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Pregled bibliografske jedinice broj: 953740

Delphinidin aggravates cisplatin-induced nephrotoxicity by augmenting renal oxidative stress, inflammation, and apoptosis


Potočnjak, Iva; Vukelić, Iva; Marinić, Jelena; Škoda, Marko; Domitrović, Robert
Delphinidin aggravates cisplatin-induced nephrotoxicity by augmenting renal oxidative stress, inflammation, and apoptosis // Book of Abstracts ; FEBS3+ conference ‘From molecules to living systems’
Siófok, Mađarska, 2018. str. 237-237 (poster, međunarodna recenzija, sažetak, ostalo)


Naslov
Delphinidin aggravates cisplatin-induced nephrotoxicity by augmenting renal oxidative stress, inflammation, and apoptosis

Autori
Potočnjak, Iva ; Vukelić, Iva ; Marinić, Jelena ; Škoda, Marko ; Domitrović, Robert

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, ostalo

Izvornik
Book of Abstracts ; FEBS3+ conference ‘From molecules to living systems’ / - Siófok, Mađarska, 2018, 237-237

Skup
FEBS3+ conference ‘From molecules to living systems’

Mjesto i datum
Siófok, Hungary, 2-5.09.2018

Vrsta sudjelovanja
Poster

Vrsta recenzije
Međunarodna recenzija

Ključne riječi
Delphinidin ; cisplatin ; oxidative stress ; inflammation ; apoptosis ; multidrug resistance protein.

Sažetak
Delphinidin is a natural anthocyanidin that possesses numerous beneficial health effects. However, its effect in cisplatin (CP)- intoxicated mice is unknown. In this study we investigated the effect of delphinidin on CP- induced kidney injury. Male BALB/cN mice were treated orally by 1 and 5 mg/kg body weight of delphinidin daily for two days, 48 h after intraperitoneal injection of CP (13 mg/kg). CP treatment resulted in increased blood urea nitrogen and serum creatinine, with histopathological signs of renal tissue injury. CP administration also increased expression of oxidative/nitrosative stress markers 3- nitrotyrosine (3-NT) and heme oxygenase-1 (HO-1), as well as expression of proinflammatory cytokine tumor necrosis factor- alpha (TNF-α). Increased expression of caspase- 8, -9, and -3, with concomitant suppression od cyclin D1 expression and increased expression of p21, suggested inhibition of the cell cycle and induction of apoptosis in the kidneys. Surprisingly, treatment by delphinidin worsen CP-induced nephrotoxicity by increasing oxidative/nitrosative stress, inflammatory response, and apoptosis. Treatment by delphinidin suppressed CP-induced activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) and increased phosphorylation of c-Jun N-terminal kinase 1 (JNK1) and p38. Deterioration of CP-induced kidney injury by delphinidin was accompanied by suppression of efflux transporters multidrug resistance protein 1 (MDR1) and multidrug resistance-associated protein 2 (Mrp2) and increased platinum (Pt) levels in renal tissue. Our results suggest that delphinidin impairs renal Pt excretion, resulting in Pt accumulation and deterioration of CP-induced nephrotoxicity.

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti, Farmacija



POVEZANOST RADA


Ustanove
Medicinski fakultet, Rijeka