Fig. 6: The comparison of pancreatic injury and inflammation between Gpihbp1−/− mice with different HTG severity in caerulein-induced acute pancreatitis.
a Triglyceride concentration of plasma before caerulein treatment between wild-type, HTG1 (triglyceride concentration, 1000–2000 mg/dL) and HTG2 mice(triglyceride concentration, å 2000 mg/dL). b, c Plasma amylase and lipase activity at 12th hour after the first injection of caerulein (50 μg/kg, 10 times, hourly) between these three groups. d Representative photomicrographs of H&E-stained section of pancreas in wild-type, HTG1 and HTG2 mice after acute pancreatitis induction. Scale bar = 500 or 100 μm. e Pathological scores of the pancreas in wild-type, HTG1 and HTG2 mice after acute pancreatitis induction. f Incidence rates of pancreatic necrosis between these three groups after acute pancreatitis induction. Each value was the mean ± SEM for n = 6. g Immunohistochemistry evaluation for myeloperoxidase and CD68 in pancreas between wild-type, HTG1 and HTG2 mice after acute pancreatitis induction. Scale bar = 100 μm. i Semiquantitative results of the area ratio of myeloperoxidase and CD68-positive cells among wild-type, HTG1 and HTG2 mice after acute pancreatitis induction. Each value was the mean ± SEM for n = 3–5. *p < 0.05 or **p < 0.01 or ***p < 0.001 vs wild-type group. #p < 0.05 or ##p < 0.01 or ###p < 0.001 vs HTG1 group. WT wild-type, TG triglyceride, Ed edema, Necr necrosis, Vac vacuolisation, Infl inflammation, FFAs free fatty acids, MPO myeloperoxidase
