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Dergiler / Eurasian Journal of Emergency Medicine / 2022 / Cilt: 21 - Sayı: 2

Can Spesific Biomarkers Be Used to Enlighten the Major Mechanisms of Acute High Dose Diclofenac Sodium-Related Nephrotoxicity?

Sinem DOĞRUYOL
Abdullah Osman KOÇAK
Serpil AYGÖRMEZ
Özge ERTENER
Habip Emrah LEYLEK
Sultan Tuna AKGÖL GÜR
İlker AKBAŞ
Sayfa
132–137
Yayın Tarihi
2022-10-11
DOI
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Yapay Zeka Hızlı Bakış & Çıkarımlar

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⚡ TL;DR(1 Cümlede Hızlı Çıkarım)

With a simple version of this panel adapted to emergency departments, we may be able to diagnose diclofenac sodium-related nephrotoxicity.

📌 3 Maddede Bu Makale

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Amaç & Hipotez:Aim: The aim of this study was to examine the basic mechanisms that play a role in the acute nephrotoxicity caused by diclofenac sodium.
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Temel Bulgular & Veri:Materials and Methods: Only water was given to the control group; however, the diclofenac sodium group was group intoxicated by giving water-soluble, 240 mg/kg, oral single dose diclofenac sodium.
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Sonuç & Katkı:With a simple version of this panel adapted to emergency departments, we may be able to diagnose diclofenac sodium-related nephrotoxicity.
🔬Tür:Modelleme & Sayısal Simülasyon
📍Kapsam:Genişletilmiş Akademik Örneklem
⚙️Değişkenler:Alan Parametreleri

Abstract

Aim: The aim of this study was to examine the basic mechanisms that play a role in the acute nephrotoxicity caused by diclofenac sodium. Materials and Methods: Only water was given to the control group; however, the diclofenac sodium group was group intoxicated by giving water-soluble, 240 mg/kg, oral single dose diclofenac sodium. After 24 hours, all animals were sacrificed and histopathological analyzes were performed. The levels of spesific biomarkers [vascular endothelial growth factor (VEGF), nuclear factor-kappa B (NF-κB), matrix metalloproteinase-9 (MMP-9), metalloproteinase tissue inhibitor-1 (TIMP-1) and carcinoembryonic antigen (CEA)] that may be related to the nephrotoxicity mechanism were evaluated. Results: As a result of biochemical analysis, we found that VEGF, TIMP-1, NF-κB and CEA levels were significantly higher and MMP-9 levels were significantly lower in diclofenac sodium group compared to control group. Nephrotoxicity related histopathological changes were observed in the sections of diclofenac sodium group. Conclusion: This study has shown that the biomarkers we evaluated in the diclofenac sodium-induced acute high-dose intoxication model we created can help us to identify the nephrotoxicity and to explain the nephrotoxicity mechanism with the three main steps (the hemodynamicrelated pathway, the inflammation-related pathway, and the oxidative stress-related pathway). With a simple version of this panel adapted to emergency departments, we may be able to diagnose diclofenac sodium-related nephrotoxicity.

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Bu Makaleye Atıf Yap

DOĞRUYOL, S., KOÇAK, A. O., AYGÖRMEZ, S., ERTENER, Ö., LEYLEK, H. E., GÜR, S. T. A., AKBAŞ, İ. (2022). Can Spesific Biomarkers Be Used to Enlighten the Major Mechanisms of Acute High Dose Diclofenac Sodium-Related Nephrotoxicity?. Eurasian Journal of Emergency Medicine, Cilt: 21 - Sayı: 2, 132–137. https://ajindex.com/articles/507420

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Kaynakça (14)

  1. Aydin G, Gökçimen A, Öncü M, Çicek E, Karahan N, Gökalp O. Histopathologic changes in liver and renal tissues induced by different doses of diclofenac sodium in rats. Turkish J Vet Anim Sci. 2003;27:1131-40
  2. FitzGerald GA, Patrono C. The coxibs, selective inhibitors of cyclooxygenase-2. N Engl J Med. 2001;345:433-2
  3. Baravalia Y, Vaghasiya Y, Chanda S. Hepatoprotective effect of Woodfordia fruticosa Kurz flowers on diclofenac sodium induced liver toxicity in rats. Asian Pac J Trop Med. 2011;4:342-6
  4. Sales GTM, Foresto RD. Drug-induced nephrotoxicity. Rev Assoc Med Bras. 2000;66(Suppl. 1):s82-s90
  5. Mousa AA, Elweza AE, Elbaz HT, Tahoun EAE, Shoghy KM, Elsayed I, et al. Eucalyptus Globulus protects against diclofenac sodium induced hepatorenal and testicular toxicity in male rats. J Tradit Complement Med. 2019;10:521-8
  6. El-Shafei RA, Saleh RM. Pharmacological effects of vitamin C & E on diclofenac sodium intoxicated rats. Biomed Pharmacother. 2016;84:314-22
  7. Choudhury D, Ahmed Z. Drug-induced nephrotoxicity. Med Clin North Am. 1997;81:705-17
  8. Hickey EJ, Raje RR, Reid VE, Gross SM, Ray SD. Diclofenac induced in vivo nephrotoxicity may involve oxidative stress-mediated massive genomic DNA fragmentation and apoptotic cell death. Free Radic Biol Med. 2001;31:139- 52
  9. Schrijvers BF, Flyvbjerg A, De Vriese AS. The role of vascular endothelial growth factor (VEGF) in renal pathophysiology. Kidney Int. 2004;65:2003-17
  10. Estrada CC, Maldonado A, Mallipattu SK. Therapeutic inhibition of VEGF signaling and associated nephrotoxicities. J Am Soc Nephrol. 2019;30:187- 200
  11. Vyas D, Laput G, Vyas AK. Chemotherapy-enhanced inflammation may lead to the failure of therapy and metastasis, OncoTargets Ther. 2014;7:1015
  12. Khames A, Khalaf MM, Gad AM, Abd El-Raouf OM, Kandeil MA. Nicorandil combats doxorubicin-induced nephrotoxicity via amendment of TLR4/P38 MAPK/NFκ-B signaling pathway. Chem Biol Interact. 2019;311:108777
  13. Fattori V, Borghi SM, Guazelli CFS, Giroldo AC, Crespigio J, Bussmann AJC, et al. Vinpocetine reduces diclofenac-induced acute kidney injury through inhibition of oxidative stress, apoptosis, cytokine production, and NF-κB activation in mice. Pharmacol Res. 2017;120:10-22
  14. Borghi SM, Fattori V, Ruiz-Miyazawa KW, Bertozzi MM, Lourenco-Gonzalez Y, Tatakihara R.I, et al. Pyrrolidine dithiocarbamate inhibits mouse acute kidney injury induced by diclofenac by targeting oxidative damage, cytokines and NF-κB activity. Life Sc