴氨大黃痠%百草枯%心髒損傷%活性氧自由基
뢰안대황산%백초고%심장손상%활성양자유기
rhein lysinate%paraquat%cardiac injury%reactive oxygen species
目的:观察赖氨大黄酸( RHL)对百草枯中毒小鼠心脏损伤的保护作用及其机制。方法小鼠随机分为对照组、百草枯模型组(腹腔注射百草枯建立活性氧自由基引起心脏损伤的小鼠模型)及RHL治疗组(造模前1周给予RHL(50 mg/kg)。用硫代巴比妥酸法检测心脏组织MDA含量,用联苯三酚自氧化法检测SOD活性,用NADPH偶联法检测GSH-Px活性。 HE染色及DCFH-DA染色分别观察心脏病理改变及活性氧水平;Western blot 检测心肌衰老相关基因的表达。结果与对照组相比,百草枯模型组小鼠心脏组织SOD和GSH-Px活性下降( P<0.05),MDA水平升高( P<0.05),RHL能减轻百草枯的作用( P<0.05);百草枯引起心肌结构破坏,心肌组织活性氧水平升高, RHL减轻上述变化( P<0.05)。百草枯能够降低SIRT1的表达,增加P53的乙酰化及P53和P66的表达。 RHL减轻上述变化( P<0.05)。结论 RHL可以减轻百草枯中毒后所致的小鼠心脏损伤。
目的:觀察賴氨大黃痠( RHL)對百草枯中毒小鼠心髒損傷的保護作用及其機製。方法小鼠隨機分為對照組、百草枯模型組(腹腔註射百草枯建立活性氧自由基引起心髒損傷的小鼠模型)及RHL治療組(造模前1週給予RHL(50 mg/kg)。用硫代巴比妥痠法檢測心髒組織MDA含量,用聯苯三酚自氧化法檢測SOD活性,用NADPH偶聯法檢測GSH-Px活性。 HE染色及DCFH-DA染色分彆觀察心髒病理改變及活性氧水平;Western blot 檢測心肌衰老相關基因的錶達。結果與對照組相比,百草枯模型組小鼠心髒組織SOD和GSH-Px活性下降( P<0.05),MDA水平升高( P<0.05),RHL能減輕百草枯的作用( P<0.05);百草枯引起心肌結構破壞,心肌組織活性氧水平升高, RHL減輕上述變化( P<0.05)。百草枯能夠降低SIRT1的錶達,增加P53的乙酰化及P53和P66的錶達。 RHL減輕上述變化( P<0.05)。結論 RHL可以減輕百草枯中毒後所緻的小鼠心髒損傷。
목적:관찰뢰안대황산( RHL)대백초고중독소서심장손상적보호작용급기궤제。방법소서수궤분위대조조、백초고모형조(복강주사백초고건립활성양자유기인기심장손상적소서모형)급RHL치료조(조모전1주급여RHL(50 mg/kg)。용류대파비타산법검측심장조직MDA함량,용련분삼분자양화법검측SOD활성,용NADPH우련법검측GSH-Px활성。 HE염색급DCFH-DA염색분별관찰심장병리개변급활성양수평;Western blot 검측심기쇠로상관기인적표체。결과여대조조상비,백초고모형조소서심장조직SOD화GSH-Px활성하강( P<0.05),MDA수평승고( P<0.05),RHL능감경백초고적작용( P<0.05);백초고인기심기결구파배,심기조직활성양수평승고, RHL감경상술변화( P<0.05)。백초고능구강저SIRT1적표체,증가P53적을선화급P53화P66적표체。 RHL감경상술변화( P<0.05)。결론 RHL가이감경백초고중독후소치적소서심장손상。
Objective To investigate the protective effects of rhein lysinate ( RHL) on cardiac tissue damage in-duced by paraquat in experimental mice , and to clarify its mechanism .Methods In this study mice were assigned to the following three groups: control, paraquat model, and RHL-treated groups.The model of oxidative damage mice was established by intraperitoneal injection of paraquat .RHL-treated group was given RHL ( 50 mg/kg ) by gavage for one week before performing model .The other two groups were given equal volume of distilled water .For making model , paraquat was intraperitoneally injected in the paraquat model and RHL-treated group .The content of MDA was detected by thiobarbituric acid assay .The activities of SOD and GSH-Px were detected by biphenyl three phenolic autoxidation assay and NADPH coupling method respectivly .The pathological profile of cardiac tis-sue was observed by hematoxylin and eosin ( HE) staining and reactive oxygen species was observed by DCFH-DA staining .The change of proteins related to myocardial damage detected by Western blot .Results Compared with control group, the activities of SOD and GSH-Px decreased (P<0.05) and the content of MDA increased (P<0.05) in paraquat model group .However , these changes were attenuated byr RHL treatmen ( P<0.05 ) .The pathologi-cal examination indicated the structure of cardiac tissue was damaged and reactive oxygen species of cardiac tissue was increased after paraquat was given , however , these changes were attenuated after RHL treatmen .It was shown in western blot analysis that compared with control group , the expression of SIRT1 decreased, the acetylation of P53 and the expression of P 53 and P66 increased in paraquat-treated group .These changes were attenuated by RHL treatmen ( P<0.05 ) .Conclusions RHL may attenuate paraquat-induced cardiac injury in mice .