Fig. 1
From: St13 protects against disordered acinar cell arachidonic acid pathway in chronic pancreatitis
Lipid metabolism was elevated in pancreatic tissues from patients and PRSS1 transgenic (PRSS1Tg) mice with ACP. Histological alterations and ultrastructural changes in pancreatic tissues from humans (A) and PRSS1Tg mice (B) with nACP/ACP were analysed by haematoxylin and eosin (H&E) staining and transmission electron microscopy (TEM); black arrows (↑): cell nuclei; white arrows (↑): ERs; blue arrows (↑): zymogen granules; purple arrows (↑): mitochondria; orange arrows (↑): fibrin; red arrows (↑): lipid droplets. C Expression of IL-1β, IL-6, and TNF-α in normal, nACP, and ACP tissues from humans and PRSS1Tg mice was measured by ELISA. The levels of fatty acids (FAs), triglycerides (TGs), cholesterol (CHOL), phospholipids, and eicosanoids in normal, nACP, and ACP tissues from humans (D) and PRSS1Tg mice (E) were assessed byGas chromatography-mass spectrometry (GC–MS) and liquid chromatography-mass spectrometry (LC–MS). Scale bars (H&E), 100 μm. ACP, alcoholic chronic pancreatitis; Cer, caerulein; EtOH, ethanol; nACP, non-alcoholic chronic pancreatitis. *P ≤ 0.05, **P ≤ 0.01, ***P ≤ 0.001. The data are presented as the means ± SDs