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目的观察核因子(NF)-κB、细胞间黏附分子(ICAM)-1和炎症细胞因子在急性胰腺炎(AP)肝损伤中的作用。方法36只SD大鼠随机分为AP组、假手术组(SO组),通过胰胆管逆行注射3.5%牛磺胆酸钠溶液制作大鼠AP模型。术后3、6、12 h胰腺组织光镜检查;肝组织光镜、电镜观察;检测血清丙氨酸氨基转移酶(ALT);放射免疫法(RIA)测定血清肿瘤坏死因子(TNF)-α、白细胞介素(IL)-1β、IL-6;酶联免疫吸附法(ELISA)检测IL-10;实时定量聚合酶链反应(Real-time PCR)检测肝组织TNF-αmRNA、IL-6 mRNA;肝组织Envision法免疫组织化学测定NF-κB、ICAM-1。结果病理学证实建立AP组,出现肝损伤的病理形态变化;与SO组比较,AP组的血清ALT以及TNF-α、IL-6、IL-1β、IL-10水平显著增高(P<0.05),其中血TNF-α水平在3 h升高、6 h达高水平,血IL-6在AP 3 h明显升高,下降缓慢。AP 6、12 h组肝NF-κB活化,AP各组间肝NF-κB活性表达差异均有统计学意义(x~2=15.048,P<0.05),ICAM-1无表达。AP 3～12 h内,AP组肝TNF-αmRNA在3 h明显升高、6 h高表达;AP组的肝IL-6 mRNA则在3 h已增加、3 h后缓慢下降,均显著高于各自时段的SO组(P<0.05)。结论AP发生后,肝脏NF-κB活化,可能介导肝TNF-αmRNA、IL-6 mRNA的表达来参与肝损伤,ICAM-1对AP早期肝损伤元明显作用。
Objective To observe the role of nuclear factor (NF) -κB, intercellular adhesion molecule (ICAM) -1 and inflammatory cytokines in hepatic injury induced by acute pancreatitis (AP). Methods Thirty - six SD rats were randomly divided into AP group, sham operation group (SO group) and AP model of rats by retrograde injection of 3.5% sodium taurocholate into the pancreatic duct. The pancreatic tissue was examined by light microscopy 3, 6, 12 h after operation. The liver tissues were observed with light microscope and electron microscope. Serum alanine aminotransferase (ALT) and serum tumor necrosis factor (TNF) -α , Interleukin (IL) -1β, IL-6 and IL-10 by enzyme-linked immunosorbent assay (ELISA) were detected by real time quantitative polymerase chain reaction Envision immunohistochemical method was used to detect NF-κB and ICAM-1 in liver tissue. Results Compared with SO group, the levels of ALT, TNF-α, IL-6, IL-1β and IL-10 in AP group were significantly increased (P <0.05) , The levels of TNF-α in blood increased at 3 h and reached the high level at 6 h, while the levels of IL-6 in blood increased significantly at 3 h and declined slowly. There was significant difference in the expression of NF-κB in hepatic tissues between AP 6 and 12 h groups (χ ~ 2 = 15.048, P <0.05), and no expression of ICAM-1. During 3 ~ 12 h AP, the expression of hepatic TNF-αmRNA in AP group increased significantly at 3 h and reached a high level at 6 h. The level of IL-6 mRNA in AP group increased at 3 h and then decreased slowly at 3 h SO groups in each time period (P <0.05). Conclusion After AP, the activation of NF-κB in liver may mediate the expression of liver TNF-αmRNA and IL-6 mRNA to participate in liver injury. ICAM-1 plays a significant role in AP early liver injury.