摘要
目的探讨巨噬细胞移动抑制因子(MIF)在实验性急性坏死性胰腺炎(ANP)发病机制中的作用以及抗炎细胞因子白介素-10(IL-10)对其的影响和意义。方法92只大鼠随机分为对照组、ANP组和IL-10治疗组。腹腔注射左旋-精氨酸制作ANP模型。治疗组于末次精氨酸注射后第2、5、8h腹腔内注射IL-1010000U。各组再分4h、12h、24h和36h点。检测血清巨噬细胞移动抑制因子(MIF)水平以及胰腺和肺组织的MIF表达。结果ANP组MIF在造模后4h已升至高值,并持续维持在较高水平,波动于(117.82±15.73)μg/L至(120.97±11.24)μg/L,显著高于对照组的血清MIF浓度(P<0.01或P<0.05);治疗组各时点血清MIF浓度低于ANP组(P<0.05)。对照组大鼠胰腺组织的外分泌部、肺组织的支气管上皮细胞及肺泡细胞有MIF弱表达,ANP组和治疗组胰腺及肺组织MIF阳性细胞数增加、染色明显增强。结论(1)MIF水平在ANP早期明显升高,ANP时肺及胰腺组织中MIF表达增强,提示MIF参与了大鼠ANP及肺损伤的发病;(2)抗炎细胞因子IL-10对血清及胰腺和肺组织的MIF水平有抑制作用,IL-10可能减轻实验性ANP的胰腺及肺的损害,对胰腺及肺组织有一定保护作用。
Objective To investigate the pathogenic role of macrophage migration inhibitory factor （MIF） in rats with acute necrotizing pancreatitis （ANP）, and to assess the inhibitory effect of anti-inflammatory cytokine IL-10 on MIF activity. Methods 92 SD male rats were randomized into control group （group C, n = 24）, acute pancreatitis group （group A, n 36）, and IL-10 intervention group （group L n - 32）. In group A, rats were injected intraperitoneally with 6% L-Arginine （3 × 1.0 rag/g） three times at 1-h intervals for ANP. In group C, rats received the same amount of saline during the same period. In group 1 , rats were injected intraperitoneally with IL-10 000 U 2 h, 5 h and 8 h after L-Arginine administration. Animals were killed at 4, 12, 24 and 36 h after the last L-Arginine injection. MIF levels in serum, pancreas and lung were determined by ELISA or immunohistochemistry. The presence of brown-yellow granules in cytoplasm was regarded as positive MIF expression. According to the number of positive cells in the same cells, the result was divided into 3 grades： negative （-）, where the staining cells were less than 5%; positive （ ＋）, where the staining cells were 5% to 25%, and strong positive （ ＋＋ ）, where the staining cells were more than 25%. Results Serum MIF levels were increased at 4 h after the induction of ANP and remained high. Serum MIFlevels fluctuated between （117.82= 15.73）/g/L and （120. 97±11.24）ptg/L. Serum MIF levels ingroup A were increased significantly, and serum MIF levels in group I were lower than those in group A. Weakly positive immunostain was observed even in the pancreas and lungs in group C, while the staining was increased in the pancreas and lungs in group A and I . Conclusions （1）Serum MIF levels were up regulated markedly early in ANP, and MIF positive expression in the lungs and pancreas was also increased. These results suggest that MIF plays a role in the pathogenesis of ANP and associated lung injury. （2）Interleukin-10 can inhibit MIF activation and alleviate histological damage to the pancreas and lung in Arginine-induced ANP.
出处
《胰腺病学》
2006年第6期326-329,共4页
Chinese JOurnal of Pancreatology
基金
2004年广西自然科学基金(No.0447054)
