NF-kappa B blockade during short-term L-NAME and salt overload strongly attenuates the late development of chronic kidney disease

Imagem de Miniatura
Arquivos
art_OLIVEIRA_NFkappa_B_blockade_during_shortterm_LNAME_and_salt_2020.PDF (5.54 MB)
Citações na Scopus
2
Tipo de produção
article
Data de publicação
2020
DOI
Scopus
Web of Science
PubMed
Título da Revista
ISSN da Revista
Título do Volume
Editora
AMER PHYSIOLOGICAL SOC
Autores
Citação
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, v.319, n.2, p.F215-F228, 2020
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Nitric oxide synthase inhibition by N-omega-nitro-L-arginine methyl ester (L-NAME) plus a high-salt diet (HS) is a model of chronic kidney disease (CKD) characterized by marked hypertension and renal injury. With cessation of treatment, most of these changes subside, but progressive renal injury develops, associated with persistent low-grade renal inflammation. We investigated whether innate immunity. and in particular the NF-kappa B system, is involved in this process. Male Munich-Wistar rats received HS + L-NAME (32 mg.kg(-1).day(-1)), whereas control rats received HS only. Treatment was ceased after week 4 when 30 rats were studied. Additional rats were studied at week 8 (n = 30) and week 28 (n = 30). As expected, HS + L-NAME promoted severe hypertension, albuminuria, and renal injury after 4 wk of treatment, whereas innate immunity activation was evident. After discontinuation of treatments, partial regression of renal injury and inflammation occurred, along with persistence of innate immunity activation at week 8. At week 28, glomerular injury worsened, while renal inflammation persisted and renal innate immunity remained activated. Temporary administration of the NF-kappa B inhibitor pyrrolidine dithiocarbamate, in concomitancy with the early 4-wk HS + L-NAME treatment, prevented the development of late renal injury and inflammation, an effect that lasted until the end of the study. Early activation of innate immunity may be crucial to the initiation of renal injury in the HS + L-NAME model and to the autonomous progression of chronic nephropathy even after cessation of the original insult. This behavior may be common to other conditions leading to CKD.
Palavras-chave
chronic kidney disease, immunity innate, N-omega-nitro-L-arginine methyl ester, NF-kappa B, salt overload
URI
https://observatorio.fm.usp.br/handle/OPI/37887
Referências
  1. Arias SCA, 2013, PLOS ONE, V8, DOI 10.1371/journal.pone.0056215
  2. Alvarez V, 2002, AM J PHYSIOL-RENAL, V283, pF1132, DOI 10.1152/ajprenal.00199.2002
  3. Anders HJ, 2007, CURR OPIN NEPHROL HY, V16, P177, DOI 10.1097/MNH.0b013e32803fb767
  4. ANDERSON S, 1988, J CLIN INVEST, V82, P1757, DOI 10.1172/JCI113789
  5. Romero CA, 2017, J MOL HISTOL, V48, P209, DOI 10.1007/s10735-017-9720-9
  6. Azadegan-Dehkordi Fatemeh, 2015, J Nephropathol, V4, P32, DOI 10.12860/jnp.2015.07
  7. BAYLIS C, 1992, J CLIN INVEST, V90, P278, DOI 10.1172/JCI115849
  8. Brown S, 2018, ARCH TOXICOL, V92, P2573, DOI 10.1007/s00204-018-2248-2
  9. Chandramohan G, 2008, AM J NEPHROL, V28, P158, DOI 10.1159/000110021
  10. Chang A, 2014, CURR OPIN NEPHROL HY, V23, P204, DOI 10.1097/01.mnh.0000444814.49755.90
  11. Correa-Costa M, 2011, PLOS ONE, V6, DOI 10.1371/journal.pone.0029004
  12. Costa JCSR, 2006, AM J NEPHROL, V26, P281, DOI 10.1159/000093960
  13. Cuzzocrea S, 2002, BRIT J PHARMACOL, V135, P496, DOI 10.1038/sj.bjp.0704463
  14. Fanelli C, 2017, SCI REP-UK, V7, DOI 10.1038/s41598-017-02915-6
  15. Faustino VD, 2018, BIOSCIENCE REP, V38, DOI 10.1042/BSR20180762
  16. Foresto-Neto O, 2018, LAB INVEST, V98, P773, DOI 10.1038/s41374-018-0029-4
  17. Zambom FFF, 2019, AM J PHYSIOL-RENAL, V317, pF1058, DOI 10.1152/ajprenal.00251.2019
  18. Fujihara CK, 2006, AM J PHYSIOL-RENAL, V290, pF632, DOI 10.1152/ajprenal.00259.2005
  19. FUJIHARA CK, 1994, AM J PHYSIOL, V266, pF697
  20. Fujihara CK, 2001, HYPERTENSION, V37, P170, DOI 10.1161/01.HYP.37.1.170
  21. Fujihara CK, 2007, AM J PHYSIOL-RENAL, V292, pF92, DOI 10.1152/ajprenal.00184.2006
  22. Goligorsky MS, 2011, KIDNEY INT, V80, P450, DOI 10.1038/ki.2011.170
  23. Han YQ, 1999, CIRC RES, V84, P695, DOI 10.1161/01.RES.84.6.695
  24. Hijmans RS, 2017, PLOS ONE, V12, DOI 10.1371/journal.pone.0178940
  25. Itani HA, 2016, CIRC RES, V118, P1233, DOI 10.1161/CIRCRESAHA.115.308111
  26. Liu HF, 2017, AM J NEPHROL, V46, P333, DOI 10.1159/000481668
  27. Ma J, 2019, SCI REP-UK, V9, DOI 10.1038/s41598-019-38811-4
  28. O'Leary R, 2016, AM J PHYSIOL-RENAL, V310, pF1000, DOI 10.1152/ajprenal.00482.2015
  29. Okabe C, 2013, AM J PHYSIOL-RENAL, V305, pF155, DOI 10.1152/ajprenal.00491.2012
  30. Orejudo M, 2019, FRONT PHARMACOL, V10, DOI 10.3389/fphar.2019.01015
  31. Patel S, 2018, CURR ALLERGY ASTHM R, V18, DOI 10.1007/s11882-018-0817-3
  32. Pons H, 2013, AM J PHYSIOL-RENAL, V304, pF289, DOI 10.1152/ajprenal.00517.2012
  33. Quiroz Y, 2001, AM J PHYSIOL-RENAL, V281, pF38
  34. RIBEIRO MO, 1992, HYPERTENSION, V20, P298, DOI 10.1161/01.HYP.20.3.298
  35. Rodriguez-Iturbe B, 2001, KIDNEY INT, V59, P2222, DOI 10.1046/j.1523-1755.2001.0590062222.x
  36. Rosin DL, 2011, J AM SOC NEPHROL, V22, P416, DOI 10.1681/ASN.2010040430
  37. Ruiz-Ortega M, 1998, J IMMUNOL, V161, P430
  38. Souza ACP, 2015, PHYSIOL REP, V3, DOI 10.14814/phy2.12558
  39. Sprangers S, 2019, MATRIX BIOL, V75-76, P190, DOI 10.1016/j.matbio.2017.11.008
  40. Su H, 2017, FRONT IMMUNOL, V8, DOI 10.3389/fimmu.2017.00405
  41. Turner JE, 2010, KIDNEY INT, V77, P1070, DOI 10.1038/ki.2010.102
  42. Volpini RA, 2004, NEPHRON PHYSIOL, V98, P97, DOI 10.1159/000081558
  43. Wolf G, 2002, KIDNEY INT, V61, P1986, DOI 10.1046/j.1523-1755.2002.00365.x
  44. WU XW, 1992, J MOL EVOL, V34, P78, DOI 10.1007/BF00163854
  45. Zhou X, 2013, PLOS ONE, V8, DOI 10.1371/journal.pone.0060332

Coleções
Artigos e Materiais de Revistas Científicas - FM/MPT
Artigos e Materiais de Revistas Científicas - FM/MCM
Artigos e Materiais de Revistas Científicas - HC/ICHC
Artigos e Materiais de Revistas Científicas - LIM/05
Artigos e Materiais de Revistas Científicas - LIM/16
Artigos e Materiais de Revistas Científicas - ODS/03