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目的探讨自噬相关因子LC3A、Beclin-1及凋亡因子Bcl-2、Bax在慢性氟中毒大鼠肝脏中的表达意义。方法将36只健康SD大鼠按体重随机分为对照组、低氟组、高氟组,分别用含氟量<1 mg/L的自来水和含氟5、50 mg/L的含氟水饲养6个月,观察氟斑牙形成情况;测定尿氟、骨氟含量以及大鼠肝功能;苏木素-伊红染色观察肝脏病理形态学改变;免疫组织化学法检测大鼠肝组织中微管相关蛋白轻链3A(LC3A)、哺乳动物ATG6同源蛋白(Beclin-1)及B细胞淋巴瘤/白血病-2蛋白(Bcl-2)、B细胞淋巴瘤/白细胞基因伴随蛋白x(Bax)的蛋白表达水平。结果与对照组比较,低、高氟组大鼠尿氟含量分别为[(2.18±0.14)、(2.40±0.19)mg/L]、骨氟含量分别为[(237.42±18.48)、(248.00±14.72)mg/kg]均明显升高(P<0.05);染氟组大鼠肝脏肝细胞索排列紊乱,肝细胞肿大,部分肝细胞胞质透亮,呈空泡样改变;与对照组比较,染氟组大鼠血清中谷丙转氨酶活性及谷草转氨酶活性明显升高(P<0.05);低、高氟组大鼠肝脏LC3A[(35.35±2.71)、(44.10±6.72)]、Beclin-1[(57.56±12.1)、(74.76±18.67)]及Bax[(51.1±9.23)、(62.32±10.3)]蛋白表达明显高于对照组,Bcl-2蛋白表达分别为[(55.18±8.36)、(39.05±6.91)]明显低于对照组(P<0.05)。结论过量氟可激活大鼠肝组织中自噬和凋亡因子,自噬和凋亡可能共同参与慢性氟中毒所致肝脏损伤的发病过程。
Objective To investigate the expression of autophagy related factors LC3A, Beclin-1 and Bcl-2 and Bax in liver of chronic fluorosis rats. Methods Thirty-six healthy SD rats were randomly divided into control group, low-fluoride group and high-fluoride group according to body weight. They were fed with tap water containing fluoride <1 mg / L and fluoride containing water containing 5 and 50 mg / Six months later, the formation of dental fluorosis was observed. Urinary fluorine and bone fluorine contents and liver function of rats were observed. Heparin-Eosin staining was used to observe the pathological changes of liver. Immunohistochemistry was used to detect the expression of microtubule-associated protein Protein expression of light chain 3A (LC3A), mammalian ATG6 homolog (Beclin-1) and Bcl-2, Bx (Bx) Level. Results Compared with the control group, the urinary fluoride contents in the low and high fluoride groups were (2.18 ± 0.14) and (2.40 ± 0.19) mg / L, respectively. The contents of fluoride in the bone were [(237.42 ± 18.48) and (248.00 ± 14.72) mg / kg] were significantly increased (P <0.05). Compared with the control group, the hepatic cells in the fluoride-exposed group were disordered, the hepatocytes enlarged, and the cytoplasm of some hepatocytes turned bright. (P <0.05); LC3A [(35.35 ± 2.71), (44.10 ± 6.72)], Beclin-1 [(57.56 ± 12.1), (74.76 ± 18.67)] and Bax [(51.1 ± 9.23), (62.32 ± 10.3)] were significantly higher than those in the control group (39.05 ± 6.91)] was significantly lower than that of the control group (P <0.05). Conclusion Excessive fluoride-induced autophagy and apoptosis in rat liver tissue may play an important role in the pathogenesis of hepatic injury induced by chronic fluorosis.