- pancreatic fibrosis
- signal pathway
This study aimed to elucidate the molecular mechanisms of the anti-pancreatic fibrosis effects of matrine in rats.
Trinitrobenzene sulfonic acid was administrated to rats to establish a pancreatic fibrosis model. Rats were divided into four groups: Control, Sham, Model, and Matrine (n=8). Hematoxylin-eosin staining, Masson staining, and Azan staining were performed to evaluate pancreatic fibrosis. Expression of transforming growth factor-β1 (TGF-β1), α-smooth muscle actin (α-SMA), and collagen I in pancreatic tissues was evaluated by immunohistochemical staining. mRNA and protein levels of TGF-β receptor 1 (TβR1), TβR2, and Smad2 in pancreatic tissues were determined by RT-PCR and Western blot, respectively.
In the model group, hyperplasia of glandules around the glandular ducts, mitochondrial swelling of acinous cells, and severe fibrosis were found. Interestingly, in the Matrine group, mitochondrial swelling was only found in a small number of acinous cells, and the fundamental structures of pancreatic tissues were intact. Moreover, pancreatic fibrosis was markedly alleviated. Comparing to the Sham group, expression of α-SMA, TGF-β1, and collagen I was sharply elevated in the Model group (p<0.05); however, their expressions were much lower in the Matrine group, compared to the Model group (p<0.05). Compared with the Sham group, mRNA and protein levels of Smad2, TβR1, and TβR2 in the Model group were notably raised (p<0.05). However, their high expression was significantly downregulated in the Matrine group (p<0.05).