Reno-protective effect of nicorandil and pentoxifylline against potassium dichromate-induced acute renal injury via modulation p38MAPK/Nrf2/HO-1 and Notch1/TLR4/NF-κB signaling pathways

J Trace Elem Med Biol. 2024 Sep:85:127474. doi: 10.1016/j.jtemb.2024.127474. Epub 2024 May 19.

Abstract

Background: Occupational and environmental exposure to chromium compounds such as potassium dichromate (PDC) (K2Cr2O7) has emerged as a potential aetiologic cause for renal disease through apoptotic, and inflammatory reactions. The known potent antioxidants such as nicorandil (NIC) and/or pentoxifylline (PTX) were studied for their possible nephroprotective effect in PDC-treated rats.

Methods: Forty male Wistar rats were divided into five groups; control, PDC group, NIC+PDC, PTX+PDC group, and combination+PDC group. Nephrotoxicity was evaluated histopathologically and biochemically. Invasive blood pressure, renal function parameters urea, creatinine, uric acid and albumin, glomerular filtration rate markers Cys-C, Kim-1 and NGAL, inflammatory markers IL-1β, IL-6, TNF-α, TGF-β, COX-II, p38MAPK, NF-κB and TLR4, oxidative stress SOD, GSH, MDA, MPO, HO-1 and Nrf2 and apoptotic mediators Notch1 and PCNA were evaluated. Besides, renal cortical histopathology was assayed as well.

Results: PDC led to a considerable increase in indicators for kidney injury, renal function parameters, invasive blood pressure, oxidative stress, and inflammatory markers. They were markedly reduced by coadministration of PDC with either/or NIC and PTX. The NIC and PTX combination regimen showed a more significant improvement than either medication used alone. Our results demonstrated the nephroprotective effect of NIC, PTX, and their combined regimen on PDC-induced kidney injury through suppression of oxidative stress, apoptosis, and inflammatory response.

Conclusion: Renal recovery from PDC injury was achieved through enhanced MAPK/Nrf2/HO-1 and suppressed Notch1/TLR4/NF-κB signaling pathways. This study highlights the role of NIC and PTX as effective interventions to ameliorate nephrotoxicity in patients undergoing PDC toxicity.

Keywords: Invasive blood pressure; Nephrotoxicity; Nicorandil; Notch1/PCNA/MAPK/TLR4/NF-κB; Pentoxifylline; Potassium dichromate.

MeSH terms

  • Acute Kidney Injury* / chemically induced
  • Acute Kidney Injury* / drug therapy
  • Acute Kidney Injury* / metabolism
  • Acute Kidney Injury* / pathology
  • Acute Kidney Injury* / prevention & control
  • Animals
  • Heme Oxygenase (Decyclizing) / metabolism
  • Male
  • NF-E2-Related Factor 2* / metabolism
  • NF-kappa B* / metabolism
  • Nicorandil* / pharmacology
  • Pentoxifylline* / pharmacology
  • Potassium Dichromate*
  • Protective Agents / pharmacology
  • Rats
  • Rats, Wistar*
  • Receptor, Notch1* / metabolism
  • Signal Transduction* / drug effects
  • Toll-Like Receptor 4* / metabolism
  • p38 Mitogen-Activated Protein Kinases* / metabolism

Substances

  • Toll-Like Receptor 4
  • NF-E2-Related Factor 2
  • NF-kappa B
  • Receptor, Notch1
  • Pentoxifylline
  • Nicorandil
  • p38 Mitogen-Activated Protein Kinases
  • Potassium Dichromate
  • Notch1 protein, rat
  • Nfe2l2 protein, rat
  • Tlr4 protein, rat
  • Heme Oxygenase (Decyclizing)
  • Hmox1 protein, rat
  • Protective Agents