中文摘要：

目的：探讨全身炎症反应综合征（SIRS）中相关共刺激分子的表达及其调控因素，并对共刺激分子在全身炎症反应综合征发展及治疗中的作用及机制进行初步探究。方法：腹腔注射脂多糖（LPS）建立全身炎症反应综合征的小鼠动物模型后，将BALB／c模型小鼠随机分为生理盐水（NS）、LPS、CD28＋LPS三组，进行脾淋巴细胞的分离，通过RT-PCR、ELISA等方法检测共刺激分子在不同组别中的表达。结果：经CD28活化型单克隆抗体（CD28mAb）刺激后的BALB／c小鼠组中共刺激分子CD40配体（CD40L）、杀伤性T细胞相关抗原-4（CTLA-4）的表达量较生理盐水组明显增高。结论：共刺激分子CD28对于全身炎症反应综合征有促进的作用。

英文摘要：

Objective： To investigate the expression level of co-stimulatory molecules in mouse model of systemic inflammatory response syndrome （SIRS）, and try to find out the primary mechanism and effect of co-stimulator cytokines in SIRS. Methods： By injecting lipopolysaccharide （LPS）, the mouse model of SIRS was established successfully. BALB/c mice were divided into 3 groups at random, and were treated with normal saline（NS）, LPS, CD28mAb＋LPS. Enzyme linked immunosorbent assay （ELISA） was used to measure IL-6 and some other cytokines in serum, such as CD40 ligand （CD40L） and Cytotoxic T lymphocyte associated antigen-4 （CTLA-4）. Spleen lymphocytes were separated to detect cytokines and co-stimulatory molecules by RT-PCR. Results： We find the positive control group with SIRS highly expresses inflammatory related cytokines and co- stimulatory molecules. For the BALB/c of injecting activated CD28mAb group, the expression of CD40L was up-regulated while CTLA-4 was down-regulated. Conclusions： CD28 as a co-stimulatory molecule plays an important role in increasing inflammatory response degree in SIRS.