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目的 探讨胰弹性蛋白酶对内毒素诱导的肝枯否细胞 (KC)炎症介质表达的影响。方法 原代培养的肝枯否细胞分为A组(对照组 )、B组 (内毒素脂多糖诱导组)、C组(胰弹性蛋白酶干预组 ) ,实验后取细胞行RT PCR检测KC的TNF α、IL 1 βmRNA表达水平、取培养上清液行ELISA测定TNF α、IL 1 β蛋白水平。结果 不论是mRNA水平还是蛋白水平 ,脂多糖诱导 (B组 )可造成KC的TNF α及IL 1 β表达增高 ,与对照组比较差异有统计学意义 (P <0 0 1 ) ;当用胰弹性蛋白酶干预后 (C组 ) ,KC的TNF α及IL 1 β表达增高更加显著 ,与B组比较差异有统计学意义 (P <0 0 1 )。结论 胰弹性蛋白酶等胰酶可显著增加枯否细胞受脂多糖诱导后对炎症因子的表达量。这可能是急性胰腺炎患者发生SIRS和MODS发生率高及高病死率的原因
Objective To investigate the effect of pancreatic elastase on the expression of inflammatory mediators induced by endotoxin in Hepatic Fibroblast (KC). Methods Primary cultured hepatocytes were divided into group A (control group), group B (endotoxin induced lipopolysaccharide group) and group C (pancreatic elastase intervention group). After the experiment, α, IL 1 β mRNA expression level, take the culture supernatant ELISA determination of TNF α, IL 1 β protein levels. Results Both mRNA and protein level induced by lipopolysaccharide (group B) increased the expression of TNFα and IL 1 β in KC, which was significantly different from the control group (P <0.01) After protease intervention (group C), the expression of TNFα and IL 1 β in KC increased more significantly, which was significantly different from that in group B (P <0.01). Conclusion Pancreatic enzymes such as pancreatic elastase can significantly increase the expression of inflammatory cytokines in Kupffer cells induced by lipopolysaccharide. This may be the reason for the high incidence and high mortality of SIRS and MODS in patients with acute pancreatitis