Chen L M, Chao L, Chao J
Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston 29425, USA.
Life Sci. 1997;60(17):1431-5. doi: 10.1016/s0024-3205(97)00094-5.
Rat kallikrein-binding protein (RKBP) is a negative acute phase protein. The potential role of RKBP in inflammation was evaluated in transgenic mice overexpressing the RKBP gene under the control of the mouse metallothionein metal-responsive promoter. Bacterial endotoxic lipopolysaccharide (LPS) was injected intraperitoneally into mice at a dose of 600 microg/25 g body weight. The death toll was recorded every 12 hours for 3 days. The survival rate of transgenic male mice (n=78) was 33.3% while that of control male mice (n=54) was 9.3% 3 days post LPS injection. In comparison, the survival rate of transgenic female mice (n=59) was 55.9% while that of control female mice (n=65) was 30.8%. Recombinant RKBP levels in the circulation of these mice increased by 3-fold after LPS treatment. The results show that RKBP transgenic mice have a higher survival rate than their non-transgenic control littermates after endotoxin shock and female mice are more resistant to lethality induced by endotoxin shock than male mice in both transgenic and control groups. These findings suggest that kallikrein-binding protein has a protective effect during acute phase inflammation.
大鼠激肽释放酶结合蛋白（RKBP）是一种负急性期蛋白。在小鼠金属硫蛋白金属反应性启动子控制下过表达RKBP基因的转基因小鼠中，评估了RKBP在炎症中的潜在作用。以600微克/25克体重的剂量将细菌内毒素脂多糖（LPS）腹腔注射到小鼠体内。连续3天每12小时记录一次死亡数。LPS注射后3天，转基因雄性小鼠（n = 78）的存活率为33.3%，而对照雄性小鼠（n = 54）的存活率为9.3%。相比之下，转基因雌性小鼠（n = 59）的存活率为55.9%，而对照雌性小鼠（n = 65）的存活率为30.8%。LPS处理后，这些小鼠循环中的重组RKBP水平增加了3倍。结果表明，在内毒素休克后，RKBP转基因小鼠比其非转基因对照同窝小鼠具有更高的存活率，并且在转基因和对照组中，雌性小鼠比雄性小鼠对内毒素休克诱导的致死性更具抵抗力。这些发现表明，激肽释放酶结合蛋白在急性期炎症期间具有保护作用。
