Effect of bilastine on diabetic nephropathy in DBA2/J mice

Autor: Maura Gurrieri, Patrizia Nardini, Cristina Grange, Benedetta Bussolati, Monica Argenziano, Roberta Cavalli, Elisa Benetti, Sara Borga, Gianluca Miglio, Alessandro Pini, Corrado Ghè, Roberta Verta, Arianna Carolina Rosa
Jazyk: angličtina
Rok vydání: 2019
Předmět:
Male
receptor
030232 urology & nephrology
030204 cardiovascular system & hematology
Kidney
Diabetic nephropathy
lcsh:Chemistry
chemistry.chemical_compound
Mice
0302 clinical medicine
Piperidines
Histamine H
Diabetes
Histamine
1
Slit diaphragm
histamine H1 receptor
Diabetic Nephropathies
lcsh:QH301-705.5
Spectroscopy
biology
General Medicine
Computer Science Applications
Mice
Inbred DBA
Histamine H1 Antagonists
medicine.medical_specialty
Renal function
Histamine H1 receptor
Catalysis
Article
Inorganic Chemistry
Nephrin
03 medical and health sciences
Internal medicine
Diabetes mellitus
medicine
Animals
Physical and Theoretical Chemistry
Molecular Biology
Bilastine
business.industry
Organic Chemistry
medicine.disease
Endocrinology
chemistry
lcsh:Biology (General)
lcsh:QD1-999
biology.protein
Synaptopodin
Benzimidazoles
business
Zdroj: International Journal of Molecular Sciences
Volume 20
Issue 10
International Journal of Molecular Sciences, Vol 20, Iss 10, p 2554 (2019)
Popis: Diabetic nephropathy is an unmet therapeutic need, and the search for new therapeutic strategies is warranted. Previous data point to histamine H1 receptor as a possible target for glomerular dysfunction associated with long term hyperglycaemia. Therefore, this study investigated the effects of the H1 receptor antagonist bilastine on renal morphology and function in a murine model of streptozotocin-induced diabetes. Diabetes was induced in DBA2/J male mice and, from diabetes onset (glycaemia &ge
200 mg/dL), mice received bilastine (1&ndash
30 mg/kg/day) by oral gavage for 14 consecutive weeks. At the end of the experimental protocol, diabetic mice showed polyuria (+195.5%), increase in Albumin-to-Creatine Ratio (ACR, +284.7%), and a significant drop in creatinine clearance (p <
0.05). Bilastine prevented ACR increase and restored creatinine clearance in a dose-dependent manner, suggesting a positive effect on glomerular filtration. The ultrastructural analysis showed a preserved junctional integrity. Preservation of the basal nephrin, P-cadherin, and synaptopodin expression could explain this effect. In conclusion, the H1 receptor could contribute to the glomerular damage occurring in diabetic nephropathy. Bilastine preserved the glomerular junctional integrity, leading to the hypothesis of anti-H1 antihistamines as a possible add-on therapy for diabetic nephropathy.
Databáze: OpenAIRE
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