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作 者:赵立娜[1] 徐健[2] 彭晓琳[1] 田利钺[1] 郝丽萍[1] 杨雪峰[1] 应晨江[1] 孙秀发[1]
机构地区:[1]华中科技大学同济医学院公共卫生学院营养与食品卫生学系,湖北武汉430030 [2]深圳市慢性病防治院
出 处:《中国公共卫生》2010年第4期454-455,共2页Chinese Journal of Public Health
基 金:国家自然科学基金(30771806)
摘 要:目的观察长期过量碘摄入对小鼠血清脂蛋白代谢影响。方法清洁级雌性断乳Balb/c小鼠60只,按体重随机分为6组(10只/组)。在饮水中以KIO3形式分别给予0(对照组),300,600,1200,2 400和4 800μg/L碘。30 d后,放射免疫法测定甲状腺激素,血清脂蛋白。PCR方法测定肝脏低密度脂蛋白受体(LDLR)、高密度脂蛋白受体(SR-BⅠ)基因表达水平。结果各剂量组小鼠尿碘水平随着碘剂量升高明显增加(P<0.01),血清四碘甲状腺原氨酸(TT4)、三碘甲状腺原氨酸(TT3)、促甲状腺激素(TSH)水平未发生明显性改变。2 400,4 800μg/L组血清总胆固醇(TC)与低密度脂蛋白-胆固醇(LDL-C)含量分别为(2.40±0.37),(2.58±0.42)和(0.39±0.11),(0.41±0.11)mmol/L,与对照组比较,差异有统计学意义(P<0.05)。LDLR mRNA表达水平呈碘剂量依赖性降低(r=-0.753,P<0.01)。结论长期过量碘摄入可致小鼠血清LDL-C水平升高。LDLR受体表达降低可能是过量碘摄入导致脂蛋白代谢紊乱的机制之一。Objective To study the effect of excessive iodine exposure on serum lipoprotein metabolism in mice and to explore its possible mechanism.Methods Sixty female Balb/c mice were randomly divided into six groups according to body weight and given iodine at different dose of 0,300,600,1200,2 400,and 4 800 μg/L,respectively,in drinking water.Serum lipoprotein and serum thyroid hormone were determined 30 days after iodine exposure.The mRNA expression of low density lipoprotein receptor(LDLR) and scavenge receptor BⅠ(SR-BⅠ) were detected by real-time PCR.Results In excessive iodine groups,urinary iodine level increased dose-dependently and serum thyroid hormones(thyroid-stimulating hormone,total triiodothyronine,and total thyroxine) were not affected by iodine intake throughout the study.A dose-dependent increase of serum low density lipoprotein-cholesterol(LDL-c) level was observed in iodine-treated groups.While there was no significant change in high density lipoprotein-cholesterol(HDL-c) level.Compared with the control group,total cholesterol and LDL-c levels increased significantly in 2400 and 4800 μg/L groups(2.40±0.37,0.39±0.11,2.58±0.42,0.41±0.11 mmol/L).A dose-dependent attenuation of hepatic LDLR mRNA(r=-0.753,P〈0.01) expression in parallel to the change of serum LDL-C was obsorved.Conclusion The findings demonstrate a dose-dependent effect of excessive iodine on LDL-c and suggest that down-regulation of hepatic LDLR gene may play a critical role in excessive iodine-induced effect.
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