Medical Laboratory, Affiliated Hospital of Putian University, Putian, Fujian, China (mainland).
School of Pharmacy and Medical Technology, Putian University, Putian, Fujian, China (mainland).
Med Sci Monit. 2020 Apr 13;26:e920684. doi: 10.12659/MSM.920684.
BACKGROUND Acute pancreatitis (AP) is a symptom of sudden pancreas inflammation, which causes patients severe suffering. In general, fibroblast growth factor (FGF) levels are increased and amylase and lipase activities are elevated during AP pathogenesis, but protein concentration are low. However, the mechanism through which FGF signaling regulates AP pathogenesis remains elusive. MATERIAL AND METHODS The concentrations of PGE2, TNF-alpha, sCRP, FGF1, and FGF2 in the serum samples of the AP group and healthy control group were detected by enzyme-linked immunosorbent assay. In addition, IkappaBalpha and p-IkappaBalpha levels were analyzed in the serum samples. Subsequently, the AP rat model was established, and FGF1, FGF2, anti-FGF1, and anti-FGF2 antibodies and Bay11-7082 were injected into AP rats. TNF-alpha, PAI-1 JNK, p-JNK, IkappaBalpha, and p-IkappaBalpha levels were also examined. RESULTS Results showed that levels of PGE2, TNF-alpha, sCRP, p-IkappaBalpha, FGF1, and FGF2, as well as amylase and lipase activity were increased in patients with AP compared with those in healthy people. In addition, protein concentrations were lower in patients with AP than in the healthy group. Activation of FGF signaling by injecting FGF1 or FGF2 also inhibited AP-induced inflammation response in the pancreas and increased amylase and lipase activities, as well as protein concentration. However, the injection of FGF1 and FGF2 antibodies accelerated AP-mediated inflammation responses in the serum. In addition, Bay11-7082 injection inhibited AP activation of inflammation response and amylase and lipase activities. Protein concentration were also increased in AP rats. CONCLUSIONS FGF signaling protects against AP-mediated damage by inhibition of AP-activating inflammatory responses.
急性胰腺炎（AP）是胰腺突然炎症的症状，会使患者遭受严重痛苦。一般来说，在 AP 发病过程中，成纤维细胞生长因子（FGF）水平升高，淀粉酶和脂肪酶活性升高，但蛋白浓度较低。然而，FGF 信号转导调节 AP 发病机制的机制仍不清楚。
通过酶联免疫吸附试验检测 AP 组和健康对照组血清样本中 PGE2、TNF-α、sCRP、FGF1 和 FGF2 的浓度。此外，还分析了血清样本中的 IkappaBalpha 和 p-IkappaBalpha 水平。随后，建立 AP 大鼠模型，并向 AP 大鼠注射 FGF1、FGF2、抗 FGF1 和抗 FGF2 抗体以及 Bay11-7082。还检查了 TNF-α、PAI-1 JNK、p-JNK、IkappaBalpha 和 p-IkappaBalpha 水平。
结果表明，与健康人相比，AP 患者的 PGE2、TNF-α、sCRP、p-IkappaBalpha、FGF1 和 FGF2 水平以及淀粉酶和脂肪酶活性均升高。此外，AP 患者的蛋白浓度低于健康组。注射 FGF1 或 FGF2 激活 FGF 信号也抑制了 AP 诱导的胰腺炎症反应，并增加了淀粉酶和脂肪酶活性以及蛋白浓度。然而，注射 FGF1 和 FGF2 抗体加速了 AP 介导的血清炎症反应。此外，Bay11-7082 注射抑制了 AP 激活的炎症反应和淀粉酶和脂肪酶活性。AP 大鼠的蛋白浓度也升高。
FGF 信号通过抑制 AP 激活的炎症反应来保护 AP 介导的损伤。
