Beclin-1、Bcl-2、Bax在慢性氟中毒大鼠肾脏中表达

发布时间：2018-04-16 02:10

本文选题：Beclin- + Bcl-　；参考：《中国公共卫生》2016年06期

【摘要】：目的观察自噬基因Beclin-1、凋亡基因Bcl-2、Bax在慢性氟中毒大鼠肾脏中的表达变化,探讨Beclin-1、Bcl-2、Bax在氟中毒肾脏损害过程中的作用。方法将SD大鼠24只随机分为3组,每组8只,对照组(饮用含氟量0.5 mg/L自来水),低、高氟组(自来水含氟量分别为50、100 mg/L);饲养9个月后,观察大鼠氟斑牙发生情况;氟离子电极法测定尿氟、骨氟含量;显微镜下观察大鼠肾组织病理形态学变化;采用免疫组织化学方法检测大鼠肾组织中Beclin-1、Bcl-2、Bax表达量;用原位杂交法测定大鼠肾脏Beclin-1 mRNA含量。结果低氟组大鼠氟斑牙检出率为75%,高氟组为100%;与对照组比较,低、高氟组大鼠尿氟和骨氟含量分别为[(10.09±0.88)、(18.09±0.89)mg/L和(5 500.84±1 093.47)、(7 477.94±1 315.88)μg/g]明显升高,差异有统计学意义(P0.05);染氟大鼠肾脏肾小管上皮细胞水肿、间质血管扩张充血,且随染氟剂量增加损伤改变逐渐加重;与对照组比较,低、高氟组大鼠肾组织中Beclin-1、Bax表达[分别为(168.90±8.68)、(146.32±10.02)和(153.74±10.56)、(134.29±9.85)]明显降低(均P0.05);与对照组比较,低、高氟组大鼠肾组织中Bcl-2表达[分别为(167.64±7.51)、(185.32±8.55)]明显升高(P0.05);与对照组比较,低、高氟组大鼠肾组织中Beclin-1 mRNA表达[分别为(166.94±13.21)、(146.11±17.66)]明显降低(P0.05)。结论慢性氟中毒可诱导肾小管上皮细胞自噬和凋亡相关分子的异常表达,自噬和凋亡可能共同参与慢性氟中毒肾脏损伤过程。
[Abstract]:Objective to observe the expression of Beclin-1 and Bcl-2nBax in the kidney of rats with chronic fluorosis and to explore the role of Beclin-1 Bcl-2Bcl-2Bax in the process of renal damage caused by fluorosis.Methods Twenty-four Sprague-Dawley rats were randomly divided into 3 groups, 8 rats in each group. The rats in the control group (drinking 0.5 mg/L tap water with fluorine content of 0.5 mg/L) and the high fluoride group (fluorine content in tap water were 50100 mg / L 路L ~ (-1)) were randomly divided into three groups.The content of fluoride in urine and bone was determined by fluorine ion electrode method, pathomorphology of renal tissue was observed under microscope, the expression of Beclin-1 Bcl-2Bcl-2Bax in rat kidney was detected by immunohistochemical method, and the content of Beclin-1 mRNA in rat kidney was determined by in situ hybridization.Results the detection rate of fluorosis teeth in low fluorine group was 75 and that in high fluorine group was 100. Compared with control group, the urinary fluorine and bone fluorine contents in high fluorine group were significantly higher than those in control group [10.09 卤0.888.09 卤0.89)mg/L and 5 500.84 卤1 093.47) 渭 g / g, respectively].The difference was statistically significant (P 0.05), renal tubular epithelial cells edema, interstitial vascular dilatation and hyperemia were observed in fluorine-exposed rats, and the changes of injury were gradually aggravated with the increase of fluoride dose, and were lower than those in the control group.The expression of Beclin-1 Bcl-2 in renal tissues of rats with high fluoride (168.90 卤8.68 卤146.32 卤10.02) and 153.74 卤10.56 (134.29 卤9.85) were significantly lower than those in the control group (P 0.05), and the expression of Bcl-2 was significantly higher in the high fluoride group than in the control group [167.64 卤7.51, 185.32 卤8.55, respectively], and was lower than that in the control group (P < 0.05).The expression of Beclin-1 mRNA in high fluoride group [166.94 卤13.21, 146.11 卤17.66] decreased significantly (P 0.05).Conclusion chronic fluorosis can induce abnormal expression of autophagy and apoptosis-related molecules in renal tubular epithelial cells. Autophagy and apoptosis may be involved in the process of renal injury caused by chronic fluorosis.
【作者单位】：贵州医科大病理学教研室;贵州毕节医学高等专科学校预防医学教研室;
【基金】：国家自然科学基金(81260419) 教育部博士点基金(博导类)(20115215110001)
【分类号】：R599.1

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