中华老年医学杂志
中華老年醫學雜誌
중화노년의학잡지
Chinese Journal of Geriatrics
2009年
11期
955-958
,共4页
杨明%石艳清%施晓芸%陈晓春
楊明%石豔清%施曉蕓%陳曉春
양명%석염청%시효예%진효춘
肝%衰老%病理学%氧化性应激%模型%动物
肝%衰老%病理學%氧化性應激%模型%動物
간%쇠로%병이학%양화성응격%모형%동물
Liver%Aging%Pathology%Oxidative stress%Models%animal
目的 评价快速老化小鼠P8(SAMP8)作为肝脏衰老动物模型的可行性,并探讨氧化应激在SAMP8肝脏衰老过程的作用机制. 方法 选择9月龄雄性SAMP8为研究对象,抗快速老化小鼠R1亚系(SAMRl)为模型对照,采用苏木精-伊红(HE)、苏丹Ⅳ和Masson染色观察两组小鼠肝脏的组织病理学改变,组织化学染色法测定肝脏衰老相关β-半乳糖苷酶活性,化学比色法测定肝组织匀浆中丙二醛(MDA)含量及超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)的活性. 结果与SAMR1组比较,SAMP8组肝组织出现肝细胞广泛的脂肪变性、局灶性坏死及炎性细胞浸润等退行性改变,衰老相关β-半乳糖苷酶染色阳性细胞明显增多(SAMP8组为78.1±11.0,SAMR1组为23.9±8.8,t=10.887,P<0.01),SOD、CAT、GSH-Px活力明显降低(SOD:SAMP8组为214.8±34.8,SAMR1组为295.3±29.7,t=4.975,P<0.01;CAT:SAMP8组为23.0±4.0,SAMR1组为36.3±8.3,t=4.084,P<0.01;GSH-Px:SAMP8组为524.0±74.2,SAMR1组为648.4±102.8,t=2.776,P<0.05),MDA含量明显增高(SAMP8组为2.3±0.2,SAMR1组为1.8±0.1,t=6.329,P<0.01). 结论 SAMP8小鼠可作为研究肝脏衰老的动物模型,氧化应激在SAMP8肝脏衰老过程中可能起重要作用.
目的 評價快速老化小鼠P8(SAMP8)作為肝髒衰老動物模型的可行性,併探討氧化應激在SAMP8肝髒衰老過程的作用機製. 方法 選擇9月齡雄性SAMP8為研究對象,抗快速老化小鼠R1亞繫(SAMRl)為模型對照,採用囌木精-伊紅(HE)、囌丹Ⅳ和Masson染色觀察兩組小鼠肝髒的組織病理學改變,組織化學染色法測定肝髒衰老相關β-半乳糖苷酶活性,化學比色法測定肝組織勻漿中丙二醛(MDA)含量及超氧化物歧化酶(SOD)、過氧化氫酶(CAT)、穀胱甘肽過氧化物酶(GSH-Px)的活性. 結果與SAMR1組比較,SAMP8組肝組織齣現肝細胞廣汎的脂肪變性、跼竈性壞死及炎性細胞浸潤等退行性改變,衰老相關β-半乳糖苷酶染色暘性細胞明顯增多(SAMP8組為78.1±11.0,SAMR1組為23.9±8.8,t=10.887,P<0.01),SOD、CAT、GSH-Px活力明顯降低(SOD:SAMP8組為214.8±34.8,SAMR1組為295.3±29.7,t=4.975,P<0.01;CAT:SAMP8組為23.0±4.0,SAMR1組為36.3±8.3,t=4.084,P<0.01;GSH-Px:SAMP8組為524.0±74.2,SAMR1組為648.4±102.8,t=2.776,P<0.05),MDA含量明顯增高(SAMP8組為2.3±0.2,SAMR1組為1.8±0.1,t=6.329,P<0.01). 結論 SAMP8小鼠可作為研究肝髒衰老的動物模型,氧化應激在SAMP8肝髒衰老過程中可能起重要作用.
목적 평개쾌속노화소서P8(SAMP8)작위간장쇠로동물모형적가행성,병탐토양화응격재SAMP8간장쇠로과정적작용궤제. 방법 선택9월령웅성SAMP8위연구대상,항쾌속노화소서R1아계(SAMRl)위모형대조,채용소목정-이홍(HE)、소단Ⅳ화Masson염색관찰량조소서간장적조직병이학개변,조직화학염색법측정간장쇠로상관β-반유당감매활성,화학비색법측정간조직균장중병이철(MDA)함량급초양화물기화매(SOD)、과양화경매(CAT)、곡광감태과양화물매(GSH-Px)적활성. 결과여SAMR1조비교,SAMP8조간조직출현간세포엄범적지방변성、국조성배사급염성세포침윤등퇴행성개변,쇠로상관β-반유당감매염색양성세포명현증다(SAMP8조위78.1±11.0,SAMR1조위23.9±8.8,t=10.887,P<0.01),SOD、CAT、GSH-Px활력명현강저(SOD:SAMP8조위214.8±34.8,SAMR1조위295.3±29.7,t=4.975,P<0.01;CAT:SAMP8조위23.0±4.0,SAMR1조위36.3±8.3,t=4.084,P<0.01;GSH-Px:SAMP8조위524.0±74.2,SAMR1조위648.4±102.8,t=2.776,P<0.05),MDA함량명현증고(SAMP8조위2.3±0.2,SAMR1조위1.8±0.1,t=6.329,P<0.01). 결론 SAMP8소서가작위연구간장쇠로적동물모형,양화응격재SAMP8간장쇠로과정중가능기중요작용.
Objective To evaluate the feasibility of liver senescence model with senescence accelerated mouse prone 8 (SAMP8), and to explore the possible mechanism of oxidative stress in the process of liver aging in SAMP8. Methods Male SAMP8 mice at the age of 9 months were chosen as research objects, and senescence accelerated mouse resistance 1 (SAMR1) mice were used for normal control. Histopathological changes in the liver of SAMR1 and SAMP8 mice were observed by hematoxylin-eosin (HE), Sudan Ⅳ and Masson staining. Senescence associated β-galactosidase activity was measured by histoehemical staining method, and the activities of superoxide dismutase (SOD), eatalase (CAT), glutathione peroxidase (GSH-Px) and the level of malondialdehyde (MDA) in liver homogenate were examined by chemical colorimetry. Results Compared with SAMR1 group, the liver degenerative changes of SAMP8 mice were observed by microscopy, such as extensive fatty degeneration, focal necrosis of hepatocytes and inflammatory cells infiltration. Meanwhile, senescence associated β-galactosidase-positive cells were significantly increased in SAMP8 group [(78.1±11.0) vs.( 23.9±8.8),t=10.887, P<0.01]. In addition, the activities of SOD, CAT and GSH-Px in liver homogenate were decreased [SOD: (214.8 ± 34.8) vs. ( 295.3 ± 29.7), t = 4.975,P<0.01;CAT: (23.0±4.0) vs. ( 36.3±8.3),t=4.084,P<0.01;GSH-Px: (524.0±74.2) vs. (648. 4±102.8) ,t=2. 776, P<0. 05]and the level of MDA was markedly increased ((2.3±0.2) vs. (1.8±0. 1),t = 6. 329, P<0. 01]. Conclusions SAMP8 mice is a feasible animal model for the study of liver senescence, and oxidative stress may play an important role in the process of liver aging in SAMP8.
