학술논문
The study on the function and cell source of interleukin‐6 in interstitial cystitis/bladder painful syndrome rat model
Document Type
Report
Author
Source
Immunity, Inflammation and Disease. December 2021, Vol. 9 Issue 4, p1520, 9 p.
Subject
Language
English
Abstract
INTRODUCTION Interstitial cystitis/bladder pain syndrome (IC/BPS) is a clinical diagnosis based on frequent urination, urgency, and symptoms of bladder and/or pelvic pain.[sup.1] IC/BPS patients with frequent urination, urgent urination, bladder [...]
: Objective: The elevated expression of interleukin‐6 (IL‐6) in patients with interstitial cystitis/bladder painful syndrome (IC/BPS) has been demonstrated, but the role of IL‐6 in IC/BPS and its source remain to be explored. Methods: IC/BPS rat model was created in female rats by using long‐term intermittent intravesical hyaluronidase (0.5 ml, 4 mg/ml). After modeling, IL‐6 stimulation group, and anti‐IL‐6R group were treated with recombinant rat IL‐6 and tocilizumab, respectively. Symptomatic changes were detected by Vonfrey pain score and urodynamics, and hematoxylin‐eosin (HE) staining, mast cell staining and Masson staining were used to evaluate the changes of inflammation in the bladder tissue of rats. Cell sources of IL‐6 was explored through enzyme linked immunosorbent assay (ELISA) test, reverse transcription polymerase chain reaction (RT‐PCR), and western‐blot test on the supernatant of coculturing rat bladder epithelial cells and rat macrophages. Results: The Vonfrey pain scores of the model group and IL‐6 stimulation group were significantly higher than those of the control group, while the anti‐IL‐6R group were significantly lower (p Conclusions: IL‐6 played an essential role in the development of IC/BPS rat model as a proinflammation cytokine. Further evidence from coculture proved that macrophages are the cell resource of IL‐6 in IC/BPS.
: Objective: The elevated expression of interleukin‐6 (IL‐6) in patients with interstitial cystitis/bladder painful syndrome (IC/BPS) has been demonstrated, but the role of IL‐6 in IC/BPS and its source remain to be explored. Methods: IC/BPS rat model was created in female rats by using long‐term intermittent intravesical hyaluronidase (0.5 ml, 4 mg/ml). After modeling, IL‐6 stimulation group, and anti‐IL‐6R group were treated with recombinant rat IL‐6 and tocilizumab, respectively. Symptomatic changes were detected by Vonfrey pain score and urodynamics, and hematoxylin‐eosin (HE) staining, mast cell staining and Masson staining were used to evaluate the changes of inflammation in the bladder tissue of rats. Cell sources of IL‐6 was explored through enzyme linked immunosorbent assay (ELISA) test, reverse transcription polymerase chain reaction (RT‐PCR), and western‐blot test on the supernatant of coculturing rat bladder epithelial cells and rat macrophages. Results: The Vonfrey pain scores of the model group and IL‐6 stimulation group were significantly higher than those of the control group, while the anti‐IL‐6R group were significantly lower (p Conclusions: IL‐6 played an essential role in the development of IC/BPS rat model as a proinflammation cytokine. Further evidence from coculture proved that macrophages are the cell resource of IL‐6 in IC/BPS.