Treatment with CernitinTM of induced urinary bladder inflammation downregulates relevant pro-inflammatory biomarkers - an experimental in vivo rodent model.

Abstract

Objective: Chronic inflammation of the urinary bladder is associated with the bladder pain syndrome. The treatment alternatives in humans are far from satisfactory and need further attention. Well-established preclinical models have shown that pro-inflammatory cytokines contribute to the progress of the inflammatory response behind pain and hyperalgesia. Previously presented results indicate that treatment with CernitinTM pollen extracts active pharmaceutical ingredients (APIs) (Cernitin GBX and Cernitin T60) significantly alleviated pain in cyclophosphamide-induced urinary bladder inflammation in a rodent model through downregulation of PGD2 and cyclooxygenase-2 (COX-2) mediators when compared to the vehicle alone. The objective was to extend the original study by exploring the correlation between the two APIs and cytokines expression and to identify a possible biomarker pattern.

Material and method: The Olink® Target 48 Mouse Cytokine assay was conducted on the homogenised tissue extracts of the bladder wall with induced inflammation from a previous study to identify the potential impacts on protein biomarkers.

Results: The test revealed that treatment with the APIs significantly downregulated the cytokines interleukin (IL)-1α, IL-2, IL-4, IL-6, and with trend to significance the biomarkers IL-12 α, β, CCL4 and fibroblast growth factor 21 when administered in combination (GBX+T60) or each component alone, compared to vehicle controls.

Conclusion: This study identified seven cytokines that were significantly or markedly reduced. The results suggest that CernitinTM APIs impact a series of key pro-inflammatory biomarkers demonstrating an ability to restrain inflammation. Therefore, they warrant further investigation as potential therapeutic candidates.