【摘要】：目的觀察慢性氟中毒大鼠腎組織自噬相關(guān)因子微管相關(guān)蛋白1(Beclin1)、微管相關(guān)蛋白1輕鏈3(LC3)、p62及抗凋亡因子B細(xì)胞淋巴瘤基因/白血病基因-2(Bcl-2)表達(dá)變化,探討自噬及凋亡在慢性氟中毒腎臟損傷中的意義。方法選擇健康SD大鼠36只,隨機(jī)分為對(duì)照組、低氟組、高氟組,每組各12只。對(duì)照組飲用含氟化鈉低于1 mg/L的自來水;低、高氟組飲用含氟化鈉分別為5、50 mg/L的自來水,干預(yù)6個(gè)月建立氟中毒模型。干預(yù)結(jié)束后股動(dòng)脈放血處死大鼠,取腎組織,光鏡下觀察腎組織病理形態(tài)學(xué)改變,免疫組織化學(xué)及RT-PCR法檢測腎組織Beclin1、LC3、p62、Bcl-2蛋白和mRNA表達(dá)。結(jié)果 HE結(jié)果示,對(duì)照組大鼠腎臟腎小球及腎小管結(jié)構(gòu)無明顯變化,腎小管上皮細(xì)胞排列整齊。低氟組、高氟組大鼠腎小管上皮細(xì)胞有不同程度的水腫,管腔狹窄,以高氟組腎小管中間質(zhì)充血更為明顯。與對(duì)照組比較,低氟組、高氟組腎組織中Beclin1、LC3蛋白及mRNA表達(dá)均升高,p62、Bcl-2蛋白及mRNA表達(dá)均下降(P均0.05)。高氟組Beclin1、LC3蛋白及mRNA表達(dá)均高于低氟組,p62、Bcl-2蛋白及mRNA表達(dá)均低于低氟組(P均0.05)。結(jié)論慢性氟中毒后大鼠腎組織自噬及凋亡均激活,且其激活程度與氟中毒的程度有關(guān),可能共同參與了慢性氟中毒腎損傷的發(fā)病機(jī)制。
[Abstract]:Objective to observe the expression of autophagy associated factor microtubule-associated protein 1 (Beclin1), microtubule-associated protein 1 light chain 3 (LC3) p62 and anti-apoptotic factor B cell lymphoma gene / leukemia gene 2 (Bcl-2) in chronic fluorosis rats. To investigate the significance of autophagy and apoptosis in renal injury caused by chronic fluorosis. Methods 36 healthy SD rats were randomly divided into control group, low fluorine group and high fluorine group with 12 rats in each group. The control group drank tap water containing sodium fluoride for less than 1 mg/L, while the high fluorine group drank the tap water containing sodium fluoride for 550 mg/L, and the model of fluorosis was established after 6 months of intervention. At the end of intervention, the rats were sacrificed by femoral artery bloodletting, the renal tissues were taken, the pathological changes of renal tissue were observed under light microscope, the expression of Bcl-2 protein and mRNA in renal tissue were detected by immunohistochemical method and RT-PCR method. Results the results of HE showed that the renal glomeruli and renal tubules in the control group had no obvious changes, and the renal tubular epithelial cells were arranged neatly. In low fluoride group and high fluoride group, renal tubular epithelial cells were edema and lumen stenosis, especially in high fluorine group. Compared with the control group, the expression of Beclin1 + LC3 protein and mRNA in renal tissue of low fluorine group and high fluorine group were significantly higher than those of control group (P < 0. 05). The expression of Beclin1 + LC3 protein and mRNA in high fluorine group was higher than that in low fluorine group. The expression of Bcl-2 protein and mRNA were lower in high fluorine group than in low fluoride group (P 0.05). Conclusion autophagy and apoptosis of renal tissue were activated after chronic fluorosis in rats, and the degree of activation was related to the degree of fluorosis, which may be involved in the pathogenesis of renal injury caused by chronic fluorosis.
【作者單位】： 貴州醫(yī)科大學(xué);
【分類號(hào)】：R595

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