【摘要】 目的 探討慢性缺氧對大鼠巖神經節神經元酸敏感離子通道（acid-sensing ion channels，ASICs）亞型3（ASIC3）和亞型2a（ASIC2a）表達的影響。 方法 將12只健康成年SD大鼠隨機分為正常組和缺氧組。用免疫組織化學法（PV）觀察正常和慢性缺氧大鼠巖神經節神經元ASIC3和ASIC2a的表達。 結果 給予慢性缺氧刺激后，巖神經節ASIC3陽性表達神經元數目增多（Plt;0.05），灰度值降低（Plt;0.05）；而ASIC2a陽性表達神經元數目和灰度值無明顯變化（Pgt;0.05）。 結論 慢性缺氧可上調大鼠巖神經節神經元ASIC3的表達，而對ASIC2a的表達無明顯影響，提示ASIC3和ASIC2a可能在巖神經節對缺氧的反應中起著不同的作用。【Abstract】 Objective To investigate the effects of chronic hypoxia on expression of acid-sensing ion channels (ASIC) 3 and ASIC2a in neurons of petrosal ganglions of rats. Methods A total of 12 SD rats were randomly assigned to control group and hypoxia group. The expressions of ASIC3 and ASIC2a of the neurons in the petrosal ganglions in the two groups were investigated with the immunohistochemical technique. Results The level of positive ASIC3 expression in the petrosal ganglions was higher in the hypoxia group than that in the control group (Plt;0.05); the difference of positive ASIC2a expression levels between the control group and the hypoxia group was not statistically significant (Pgt;0.05). Conclusion Chronic hypoxia can significantly increase the expression of ASIC3, but not that of ASIC2a, of the neurons in the petrosal ganglions, suggesting their different roles in mediating a cellular response to chronic hypoxia.
Objective
To study the impact of chronic hypoxia on white matter (WM) injury and brain development delay using a neonatal rat model, and to explore its value in simulating chronic hypoxic brain damage in cyanotic congenital heart disease (CHD).
Methods
Three-day-old Sprague-Dawley (SD) rats were randomly distributed to an experiment group (n=36, FiO2 10.5%±1.0%) and a control group (n=36, FiO2 21.0%±0.0%) and were raised for 12 days. (1) Body weight of SD rats was recorded every day and fresh brain weight was measured on P14. (2) H&E staining was performed on sections of brain tissue to observe pathological changes and ventricular size. (3) Immunohistochemistry (IHC) was applied to reveal alterations of oligodendroglial progenitor cells (OPC), preoligodendrocytes (PreOL) and myelin basic protein (MBP) in brain WM area. (4) Protein was extracted from 50 mg of brain tissue in WM area and expression of MBP was determined using Western blotting. (5) Motor function and coordination of rats (P30) were assessed via rotation experiment.
Results
(1) Body weight and brain weight were significantly less in the experiment group compared with the control group on P14 (body weight 14.92±1.26 gvs. 30.26±1.81 g, t=7.51, P<0.01; brain weight 0.68± 0.05 gvs.0.97±0.04 g, t=13.26, P<0.01); (2) HE staining: Sections of brain tissue from the experiment group showed ventricular size enlargement with a statistical difference (P<0.01), disordered cell organization, local neuronal death and leukomalacia. (3) The number of OPC and PreOL in the experiment group were significantly less than those in the control group (64.8±6.3vs. 126.2±8.4, t=11.19, P<0.01; 19.1±7.6vs. 46.7±9.5, t=7.28, P<0.01, respectively). MBP distribution was sparse and disorganized in the experiment group. (4) Western blotting: Expression of MBP was less in the experiment group (P<0.01). (5) Behavioral test: Time on rotarod was less in the experiment group with a statistical difference (P<0.01).
Conclusion
Chronic hypoxia can result in WM injury and brain development delay in neonatal rats, with features comparable to those seen in infants with cyanotic CHD.
