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SIP24/24p3为一小鼠分泌的应急时相反应蛋白,SIP24/24p3在体内的表达是高度组织特异的,其功能包括抗炎症及特异性诱导白细胞凋亡。为研究SIP24/24p3的调控因子及机制,我们在细胞培养中通过35S代谢标记方法定量检测了炎症因子IL-6和TNF-α对SIP24/24p3蛋白的诱导作用。结果显示:IL-6在BALB/c 3T3细胞中诱导SIP24/24p3.在BNL细胞中无诱导作用,而TNF-α在BMLB/c 3T3和BNL细胞中对SIP24/24p3都有诱导作用;IL-6对SIP24/24p3表达的剂量效应在BALB/c 3T3细胞中呈正相关,在BNL细胞中无相关性;TNF-α对SIP24/24p3表达的剂量效应在BALB/c 3T3和BNL细胞中都呈正相关,但在BNL细胞中高浓度的TNF-α导致SIP24/24p3表达量有所降低;在BALB/c 3T3细胞中IL-6和TNF-α对SIP24/24p3的表达有同等诱导作用;而在BNL细胞中FNF-α对SIP24/24p3的表达起主导作用,IL-6是一种起扩增作用的第二诱导信号。这有助于解释SIP24/24p3在体内的高度特异表达,也为阐明应急时相反应蛋白在不同组织中的调控机制提供了依据。
SIP24 / 24p3 is an emergent phase response protein secreted by a mouse. The in vivo expression of SIP24 / 24p3 is highly tissue-specific and its function includes anti-inflammatory and specific induction of leukocyte apoptosis. To investigate the regulatory factors and mechanisms of SIP24 / 24p3, we used the 35S metabolic labeling method to quantitatively detect the induction of SIP24 / 24p3 protein by inflammatory cytokines IL-6 and TNF-α in cell culture. The results showed that IL-6 induced SIP24 / 24p3 in BALB / c 3T3 cells without induction in BNL cells, while TNF-α induced SIP24 / 24p3 in BMLB / c 3T3 and BNL cells. IL- 6 had a positive correlation with dose-effect of SIP24 / 24p3 expression in BALB / c 3T3 cells and no correlation in BNL cells. The dose effect of TNF-α on SIP24 / 24p3 expression was positively correlated with BALB / c 3T3 and BNL cells , But the expression of SIP24 / 24p3 was decreased in high concentrations of TNF-α in BNL cells; IL-6 and TNF-α in BALB / c 3T3 cells induced SIP24 / 24p3 expression equally; while in BNL cells FNF-α plays a leading role in the expression of SIP24 / 24p3, a second inducing signal that plays an amplification role. This helps to explain the highly specific expression of SIP24 / 24p3 in vivo and provides a basis for clarifying the regulatory mechanism of the phase reaction protein in different tissues in emergency.