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目的探讨核因子(NF)κB在重症急性胰腺炎(SAP)合并肝损伤过程中的作用及雷公藤内脂醇对SAP合并肝损伤的保护作用。方法Wistar大鼠随机分为3组:重症急性胰腺炎组(P组),雷公藤内脂醇治疗组(T组),假手术组(S组)。SAP模型由5%牛磺胆酸钠大鼠胆胰管逆行注射诱发而成。模型成功后,P组不做处理;T组立即行雷公藤内脂醇(0.05g/L)腹腔注射0.2mg/kg体重;S组仅开腹,不制作SAP模型。术后各组于2、6、12h三个时间点处死大鼠。各时间点测血清淀粉酶(AMY),丙氨酸氨基转移酶(ALT);肿瘤坏死因子(TNF)α、白细胞介素(IL)-6水平;取肝组织测NFκB活性,并行苏木素伊红(HE)染色及电镜观察。结果AMY、ALT水平随SAP病情的的进展而升高(P<0.05),其水平P组及T组各时间点均较S组高,AMY水平在术后12hT组显著低于P组(P<0.05);ALT水平在术后6、12hT组显著低于P组(P<0.05);血清TNFα、IL-6水平随SAP病情的进展而升高(P<0.05),其水平P组及T组各时间点均较S组高,但TN-Fα、IL-6水平T组各时间点显著低于P组(P<0.05);肝组织NFκB活性随SAP病情的的进展而升高(P<0.05),2、6、12h三个时间点P组及T组均升高(P<0.05),但T组活性显著低于P组(P<0.05);T组肝脏病理损害较P组减轻。结论NFκB参与了大鼠SAP合并肝损伤发病过程,雷公藤内脂醇可以减轻SAP?
Objective To investigate the role of nuclear factor (NF) κB in the process of severe acute pancreatitis (SAP) combined with liver injury and the protective effect of triptolide on SAP-associated liver injury. Methods Wistar rats were randomly divided into three groups: severe acute pancreatitis group (P group), triptolide treatment group (T group), sham operation group (S group). The SAP model was induced by retrograde injection of 5% sodium taurocholate into the bile ducts. After the model was successful, the P group was not treated; the T group immediately received triptolide (0.05g/L) intraperitoneal injection of 0.2mg/kg body weight; in the S group, only the abdomen was opened and the SAP model was not made. Rats were sacrificed at 3, 2, and 12 hours after surgery. Serum amylase (AMY), alanine aminotransferase (ALT), tumor necrosis factor (TNF) alpha, and interleukin (IL)-6 levels were measured at each time point; NFκB activity in hepatic tissue was measured, and hematoxylin and eosin was measured. (HE) staining and electron microscopy. Results The levels of AMY and ALT increased with the progression of SAP (P<0.05). The levels of PYY and A group were higher than those of S group at various time points. The AMY level was significantly lower in group T than in group P at 12 hours after operation (P). <0.05); ALT levels were significantly lower in the T group than in the P group at 6 and 12h postoperatively (P<0.05); serum TNFα and IL-6 levels increased with progression of the SAP condition (P<0.05). T group was higher than S group at all time points, but TN-Fα and IL-6 levels in T group were significantly lower than P group at each time point (P<0.05); NFκB activity in liver tissue increased with the progress of SAP condition ( P<0.05). Both P, T groups were increased at 2, 6, and 12h (P<0.05), but T group activity was significantly lower than P group (P<0.05); T group had more pathological lesions than liver P. Group relief. Conclusion NFκB is involved in the pathogenesis of SAP and hepatic injury in rats. Triptolide can reduce SAP.