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目的探讨膳食钙对氟暴露致子代肝脏损伤的分子机制。方法取初断乳SD大鼠雌鼠100只,雄鼠50只。雌鼠随机分成对照、染氟、低钙、低钙染氟、高钙染氟5组。3个月后合笼,取14和28日龄仔鼠进行相关实验。结果与对照组相比,其他各组仔鼠肝细胞的凋亡数量明显增多,28日龄仔鼠低钙染氟组Bcl-2蛋白表达降低(P<0.05),染氟组和低钙染氟组14日龄雄性、28日龄雌雄仔鼠肝组织Caspase12蛋白表达水平升高(P<0.01);与染氟组相比,低钙染氟组的细胞凋亡数量明显增多,高钙染氟组的细胞凋亡数量有所下降,各日龄仔鼠低钙染氟组Bcl-2蛋白表达降低(P<0.05),28日龄雄性仔鼠高钙染氟组Caspase12蛋白表达降低(P<0.05),低钙组降低(P<0.01)。结论氟中毒致子代肝损伤的机制可能是氟暴露导致子代肝组织上调内质网途径凋亡通路中Caspase12表达,下调Bcl-2的表达,低钙与染氟表现出协同作用,高钙则能缓解氟中毒症状。
Objective To investigate the molecular mechanism of dietary calcium on liver damage induced by fluoride exposure in offspring. Methods 100 female SD rats and 50 male rats were weaned. Female rats were randomly divided into control, stained with fluorine, low calcium, low calcium fluoride, high calcium fluoride group. After 3 months cage, taking 14 and 28-day-old offspring related experiments. Results Compared with the control group, the apoptosis of hepatocytes in other groups was significantly increased. The expression of Bcl-2 protein in fluorosis group was lower than that in control group (P <0.05) The expression of Caspase 12 protein in liver tissue of 14-day-old male and 28-day-old male and female offspring rats in fluoride group increased significantly (P <0.01). Compared with fluoride-treated group, the number of apoptotic cells in fluoride- (P <0.05). The expression of Caspase12 protein in fluoroux group was decreased (P <0.05), while the expression of Caspase12 protein in fluoroux group <0.05), low-calcium group decreased (P <0.01). Conclusions The mechanism of liver injury induced by fluorosis may be that fluoride exposure leads to upregulation of Caspase12 in the apoptotic pathway of endoplasmic reticulum pathway in the liver of offspring, down-regulating the expression of Bcl-2, synergistic effect of low calcium and fluoride, and high calcium You can alleviate the symptoms of fluorosis.