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目的探讨刺猬信号通路(Hh)在慢性氟中毒大鼠肝脏损伤中作用及机制。方法选择健康成年SD大鼠36只,按体重随机分为对照组、低、高剂量染氟组(饮水中含氟量分别为5、50 mg/L),每组12只(雌雄各半),饲养6个月后检测大鼠尿氟、骨氟含量;应用自动生化分析仪检测大鼠肝功能;免疫组织化学(IHC)、Western blot和逆转录PCR(RT-PCR)法检测大鼠肝脏组织中印度刺猬蛋白(Ihh)、跨膜蛋白(Smo)、胶质瘤相关癌基因(Gli1)蛋白和mRNA表达;试剂盒法检测肝组织中总超氧化物歧化酶(T-SOD)、谷胱甘肽过氧化物酶(GSH-Px)和谷氨酰胺合成酶(GS)活力及脂质过氧化物(LPO)含量。结果与对照组比较,染氟组大鼠尿氟、骨氟含量、高剂量染氟组大鼠血清谷丙转氨酶、谷草转氨酶活性[分别为(73.42±6.98)、(161.08±8.59)U/L]明显增加,高剂量染氟组大鼠肝组织中Ihh、Smo、Gli1蛋白和mRNA的表达[分别为(71.41±4.18)、(83.83±5.26)、(81.14±25.44)及(1.20±0.17)、(3.13±0.19)、(5.35±0.52)]明显增加,高剂量染氟组大鼠肝组织中T-SOD、GSH-Px、GS活性[(5.08±0.64)、(5.53±0.83)、(19.22±1.84)U/mgprot]明显降低,LPO含量[(10.29±1.81)μmol/gprot]升高,差异均有统计学意义(P<0.05)。结论 Hh信号通路与氧化应激可能共同参与慢性氟中毒所致肝脏损伤发病过程。
Objective To investigate the role and mechanism of hedgehog signaling pathway (Hh) in the liver of chronic fluorosis rats. Methods Thirty - six healthy adult SD rats were randomly divided into control group, low and high dose fluoride group (fluoride content in drinking water was 5 and 50 mg / L, respectively), 12 in each group (male and female respectively) , And the urinary fluoride and bone fluoride contents of rats were detected after 6 months of feeding. The liver function of rats was detected by automatic biochemical analyzer. The liver of rat was detected by IHC, Western blot and reverse transcription polymerase chain reaction (RT-PCR) The expressions of Ihh, Smo, Gli1 and Gli1 mRNA and protein were detected in all the groups. The levels of total superoxide dismutase (T-SOD) and glutathione Glutathione peroxidase (GSH-Px) and glutamine synthetase (GS) activity and lipid peroxide (LPO) content. Results Compared with the control group, the levels of serum alanine aminotransferase (AST) and aspartate aminotransferase (AST) in the fluoride group and the fluoride group were significantly higher than those in the control group [(73.42 ± 6.98), (161.08 ± 8.59) U / L (71.41 ± 4.18), (83.83 ± 5.26), (81.14 ± 25.44) and (1.20 ± 0.17), respectively, in the liver tissue of the rats in the high-dose and high- , (3.13 ± 0.19) and (5.35 ± 0.52)], respectively. The activities of T-SOD, GSH-Px and GS in the liver tissue of high- 19.22 ± 1.84) U / mgprot], LPO content [(10.29 ± 1.81) μmol / gprot] was significantly higher than that of control group (P <0.05). Conclusion Hh signaling pathway and oxidative stress may participate in the pathogenesis of liver injury induced by chronic fluorosis.