中文摘要：

目的 观察脓毒症大鼠血清补体及细胞因子的变化规律,并探讨其可能的发生机制.方法 按随机数字表法将120只雄性Wistar大鼠分为正常对照组（n=15）、假手术组（n=15）、脓毒症组〔盲肠结扎穿孔术（CLP）制模,n=90〕,脓毒症组再分为24、48、72 h 3个亚组.采用固相夹心法酶联免疫吸附试验（ELISA）检测血清补体C5、C5a及肿瘤坏死因子-α（TNF-α）、白细胞介素（IL-1β、IL-6）、高迁移率族蛋白B1（HMGB1）、巨噬细胞移动抑制因子（MIF）水平.结果 与正常对照组及假手术组相比,脓毒症组制模后24 h,C5、C5a、IL-1β水平显著升高〔C5（ng/L）：1.60±0.19比1.04±0.20、1.09±0.09,C5a（ng/L）：0.20±0.02比0.18±0.01、0.18±0.02,IL-1β（ng/L）：700.20±111.41比475.87±108.96、592.29±121.57,均P〈0.05〕,随后有所下降,48 h和72 h时C5仍显著高于正常对照组（1.17±0.24、1.27±0.24比1.04±0.20,均P〈0.05）.制模后48 h和72 h,脓毒症组TNF-α（ng/L：51.33±1.96、51.06±1.64）显著低于正常对照组（59.53±3.06）和假手术组（57.91±2.72,均P〈0.05）.脓毒症组HMGB1水平逐渐升高,72 h已显著高于正常对照组和假手术组（ng/L：472.21±20.94比406.00±43.16、404.41±35.39,均P〈0.05）.各组间MIF、IL-6水平差异均无统计学意义.结论 补体系统通过促进促炎细胞因子及炎性介质释放,导致炎症反应失控和免疫功能紊乱,是脓毒症重要发病机制之一.

英文摘要：

Objective To observe the changes of serum complements and proinflammatory cytokines in rats with sepsis, and to explore the possible mechanism.Methods 120 healthy male Wistar rats were randomly divided into three groups： normal control group （n = 15）, sham operation group （n = 15） and sepsis group [cecum ligation and puncture （CLP） operation,n = 90]. The sepsis rats were sacrificed on 24, 48 and 72 hours after modeling. The level of serum complements （C5, C5a） and cytokines tumor necrosis factor-α （TNF-α）, interleukin （IL-1, IL-6）, high mobility group box 1 （HMGB1）, macrophage migration inhibitory factor （MIF） were detected by enzyme linked immunosorbent assay （ELISA）.Results Compared with normal control group and sham operation group, the levels of serum complements C5, C5a and IL-1β were significantly increased at 24 hours after CLP in sepsis group [C5 （ng/L）： 1.60±0.19 vs. 1.04±0.20, 1.09±0.09; C5a （ng/L）： 0.20±0.02 vs. 0.18±0.01, 0.18±0.02; IL-1β （ng/L）： 700.20±111.41 vs. 475.87±108.96, 592.29±121.57; allP 〈 0.05]; then the levels of C5, C5a and IL-1β declined, the level of serum C5 were also higher than normal control group at 48 hours and 72 hours after CLP （ng/L： 1.17±0.24, 1.27±0.24 vs. 1.04±0.20, bothP 〈 0.05）. In sepsis group the level of serum TNF-α （ng/L： 51.33±1.96, 51.06±1.64） was lower than that in normal control group （59.53±3.06） and sham operation group （57.91±2.72） at 48 hours and 72 hours （allP 〈 0.05）. There was a time dependent rise of serum HMGB1 in sepsis group, which level was much higher than that in normal control group and sham operation group at 72 hours after CLP （ng/L： 472.21±20.94 vs. 406.00±43.16, 404.41±35.39, bothP 〈 0.05）. There were no significant differences of MIF, and IL-6 level between groups at each time points.Conclusions Complement system led to uncontrolled inflammatory response and immune dysfunction through the release of proinflammatory cytokines an