Picroside II is an important ingredient agent in
Traditional Chinese medicine and hoped to reduce hepatocellular injury caused by severe
acute pancreatitis (SAP). An SAP-induced hepatocellular injury model was established in rats by using
pentobarbital sodium. 27 rats were divided into 3 groups: the
sham group (SG), model group (MG), and Picroside groups (PG). SAP-induced hepatocellular injury was assessed using
hematoxylin and
eosin staining. We measured hepatocellular
enzymes (
amylase (AMY),
alanine aminotransferase (ALT), and
aspartate aminotransferase (AST)), oxidative stress factors (superoxidase dismutase (SOD) and
malondialdehyde (MDA)), and inflammatory factors (
tumor necrosis factor α (TNF-α),
interleukin- (IL-) 6, and IL-10), apoptotic factors (BAX and cleaved
caspase 3), and inflammatory signaling (
Janus kinase 2 (JAK2)/
signal transducer and activator of transcription 3 (STAT3), p-JAK2, and p-STAT3) in hepatocellular tissues. The SAP-induced hepatocellular injury model was successfully established.
Picroside II treatment repaired hepatocellular injury by reducing the activities of AMY, ALT, and AST; reducing the levels of MDA, TNF-α,
IL-1,
IL-6, p-JAK2, p-STAT3, BAX, and cleaved
caspase 3; and increasing the levels of SOD and
IL-10.
Picroside II exerted protective function for the SAP-induced hepatocellular injury model.
Picroside II improved SAP-induced hepatocellular injury and
antioxidant and anti-inflammatory properties by affecting JAK2/STAT3 phosphorylation signaling.