Department of Otorhinolaryngology-Head and Neck Surgery, Soonchunhyang University Cheonan Hospital, Soonchunhyang University College of Medicine, Cheonan, Korea.
Department of Biochemistry, Soonchunhyang University College of Medicine, Cheonan, Korea.
J Korean Med Sci. 2020 Dec 28;35(50):e420. doi: 10.3346/jkms.2020.35.e420.
Studies have reported that epithelial cell proliferation may be involved in the pathogenesis of nasal polyps (NPs). Estrogen receptor (ER)-α, one type of ER, is related to anti-inflammatory action and cell survival in certain tissues. In this study, we examined the presence or absence of ER-α in NPs and healthy inferior turbinate mucosae. We also investigated the effect of dexamethasone on ER-α expression, cell viability, and apoptosis in RPMI 2650 cells.
Immunohistochemical staining and Western blot analysis were conducted to determine the expression of ER-α in 15 NPs and 15 healthy inferior turbinate mucosae. After treating RPMI 2650 cells with dexamethasone, ER-α expression was analyzed using Western blot analysis and cell viability was determined using the MTT assay. Western blot analysis and annexin V-phycoerythrin (PE) staining were used to examine apoptotic cell death.
Western blot analysis showed that ER-α expression was upregulated in 13 of the 15 NP tissues. Immunohistochemical staining for ER-α confirmed the results of the Western blot analysis. When RPMI 2650 cells were treated with dexamethasone, both ER-α expression and cell viability were decreased. Furthermore, the treatment of RPMI 2650 cells with dexamethasone increased apoptotic cell death, as shown by increased levels of BAX and cleaved caspase-3, decreased levels of Bcl-2, and an increased percentage of positive annexin V-PE stained cells.
ER-α expression was higher in NPs than in healthy inferior turbinate mucosae. When RPMI 2650 cells were treated with dexamethasone, ER-α expression was downregulated, cell viability decreased, and apoptosis increased. The decreased cell viability may be related, at least in part, to the decreased ER-α protein levels, which likely contributed to the induction of apoptotic cell death in RPMI 2650 cells.
研究报告称，上皮细胞增殖可能与鼻息肉（NPs）的发病机制有关。雌激素受体（ER）-α是 ER 的一种类型，与某些组织中的抗炎作用和细胞存活有关。在这项研究中，我们检查了 ER-α在 NPs 和健康下鼻甲黏膜中的存在情况。我们还研究了地塞米松对 RPMI 2650 细胞中 ER-α表达、细胞活力和细胞凋亡的影响。
通过免疫组织化学染色和 Western blot 分析，确定了 15 例 NPs 和 15 例健康下鼻甲黏膜中 ER-α的表达。用地塞米松处理 RPMI 2650 细胞后，通过 Western blot 分析分析 ER-α的表达，通过 MTT 法测定细胞活力。Western blot 分析和膜联蛋白 V-藻红蛋白（PE）染色用于检测凋亡细胞死亡。
Western blot 分析显示，15 例 NP 组织中有 13 例 ER-α表达上调。ER-α的免疫组织化学染色证实了 Western blot 分析的结果。当 RPMI 2650 细胞用地塞米松处理时，ER-α的表达和细胞活力均降低。此外，地塞米松处理 RPMI 2650 细胞增加了凋亡细胞死亡，表现为 BAX 和裂解 caspase-3 水平升高，Bcl-2 水平降低，以及阳性膜联蛋白 V-PE 染色细胞的百分比增加。
与健康下鼻甲黏膜相比，NP 中的 ER-α表达更高。当 RPMI 2650 细胞用地塞米松处理时，ER-α的表达下调，细胞活力降低，凋亡增加。细胞活力的降低可能与 ER-α蛋白水平的降低有关，这可能至少部分导致了 RPMI 2650 细胞中凋亡细胞死亡的诱导。
