IL-8、IL-10在大鼠急性胰腺炎并发肺损伤中的作用

目的　探讨IL- 8、IL- 10在大鼠胰腺炎肺损伤中的作用。方法　采用胰胆管逆行注射3.5%牛磺胆酸钠的方法,制作大鼠重症急性胰腺炎并发肺损伤模型。分别对胰腺损伤、肺损伤程度进行病理评分,测定肺组织湿/干质量比;ELISA法测定大鼠血清IL- 8、IL -10水平。结果　造模后1 h,大鼠即出现较明显的胰腺损伤,随着时间的延长,胰腺损伤逐渐加重,以12 h为最。造模后1 h,即出现肺损伤,光镜下表现为白细胞浸润、肺泡间隔增厚、肺水肿及肺泡腔萎陷;至4 h肺组织湿/干质量比开始增加,此后,肺损伤程度逐渐增加,以24 h为最。造模后1 h,大鼠血清IL- 8、IL- 10水平逐渐升高,至24h达最高。结论　IL -8、IL- 10参与了大鼠胰腺炎肺损伤的病理过程,胰腺炎肺损伤的过程可能是体内全身性炎症反应综合征(SIRS)和代偿性抗炎症反应综合征(CARS)失衡的结果。

Effects of IL-8, IL-10 in Acute Pancreatitis Associated with Acute Lung Injury in Rats

Objective To explore the roles of IL-8 and IL-10 in pathogenesis of pancreatitis associated lung injury(PALI) in rats. Methods Pancreatitis was induced with 3.5% sodium taurocholate through of Aho et al. The severity of pancreatitis was evaluated by quantitating pancreatic pathologic score. Lung injury was evaluated by lung pathologic score and lung water content. Serum IL-8 and IL-10 were quantitated by enzyme-linked immunosorbent assay. Results Lung injury could be found at 1 h after induction of pancreatitis with 3.5% sodium taurocholate. The microscopic findings of lung injury included leukocytes infiltration in lung tissue, pulmonary sepatal thickening, pneunoedema and collapse of alveolar cavity. Lung water content increased from 4 h after induction of pancreatitis. The levels of serum IL-8 and IL-10 increased from 1 h after induction of pancreatitis, and peaked at 24 h. Conclusion Both IL-8 and IL-10 are involved in the pathogenesis of pancreatitis acute lung injury (PALI) and PALI may be the result of imbalance of systemic inflammatory response syndrome(SIRS) and compensatory anti-inflammatory response syndrome(CARS).