老年大鼠线粒体呼吸功能及氧应激水平与茶多酚

Effect of tea polyphenols on the mitochondria respiratory function and level of oxygen stress in aging rat

目的:研究茶多酚对老年大鼠心肌、肝脏线粒体呼吸控制率和氧应激水平的影响,探索茶多酚在抗衰老方面的应用价值。方法:实验于2004-01/07在邯郸市第一医院预防保健科实验室完成。提取大鼠心肌、肝脏线粒体。采用测氧仪测定密闭系统中态3呼吸、态4呼吸速率,计算呼吸控制率。采用南京建成生物工程公司试剂盒测定心肌、肝脏线粒体总抗氧化力、超氧化物歧化酶活性以及丙二醛水平。结果:老年对照组大鼠心肌线粒体呼吸控制率(2.24±0.55)和肝脏线粒体呼吸控制率(2.65±0.42)均低于青年对照组(心肌3.76±0.41,肝脏4.41±0.53)(P<0.05)。而老年结合茶多酚干预组心肌线粒体呼吸控制率(3.46±0.40)和肝脏线粒体呼吸控制率(4.83±0.37)均高于老年对照组(P<0.05)。老年对照组心肌线粒体总抗氧化能力(1.76±0.33)μkat/g)和肝脏线粒体总抗氧化能力(1.20±0.22)μkat/g)低于青年对照组心肌(2.45±0.20)μkat/g,肝脏(1.78±0.18)μkat/g(P<0.05)。老年结合茶多酚干预组心肌线粒体总抗氧化能力(2.26±0.25)μkat/g)高于老年对照组(P<0.05)。老年对照组肝脏线粒体丙二醛水平(5.11±1.05)μkat/g)明显高于青年对照组(2.27±0.72)μkat/g)(P<0.05)。老年结合茶多酚干预组肝脏线粒体丙二醛水平(3.35±1.12)μkat/g)

AIM: To study the effect of tea polyphenols (TP) on the myocardial and liver mitochondria respiration control ratio (RCR) and the level of oxygen stress in aging rat, and investigate the practical value of TP against aging. METHODS: The experiment was carried out in the laboratory of Department of Prevention and Health Care,Handan First Hospital in 2004.Myocardial and liver mitochondria of rat were extracted.The respiratory rates of State 3 and State 4 in close system were determined with oxygen measuring meter to calculate RCR.The total anti-oxidation capacity (TAOC), activity of superoxide dismutase (SOD) and concentration of malondialdehyde (MDA) of myocardial and liver mitochondria were detected with the reagent kit produced by Nanjing Jiancheng Biology Engineering Corporation. RESULTS: The RCR of myocardial and liver mitochondria in the aging control group (2.24±0.55, 2.65±0.42) were significantly lower than those in the young control group (3.76±0.41, 4.41±0.53) (P< 0.05). The RCR of myocardial and liver mitochondria in the aging TP intervention group (3.46±0.40, 4.83±0.37) were higher than those in the aging control group (P< 0.05).The TAOC of myocardial and liver mitochondria were lower in the aging control group [(1.76±0.33), (1.20±0.22) μkat/g] than in the young control group [(2.45±0.20),(1.78±0.18) μkat/g](P< 0.05), while the TOAC of myocardial mitochondria in the aging TP intervention group [(2.26±0.25) μkat/g] was higher than that in the aging control group(P< 0.05).The MDA level of liver mitochondria was obviously higher in the aging control group [(5.11±1.05) μkat/g] than in the young control group [(2.27±0.72) μkat/g](P< 0.05), while it was lower in the aging TP intervention group [(3.35±1.12) μkat/g] (P< 0.05). CONCLUSION: The RCR is obviously decreased, and oxidative phosphorylation function declines in aging mitochondria.TP can effectively increase the RCR of myocardial and liver mitochondria of aging rats, and improve the oxidative-phosphorylation function of aging mitochondria. In addition, TP can antagonize the decrease the TAOC of myocardial mitochondria of aging organs, obviously inhibit the injury of oxygen-derived free radicals to liver mitochondria, and protect mitochondria of aging rats.