Naslov
Antifibrotic activity of anthocyanidin delphinidin in carbon tetrachloride-induced hepatotoxicity in mice

Autori
Domitrović, Robert ; Jakovac, Hrvoje

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

Izvornik
Book of Abstracts / Kovarik, Zrinka ; Varljen, Jadranka - Rijeka : Hrvatsko Društvo za Biotehnologiju, 2010, 105-105

Skup
10th Congress of the Croatian Society of Biochemistry and Molecular Biology with International Participation

Mjesto i datum
Opatija, Hrvatska, 15.09.2010. - 18.09.2010

Vrsta sudjelovanja
Poster

Vrsta recenzije
Nije recenziran

Ključne riječi
liver fibrosis; carbon tetrachloride; hepatic stellate cells; oxidative stress; delphinidin

Sažetak
Liver fibrosis is a frequent event which follows chronic damage to the liver, characterized by excess deposition of connective tissue in extracellular matrix and a distortion of the liver tissue architecture by forming a fibrous scar. The aim of this study was to investigate the hepatoprotective effects of anthocyanidin delphinidin in carbon tetrachloride (CCl4)-induced liver fibrosis in mice. Male Balb/C mice were treated with CCl4 (20% CCl4 in olive oil, 2 mL/kg) intraperitoneally (i.p.), twice a week for 7 weeks. Delphinidin was administered i.p. once daily for next 2 weeks, in doses of 10 and 25 mg/kg of body weight. The CCl4 control group has been observed for spontaneous reversion of fibrosis. CCl4-administration increased serum transaminase and alkaline phosphatase levels, and oxidative stress in the liver. Delphinidin has attenuated oxidative stress, increased matrix metalloproteinase-9 and metallothionein I/II expression, and restored hepatic architecture in a dose-dependent manner. Hepatic overexpression of tumor necrosis factor-α and transforming growth factor-β1 has been completely withdrawn by delphinidin. Concomitantly, the expression of α-smooth muscle actin indicated returning of hepatic stellate cells (HSC) into inactive state. Our results suggest the therapeutic effects of delphinidin in CCl4-induced liver fibrosis by promoting extracellular matrix degradation, HSC inactivation and down-regulation of fibrogenic stimuli, with strong enhancement of hepatic regenerative capability.

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti, Farmacija

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