Pretreatment of carprofen impaired initiation of inflammatory- and overlapping resolution response and promoted cardiorenal syndrome in heart failure

In response to injury, initiation of leukocytes-directed intense inflammation is part of the innate immune response of the body and plays a vital role in resolution, and tissue repair as the response eliminates damaged tissue and cell debris

Veena Krishnan; David Booker; Gabrielle Cunningham; Jeevan Kumar Jadapalli; Vasundhara Kain; Amanda B. Pullen; Ganesh V. Halade

2018

Scholarcy highlights

  • In response to injury, initiation of leukocytes-directed intense inflammation is part of the innate immune response of the body and plays a vital role in resolution, and tissue repair as the response eliminates damaged tissue and cell debris
  • Gene expression levels of inflammatory cytokines and renal injury markers were measured in the kidney and compared to +/−CAP naïve controls
  • After 2 weeks CAP treatment and 24 hours post-myocardial infarction, the +CAP+MI-d1 mice were compared with -CAP+MI-d1 mice to determine whether the inflammation and resolution response was impaired by CAP treatment in kidney
  • CAP pretreatment elevated plasma creatinine levels compared with -CAP-no-MI mice, indicating that CAP treatment, without MI, triggered renal injury
  • The glomerular filtration studies revealed that there were no significant differences in Glomerular filtration rate between -CAPno-MI and +CAP-no-MI mice, demonstrating that the CAP treatment does not lead to renal dysfunction, but does induce molecular and cellular renal injury
  • Presented results are indicative of immune suppressive and impaired resolution of inflammation mechanisms due to the subacute treatment of pain-killer carprofen thereby cardiorenal syndrome in acute heart failure

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