fig3

Figure 3. PgNVs administration ameliorates acute pancreatitis in vivo. (A) Representative images showing the mouse pancreas from each experimental group and injury score: control group showing preserved pancreatic architecture, AP group displaying marked tissue injury characterized by loss of acinar structure and inflammatory cell infiltration (black arrows), and PgNVs group demonstrating partial preservation of pancreatic architecture. Samples were taken at 3 days post pancreatitis, and stained with hematoxylin-eosin staining (n = 5). Scale bar: 100 µm; (B) Determination of plasma amylase activity in control, AP, and AP+PgNVs groups at 3 days post pancreatitis (n = 5); (C) Relative mRNA expression of Tnfa, Il6 and Il1b in the pancreas of mice three days after induction of acute pancreatitis (AP) in control, AP and AP + PgNVs groups. The levels were determined by RT-qPCR analysis, using Tbp as housekeeping gene (n = 5); (D) Representative western blot image of p-p65 and densitometry using beta-tubulin as a loading control (n = 3); (E) Plasma IL6 levels in control, AP, and AP+PgNVs groups at 3 days post pancreatitis (n = 5). Measurements expressed as mean ± SD. *Significantly different from control group, P < 0.05; **significantly different from control group, P < 0.01; ^#significantly different from AP group, P < 0.05; ^##significantly different from AP group, P < 0.01. AP: Acute pancreatitis; EVs: extracellular vesicles; PgNVs: pomegranate-derived nanovesicles; mRNA: messenger RNA; Tnfa: tumor necrosis factor alpha; Il6: interleukin 6 (IL6); Il1b: interleukin 1 beta; RT-qPCR: reverse transcription-quantitative polymerase chain reaction; Tbp: TATA-box binding protein; p-p65: phosphorylated p65; SD: standard deviation.