Expressions of P-NMDAR and CaMKⅡin brain tissue of rats with chronic fluorosis
10.3760/cma.j.cn231583-20191220-00360
- VernacularTitle:慢性氟中毒大鼠脑组织P-NMDAR及CaMKⅡ的表达
- Author:
Jianxia WEN
1
;
Na WEI
;
Fan BI
Author Information
1. 贵州医科大学病理学教研室，贵阳 550004
- From:
Chinese Journal of Endemiology
2020;39(9):636-640
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To observe the changes of phosphorylated N-methyl-D-aspartate receptor (P-NMDAR) subunit and calmodulin-dependent protein kinase Ⅱ (CaMK Ⅱ) protein expression in the brain tissue of rats with chronic fluorosis, and to explore the molecular pathogenesis of chronic fluorosis nerve injury.Methods:Eighteen one-month-old SD rats (half male and half female), weighing (100 ± 20) g, were randomly divided into three groups after adaptive feeding for 1 week: control group (drinking tap water, fluoride content < 0.5 mg/L), low fluoride group (drinking water fluoride content was 10.0 mg/L) and high fluoride group (drinking water fluoride content was 100.0 mg/L), with 6 rats in each group (half male and half female). Brain tissue was harvested after 180 days of feeding. HE staining was used to observe the morphological changes of rat brain tissue, Nissl staining was used to observe the changes of Nissl bodies in nerve cells, and immunohistochemical staining was used to observe the expressions of P-NMDAR subunits (P-NMDAR1, P-NMDAR2A) and CaMK Ⅱ protein in rat brain tissue.Results:Under light microscope, HE staining showed disordered arrangement of hippocampal neurons, nuclear hyperstaining and basophilic enhancement in the high fluoride group. The results of Nissl staining showed that the average optical density of Nissl bodies in nerve cells in the hippocampus of rats in the control group, low fluoride group, and high fluoride group were 0.024 4 ± 0.009 7, 0.024 0 ± 0.003 1, and 0.023 9 ± 0.013 8, respectively. There was no statistically significant difference between the groups ( F = 0.010, P > 0.05). Compared with the control group (0.011 8 ± 0.006 5, 0.065 6 ± 0.011 1, 0.143 8 ± 0.029 9) and low fluoride group (0.017 2 ± 0.006 8, 0.062 6 ± 0.017 8, 0.135 6 ± 0.029 6), the protein expressions of P-NMDAR1, P-NMDAR2A and CaMK Ⅱ in high fluoride group were significantly increased (0.026 3 ± 0.005 7, 0.086 3 ± 0.009 0, 0.210 9 ± 0.048 7, P < 0.05); and the protein expression of P-NMDAR1 in low fluoride group was higher than that in the control group ( P < 0.05). Conclusion:Long-term excessive fluoride intake can lead to nerve cell injury in rats, and the mechanism of injury maybe related to the excitotoxicity induced by calcium ion (Ca 2+) overload caused by overactivation of NMDAR subunits.
