针对衰老引起的大脑微环境的变化，小胶质细胞可以极化为促炎性M1型和抗炎性M2型。此外，星形胶质细胞可极化为A1表型，表现出神经毒性，或A2表型，表现出神经保护作用。这项研究旨在调查随着年龄的增长中脑胶质细胞和多巴胺能（DA）神经元的变化。收集了2、6、18和28个月大的大鼠大脑。使用抗TH和抗DAT抗体检测DA神经元。星形胶质细胞标记物（神经胶质纤维酸性蛋白，GFAP），小胶质细胞标记物（离子钙结合衔接子分子1，Iba-1），M1标记物（肿瘤坏死因子-α（TNF-α）和白介素-1β（IL-1β）的表达），M2标志物（精氨酸酶1（Arg1）和IL-10），A1标志物（lipocalin-2（Lcn2）和补体C3（C3），在18、28个月大的大鼠大脑中，DA神经元表达下降。另外，小胶质细胞和星形胶质细胞随着年龄的增长具有不同程度的激活。此外，衰老大鼠的M1标志物（TNF-α和IL-1β）升高，而M2标志物（Arg1和IL-10）降低。此外，在老年大鼠中，A2标记（BDNF和GDNF）减少，而A1标记（Lcn2和C3）增加。年龄引起DA神经元丢失并影响中脑神经胶质细胞表型极化，这可能解释了帕金森氏病的发生和发病机理。在18、28个月大的大鼠大脑中，DA神经元表达下降。另外，小胶质细胞和星形胶质细胞随着年龄的增长具有不同程度的激活。此外，衰老大鼠的M1标志物（TNF-α和IL-1β）升高，而M2标志物（Arg1和IL-10）降低。此外，在老年大鼠中，A2标记（BDNF和GDNF）减少，而A1标记（Lcn2和C3）增加。年龄引起DA神经元丢失并影响中脑神经胶质细胞表型极化，这可能解释了帕金森氏病的发生和发病机理。在老年大鼠中，A2标记（BDNF和GDNF）减少，而A1标记（Lcn2和C3）增加。年龄引起的DA神经元丢失并影响中脑神经胶质细胞表型极化，这可能是帕金森氏病的发生和发病机制。在老年大鼠中，A2标记（BDNF和GDNF）减少，而A1标记（Lcn2和C3）增加。年龄引起DA神经元丢失并影响中脑神经胶质细胞表型极化，这可能解释了帕金森氏病的发生和发病机理。
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Age-Associated Dopaminergic Neuron Loss and Midbrain Glia Cell Phenotypic Polarization.
In response to changes in brain micro-environment caused by aging, microglia could polarize into proinflammatory M1 phenotype and anti-inflammatory M2 phenotype. Besides, astroglia could polarize into A1 phenotype, exhibiting neurotoxicity, or A2 phenotype, showing neuroprotection. This study aimed to investigate the change of glial cells and dopaminergic (DA) neuron in midbrain with age. Two-, 6-, 18- and 28- months old rat brains were collected. The DA neurons were detected using anti-TH and anti-DAT antibodies. The expressions of astroglia markers (glial fibrillary acidic protein, GFAP), microglia markers (ionized calcium binding adaptor molecule 1, Iba-1), M1 markers (tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), M2 markers (arginase 1 (Arg1) and IL-10), A1 markers (lipocalin-2 (Lcn2) and complement C3 (C3), A2 markers (brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF) were examined by real time RT-PCR and Western Blotting. DA neuron expressions decreased in 18-, 28- months old rat brains. In addition, microglia and astroglia have different degrees of activation with age. Besides, M1 markers (TNF-α and IL-1β) increased and M2 markers (Arg1 and IL-10) decreased in aged rats. Furthermore, A2 markers (BDNF and GDNF) decreased and A1 markers (Lcn2 and C3) increased in aged rats. Age induced DA neuron loss and influenced midbrain glial cells phenotypic polarization, which might account for the occurrence and pathogenesis of Parkinson's diseases.
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