摘要
目的 探讨锌对血栓素 B2 (TXB2 )、6 -酮 -前列腺环素 F1α(6 - keto- PGF1α)、脂代谢及抗氧化功能的影响。方法 纯系新西兰雄性大白兔 2 0只 ,分为对照组和加锌组 ,加锌组饮水中加葡萄糖锌 (锌浓度 15 .3 mm ol/L )。实验前后 3次观察 TXB2 、6 - keto- PGF1α、超氧化物歧化酶 (SOD)、脂质过氧化物 (L PO)、血清总胆固醇 (T、C)、脂蛋白 (L DL- C、HDL- C)、载脂蛋白 (Apo B1 0 0 、Apo AI)变化。结果 加锌组血清锌在补锌后持续升高 (P <0 .0 1) ,心、肝、肾、肌肉锌也升高 (P <0 .0 5或 0 .0 1)。血液及组织 SOD活性下降 (P <0 .0 5或 0 .0 1) ,L PO含量升高 (P <0 .0 5或 0 .0 1) ,血液及肝 SOD/ L PO比值变小 (P <0 .0 1)。TC、L DL- C、Apo B1 0 0 较实验前及对照组升高 (P<0 .0 5或 0 .0 1) ,HDL- C、Apo AI降低 (P <0 .0 5或 0 .0 1)。 TXB2 较实验前及对照组升高 (P <0 .0 1) ,6 - keto-PGF1α3个月时有升高趋势 ,6个月明显降低 (P <0 .0 1)。结论 高锌摄入能升高 TXB2 ,降低 6 - keto- PGF1α,干扰脂代谢 。
Objective To study the effect of zinc on thromboxane B 2(TXB 2),6 keto prostaglandin F 1α (6 keto PGF 1α ),lipid metablism and anti oxidation function.Methods Twenty New Zealand white rabbits were divided into 2 groups (control group and zinc gluconate supplemented group).The changes of TXB 2,6 keto PGF 1α ,superoxide dismutase (SOD),lipid peroxide (LPO) and serum lipids (T.C,HDL C,LDL C,Apo AI and Apo B 100 ) were observed for three times during the 6 month experiment.Results Serum zinc was significantly increased (P<0.01) and zinc levels in heart,liver,kidney and skeletal muscle were also incaeased (P<0.05 or 0.01) in zinc gluconate supplemented group following zinc intaking.SOD activities in blood and tissue were markedly decreased (P<0.05 or 0.01),but LPO content was increased (P<0.05 or 0.01),the ratio of SOD/LPO in blood and tissue became reduced (P<0.01) in zinc glaconate supplemented group.Serum total cholesterol,low density lipoprotein cholesterol (LDL C) and apolipoprotien B 100 (Apo B 100 ) levels were increased (P<0.05 or 0.01),high density lipoprotein (HDL C) and apolipoprotien AI(Apo AI ) levels were decreased (P<0.05 or 0.01) in zinc gluconate supplemented group.TXB 2 level was significantly higher (P<0.01) but 6 keto PGF 1α lower (P<0.01) in zinc gluconate supplemented group than in control group.Conclusions Zinc intaking could increase TXB 2 levels,decrease 6 keto PGF 1α ,affect lipid metabolism and inhibit anti oxidation function.
出处
《中国地方病学杂志》
CAS
CSCD
2000年第6期426-428,共3页
Chinese Jouranl of Endemiology
基金
山东省卫生厅科研基金资助