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目的观察生理水平(100 pg/ml)和妊娠水平(50 ng/ml)的雌二醇(E_2)对体外培养的小鼠T淋巴细胞白细胞介素(IL)-2、IL-4 mRNA表达的影响,并进一步探讨E_2对自身免疫性疾病的调节机制。方法Balb/c小鼠断颈处死后,制备脾T淋巴细胞并分3组,分别为ConA 5μg/ml(对照组),ConA 5μg/ml+E_2：100 pg/ml,ConA 5μg/ml+E_2 50 ng/ml。每组6个样本。并将各组T细胞置于37℃,5％CO_2条件下分别孵育0、24、48 h。采用半定量反转录一聚合酶链反应(QRT-PCR)法检测0、24、48 h IL-2、IL-4 mRNA表达。结果生理水平和妊娠水平E_2可下调活化48 h的T细胞IL-2基因的转录水平,与对照组相比具有统计学意义。E_2对活化后24、48 h的T细胞IL-4基因转录的调节作用呈剂量选择性。生理水平E_2使活化T细胞IL-4 mRNA水平显著降低,而妊娠水平E_2使活化T细胞IL-4 mRNA水平显著升高。结论①生理水平E_2下调IL-2、IL-4基因的转录。②妊娠水平E_2下调IL-2基因的转录、上调IL-4基因的转录。③E_2对自身免疫病发病机制过程中起重要的调节作用。
Objective To observe the effects of estradiol (E_2) at physiological level (100 pg / ml) and pregnancy level (50 ng / ml) on the expression of interleukin (IL) -2 and IL-4 mRNA in mouse T lymphocytes cultured in vitro Influence and further explore the regulatory mechanism of E 2 on autoimmune diseases. Methods Balb / c mice were sacrificed and the splenic T lymphocytes were prepared and divided into 3 groups: ConA 5μg / ml (control group), ConA 5μg / ml + E 2: 100 pg / ml, ConA 5μg / ml + 50 ng / ml. 6 samples in each group. Each group of T cells were incubated at 37 ℃, 5% CO 2 conditions were incubated for 0,24,48 h. The mRNA expressions of IL-2 and IL-4 at 0, 24 and 48 h were detected by semi-quantitative reverse transcription-polymerase chain reaction (QRT-PCR) Results Physiological level and gestational level E 2 decreased the transcription level of IL-2 gene in T cells activated for 48 h, which was statistically significant compared with the control group. The effect of E_2 on the transcription of IL-4 gene in T cells 24 and 48 h after activation was dose-selective. Physiological level of E_2 significantly decreased the level of IL-4 mRNA in activated T cells, whereas pregnancy level of E_2 significantly increased the level of IL-4 mRNA in activated T cells. Conclusion Physiological level E 2 down-regulates the transcription of IL-2 and IL-4. Pregnancy level E2 decreased the transcription of IL-2 gene and up-regulated the transcription of IL-4 gene. ③ E2 plays an important regulatory role in the pathogenesis of autoimmune diseases.