PI3K-Akt1 expression and its significance in liver tissues with chronic fluorosis.
PI3K-Akt1 expression and its significance in liver tissues with chronic fluorosis.
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发表时间：
2015-02
影响因子：
1.4
通讯作者：
Bin Fan;Yan-ni Yu;Ying Zhang
中科院分区：
文献类型：
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作者：
Bin Fan;Yan-ni Yu;Ying Zhang
本研究旨在探讨PI3K信号通路在慢性氟中毒肝损伤机制中的作用及意义。我们选用48只Sprague - Dawley大鼠，根据体重随机分为4组，每组12只，雌雄各半。对照组给予固体饲料（氟含量为1.5 mg/kg）。氟中毒组给予来自地方性氟中毒地区氟含量为17 mg/kg的玉米。阻断组在实验结束前1周于尾静脉注射阻断剂LY294002，阻断对照组注射磷酸盐缓冲液，剂量均为10 mg/kg，每隔1天注射1次。动物自由饮用自来水。采用氟离子选择性电极法测定尿液和骨骼中的氟含量。采用实时聚合酶链反应、链霉亲和素 - 过氧化物酶法和蛋白质印迹法分别测定肝组织中PI3K、Akt1的mRNA和蛋白质表达。结果显示，与对照组相比，氟中毒组尿液和骨骼中的氟含量增加。氟中毒肝细胞中PI3K和Akt1的mRNA及蛋白质表达显著增加，而阻断组低于氟中毒组。细胞凋亡和细胞内钙浓度增加。因此，我们得出结论：PI3K - Akt信号通路可能是氟中毒所致肝损伤发病机制中的信号通路之一。
This study was to explore the effect and significance of PI3K signal pathway on mechanism of liver injury in chronic fluorosis. We used 48 Sprague-Dawley rats which were randomly divided into 4 groups according to the body weight, 12 in each group, half of male and female. The control group was fed with the solid feed (the fluorine content was 1.5 mg/kg). The fluorosis animals were fed with the corn containing fluorine content of 17 mg/kg from the endemic fluorosis areas. Blocking agent LY294002 was injected in the blocking group and phosphate buffer solution was injected in the blocking control in the caudal vein with 10 mg/kg once every other day in the one week before the end of the experiment. The animals were drunk by tap water freely. The fluoride contents of urinary and skeletal were determined by the F-ion selective electrode method. The mRNA and protein expressions of PI3K, Akt1 in the liver tissues were determined by real-time polymerase chain reaction, and streptavidin-perosidase and Western blot, respectively. Results showed that fluoride contents of the urine and bone were increased in the fluorosis compared to those in the control. The expression of PI3K and Akt1 mRNA and proteins was significantly increased in fluorosis hepatocytes, and lower than that of the fluorosis in the blocking. The apoptosis and the intracellular calcium concentration were increased. Therefore, we conclude that PI3K-Akt signaling pathway may be one of the signaling pathways in the pathogenesis of liver injury caused by fluorosis.