Background
Long-term abuse of ketamine can cause irreversible bladder fibrosis, but the mechanism of bladder fibrosis is still under investigation. This study aims to explore the mechanism of bladder fibrosis utilizing proteomic analysis in a rat model.
Conclusions
We consider that MC protease 1 and platelet activation pathways may play an important role in ketamine-induced bladder fibrosis.
Methods
After building a rat model, hematoxylin and eosin (HE) staining, Masson's trichrome staining, and western blotting (WB) of collagen I were used to assess bladder pathology and fibrosis in a rat model. Next, protein expression changes in the rat bladder by proteomic technology were quantitatively detected, and reverse transcription-polymerase chain reaction (RT-PCR) and WB were used to verify the expression of proteins. Bioinformatic techniques and functional analysis were also performed.
Results
Compared to the control group, thinning of the bladder epithelium layer, infiltration of submucosal inflammatory cells, deposition of many collagen fibers, and an elevated expression of collagen I were observed in the experimental group. A total of 3,690 proteins were identified, of which 423 proteins were upregulated, and 304 proteins were down-regulated. Eight out of ten mRNA expressions and acyloxyacyl hydrolase (AOAH), mast cell (MC) protease 1 protein expressions were in line with the proteomic results. Sixty-five differential expression proteins (DEPs) were found to belong to the immune system, and 18 of them were involved in immune diseases, according to KEGG analysis. Conclusions: We consider that MC protease 1 and platelet activation pathways may play an important role in ketamine-induced bladder fibrosis.