Panax notoginseng
saponins are extracted from Chinese
ginseng—
Panax notoginseng Ledeb
—and are known to have
therapeutic anti-inflammatory effects. However, the precise mechanism behind
their anti-inflammatory effects remains relatively unknown. To better understand
how
Panax notoginseng
saponins exert their therapeutic benefit,
we tested them in a rat model of severe acute pancreatitis (SAP). Rats received
a tail vein injection of
Panax notoginseng
saponins and were
administered 5% sodium taurocholate 2 h later. Pancreatic tissue was then
harvested and levels of miR-181b, FSTL1, TREM1, TLR4, TRAF6, IRAK1, p-Akt,
p-p38MAPK, NF-κBp65, and p-IκB-α were determined using Western blot and
quantitative real-time polymerase chain reaction (qRT-PCR). Enzyme-linked
immunosorbent assays were used to determine serum levels of tumor necrosis
factor-α (TNF-α), TREM1, interleukin (IL)-6, ACAM-1, IL-8, and IL-12 and
DNA-bound levels of NF-KB65 and TLR4 in pancreatic and ileum tissue. Serum
levels of lipase and amylase, pancreatic myeloperoxidase (MPO) activity, and
pancreatic water content were also measured. Hematoxylin and eosin staining was
used for all histological analyses. Results indicated upregulation of miR-181b,
but negligible levels of FSTL1, p-p38MAPK, TLR4, TRAF6, p-Akt, IRAK1, TREM1,
p-NF-κBp65, and p-IκB-α, as well as negligible DNA-bound levels of NF-KB65 and
TLR4. We also observed lower levels of IL-8, IL-6, ACAM-1, TNF-α, MPO, and IL-12
in the
Panax notoginseng
saponin–treated group when compared
with controls. In addition,
Panax notoginseng
saponin–treated
rats had significantly reduced serum levels of lipase and amylase. Histological
analyses confirmed that
Panax notoginseng
saponin treatment
significantly reduced taurocholate-induced pancreatic inflammation.
Collectively, our results suggest that
Panax notoginseng
saponin treatment attenuated acute pancreatitis and pancreatic inflammation by
increasing miR-181b signaling. These findings suggest that
Panax
notoginseng
saponins have therapeutic potential in the treatment of
taurocholate-induced SAP.