Therapeutic Effect of Platelet-Rich Plasma Improves Bladder Overactivity in the Pathogenesis of Ketamine-Induced Ulcerative Cystitis in a Rat Model.
Kuang-Shun ChuehKuan-Hua HuangJian-He LuTai-Jui JuanShu-Mien ChuangRong-Jyh LinYi-Chen LeeCheng-Yu LongMei-Chen ShenTing-Wei SunYung-Shun JuanPublished in: International journal of molecular sciences (2022)
The present study attempted to elucidate whether intravesical instillation of platelet-rich plasma (PRP) could decrease bladder inflammation and ameliorate bladder hyperactivity in ketamine ulcerative cystitis (KIC) rat model. Female Sprague Dawley (S-D) rats were randomly divided into control group, ketamine-treated group, ketamine with PRP treated group, and ketamine with platelet-poor plasma (PPP) treated group. Cystometry and micturition frequency/volume studies were performed to investigate bladder function. The morphological change of bladder was investigated by Mason's trichrome staining. Western blotting analysis were carried out to examine the protein expressions of inflammation, urothelial differentiation, proliferation, urothelial barrier function, angiogenesis and neurogenesis related proteins. The results revealed that treatment with ketamine significantly deteriorated bladder capacity, decreased voiding function and enhanced bladder overactivity. These pathological damage and interstitial fibrosis may via NF-κB/COX-2 signaling pathways and muscarinic receptor overexpression. PRP treatment decreased inflammatory fibrotic biosynthesis, attenuated oxidative stress, promoted urothelial cell regeneration, and enhanced angiogenesis and neurogenesis, thereafter recovered bladder dysfunction and ameliorate the bladder hyperactivity in KIC rat model. These findings suggested that the PRP therapy may offer new treatment options for those clinical KIC patients.
Keyphrases
- platelet rich plasma
- urinary tract
- oxidative stress
- spinal cord injury
- signaling pathway
- pain management
- newly diagnosed
- diabetic rats
- stem cells
- ejection fraction
- high grade
- endothelial cells
- systemic sclerosis
- inflammatory response
- end stage renal disease
- vascular endothelial growth factor
- bone marrow
- lps induced
- chronic kidney disease
- ischemia reperfusion injury
- south africa
- epithelial mesenchymal transition
- induced apoptosis
- pi k akt
- mass spectrometry
- combination therapy
- blood brain barrier
- toll like receptor
- single molecule
- binding protein
- high speed
- endoplasmic reticulum stress
- protein protein