老年大鼠单核/巨噬细胞分泌和表达肿瘤坏死因子增多

INCREASE OF MONOCYTES/MACROPHAGES DERIVED TNF-α RELEASE AND GENE EXPRESSION IN AGING RATS

为研究老年时肿瘤坏死因子（ＴＮＦ－α）分泌及表达的改变，在内毒素（ＬＰＳ）１．０μｇ／ｍｌ刺激大鼠单核／巨噬细胞后，用酶联免疫法（ＥＬＩＳＡ）测定培养液中ＴＮＦ－α含量，用半定量逆转录－聚合酶链反应（ＲＴ－ＰＣＫ）测定ＴＮＦ－αｍＲＮＡ。同时测定培养液中一氧化氮（ＮＯ）和前列腺素Ｉ２（ＰＧＩ２）的含量。结果显示：老年鼠ＴＮＦ－α分泌量及其ｍＲ－ＮＡ明显高于青年鼠。ＮＯ产量在老年鼠与青年鼠之间无明显差异。老年鼠ＰＧＩ２分泌明显低于青年鼠。由于ＰＧ能抑制ＴＮＦ－α释放，从而推测，ＰＧＩ２产生能力的降低可能是老年大鼠单核／巨噬细胞ＴＮＦ－α分泌量明显高于青年鼠的原因之一。

o investigate the changes of both release and synthesis of TNF-α (tumor necrosis factor- α) in aging rats, the rat monocytes or macrophages were stimulated by lipopolysaccharide (LPS) 1.0 μg/ml. The level of TNF-α in culture supernatant was measured by ELISA (enzymelinkedimmunosorbentassays) and the TNF-α was determined by semiquantity RT-PCR (reverse transcriptpolymerase chain reaction). At the same time, the levels of NO (nitric oxide)and PGI-2 (prostglandin I2) in the culture supernatant were measured. The result showed that the monocytes or macrophages from the aging rats produced more TNF-α and it's mRNA than those form the young rats. There was no difference in NO level between the aging and the young rats. The production of PGI-2 from the aging rats was lower than that from the young ones. Since PGI-2 may inhibit TNF-α production from macrophages, the decrease output of PGI-2 might is be one of the mechanisms that the aging rats produced more TNF-α and it's mRNA than those from the young rats.