Effects of Apis mellifera venom on anti-type II collagen antibody, interleukin 6 a...
| Grant number: | 17/18730-6 |
| Support type: | Scholarships in Brazil - Scientific Initiation |
| Effective date (Start): | February 01, 2018 |
| Effective date (End): | January 31, 2019 |
| Field of knowledge: | Health Sciences - Medicine |
| Principal Investigator: | Carla Patrícia Carlos |
| Grantee: | Rodrigo Piloto de Oliveira Batanero |
| Home Institution: | Faculdade Faceres. Instituto Superior de Educação Ceres (UNICERES). São José do Rio Preto , SP, Brazil |
Abstract Introduction: kidney damage caused directly by the rheumatoid arthritis (RA) is not well elucidated, and there is evidence of the involvement of the Renin-Angiotensin System (RAS) in extra-articular manifestations of RA. Objective: the aim of this study is to propose an experimental model to investigate the renal manifestation of the RA in rats, as well as the participation of RAS in the mechanism of this injury. Methods: male Wistar rats, weighing 200 g, ingesting salt depleted diet, will be distributed in three groups (8 rats/group): Control, Arthritis and Arthritis + AT1 blocker (Losartan 1 mg/Kg daily, s.c.). Arthritis is induced with the injection of 100 µ l of an emulsion of dissected Mycobacterium tuberculosis (50 mg/mL) on the intradermal paw. The animals will be sacrificed 60 days after immunization. This time was established after analysis of preliminary results obtained in a pilot study. The following parameters will be evaluated: renal function through the quantification of proteinuria, urea and creatinine levels, creatinine clearance and fraction of excretion of sodium and potassium; renal injury and inflammation by histopathological analysis, apoptosis, influx of neutrophils and macrophages and TGF-B expression; oxidative stress by renal expression of iNOS and nitrotyrosine and plasma dosage of TBARS (thiobarbituric acid reactive substances); renal expression of AT1 and AT2 receptors; and plasma concentration of angiotensin II. This study can contribute to a better understanding of the mechanisms involved in the genesis of the disease, and the development of therapies against kidney injury in patients affected by RA. (AU) | |