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目的研究催乳素(PRL)对刀豆蛋白A(ConA)诱导活化T淋巴细胞的影响,探讨PRL在T淋巴细胞活化中的作用。方法用25μg/L的PRL与500μg/L的溴隐亭(Brc)单独或联合刺激5 mg/LConA诱导活化的CD4+T淋巴细胞系JurkatE6-1细胞,实验设置空白对照组、ConA组、ConA和PRL联合刺激组(PRL组)、ConA和Brc联合刺激组(Brc组)、ConA和PRL及Brc联合刺激组(PRL-Brc组),药物刺激48 h后,Trizol法提取Jurkat E6-1细胞总RNA,反转录后,利用PCR技术检测TNF受体相关因子6(TRAF6)基因的表达,利用反转录酶PCR技术检测TNF超家族成员4(TNFSF4)和相对分子质量为37 000的杀伤特异性分泌蛋白(KSP37)基因的表达。结果与空白对照组、ConA组比较,PRL组和Brc组活化T淋巴细胞TRAF6、TNFSF4、KSP37基因的表达显著降低(Pa<0.05);与PRL组和Brc组比较,PRL-Brc组可明显逆转PRL对活化T淋巴细胞TRAF6、TNFSF4、KSP37基因表达的抑制(Pa<0.05);与空白对照组比较,PRL-Brc组可明显抑制活化T淋巴细胞TRAF6基因的表达(Pa<0.01),KSP37及TNFSF4的表达高于空白对照组但是无统计学意义(Pa>0.05);与ConA组比较,PRL-Brc组可明显抑制活化T淋巴细胞TRAF6、TNFSF4、KSP37基因的表达(Pa<0.01)。结论生理浓度的PRL可以通过抑制活化T淋巴细胞中TRAF6、TNFSF4、KSP37的表达参与T淋巴细胞应答;Brc可通过拮抗PRL对活化T淋巴细胞的TRAF6、TNFSF4、KSP37的抑制用于治疗PRL引起的疾病。
Objective To investigate the effect of prolactin (PRL) on activated T lymphocytes induced by ConA and to explore the role of PRL in the activation of T lymphocytes. Methods Jurkat E6-1 cells, activated by 5 mg / L LCA, were stimulated with 25 μg / L PRL and 500 μg / L bromocriptine (Brc) alone or in combination. The blank control group, ConA group, ConA (PRL group), ConA and Brc combined group (Brc group), ConA and PRL group and Brc combined group (PRL-Brc group). After 48 h of drug stimulation, Jurkat E6-1 cells Total RNA was reverse transcribed and the expression of TNF receptor related factor 6 (TRAF6) gene was detected by PCR. The TNF superfamily member 4 (TNFSF4) and the relative molecular weight of 37 000 were detected by reverse transcriptase PCR Specific secreted protein (KSP37) gene expression. Results Compared with the blank control group and the ConA group, the expression of TRAF6, TNFSF4 and KSP37 in activated T lymphocytes of PRL group and Brc group was significantly decreased (P <0.05). Compared with PRL group and Brc group, PRL-Brc group was significantly reversed (P <0.05). Compared with the blank control group, PRL-Brc group could significantly inhibit the expression of TRAF6 gene in activated T lymphocytes (Pa <0.01), KSP37 and The expression of TNFSF4 was higher than that of the blank control group (P> 0.05). Compared with the ConA group, PRL-Brc group could significantly inhibit the expression of TRAF6, TNFSF4 and KSP37 in activated T lymphocytes (Pa <0.01). Conclusion Physiological concentrations of PRL can inhibit the expression of TRAF6, TNFSF4 and KSP37 in activated T lymphocytes and participate in the T lymphocyte response. Brc inhibits PRL-induced activation of T lymphocytes by antagonizing PRL on TRAF6, TNFSF4 and KSP37 disease.