Tnf-α inhibition by infliximab as a new target for the prevention of glycerol-contrast-induced nephropathy

Environ Toxicol Pharmacol. 2015 Mar;39(2):577-88. doi: 10.1016/j.etap.2015.01.002. Epub 2015 Jan 20.

Abstract

Contrast medium-induced nephropathy (CIN) remains as a problem with high incidence and mortality rates. The aim of this study is to examine the roles of infliximab (INF) in the glycerol (GLY) and CIN model in rats. The rats were separated into five groups (n=8): Healthy, GLY, GLY+CM, GLY+CM+INF 5mg/kg intraperitoneally (i.p.), and GLY+CM+INF 7 mg/kg (i.p.). Antioxidant levels in the therapy groups were observed to be quite similar to those in the healthy group. In this study, while the kidney TNF-α, IL-1β, TGF-1β and Caspase 3 gene expressions' levels increased in the nephrotoxic groups, these levels were found to have decreased in the treatment groups. Moreover, histopathologic examination showed that hyaline, haemorrhagic casts and necrosis were increased in nephrotoxicity group, whereas they decreased in the therapy group. Furthermore, TNF-α and NF-κB expression were decreased with infliximab administrated groups similar to control group. In conclusion, we suggest that infliximab have protective roles on CIN.

Keywords: Contrast-media; Infliximab; Nephrotoxicity; Rat.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / pharmacology
  • Anti-Inflammatory Agents / therapeutic use*
  • Blood Urea Nitrogen
  • Caspase 3 / genetics
  • Contrast Media*
  • Creatinine / blood
  • Glutathione / metabolism
  • Glycerol*
  • Infliximab / pharmacology
  • Infliximab / therapeutic use*
  • Interleukin-1beta / genetics
  • Kidney / drug effects
  • Kidney / metabolism
  • Kidney / pathology
  • Kidney Diseases / chemically induced*
  • Kidney Diseases / drug therapy*
  • Kidney Diseases / metabolism
  • Kidney Diseases / pathology
  • Male
  • Malondialdehyde / metabolism
  • RNA, Messenger / metabolism
  • Rats, Wistar
  • Superoxide Dismutase / metabolism
  • Transforming Growth Factor beta1 / genetics
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors*
  • Tumor Necrosis Factor-alpha / genetics

Substances

  • Anti-Inflammatory Agents
  • Contrast Media
  • Interleukin-1beta
  • RNA, Messenger
  • Tgfb1 protein, rat
  • Transforming Growth Factor beta1
  • Tumor Necrosis Factor-alpha
  • Malondialdehyde
  • Creatinine
  • Infliximab
  • Superoxide Dismutase
  • Casp3 protein, rat
  • Caspase 3
  • Glutathione
  • Glycerol