Pathogenic role of innate immunity in a model of chronic NO inhibition associated with salt overload.

Pathogenic role of innate immunity in a model of chronic NO inhibition associated with salt overload. Am J Physiol Renal Physiol. 2019 Aug 14;: Authors: Zambom FFF, Oliveira KC, Foresto-Neto O, Faustino VD, Ávila VF, Albino AH, Arias SCA, Volpini RA, Malheiros DMAC, Saraiva Câmara NO, Zatz R, Fujihara CK Abstract Nitric oxide inhibition with Nw-nitroarginine-methylester (L-NAME) along with salt overload leads to hypertension, albuminuria, glomerulosclerosis, glomerular ischemia and interstitial fibrosis, characterizing a chronic kidney disease (CKD) model. Previous findings of this laboratory and elsewhere suggest that activation of at least two pathways of innate immunity, TLR4/NF-κB and NLRP3 inflammasome/IL-1β, occurs in several experimental models of CKD, and that progression of renal injury can be slowed with inhibition of these pathways. In the present study, we investigated whether activation of innate immunity, through either the TLR4/NF-κB or NLRP3/IL-1β pathway, is involved in the pathogenesis of renal injury in chronic NO inhibition with salt overload model. Adult male Munich-Wistar rats receiving L-NAME in drinking water and salt overload (Group HS+N) were treated with Allopurinol (ALLO), as an NLRP3 inhibitor (Group HS+N+ALLO), or Pyrrolidine Dithiocarbamate (PDTC) a NF-κB inhibitor (Group HS+N+PDTC). After 4 wks, HS+N rats developed hypertension, albuminuria and renal injury, along with renal inflammation, oxidat...
Source: American Journal of Physiology. Renal Physiology - Category: Physiology Authors: Tags: Am J Physiol Renal Physiol Source Type: research