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The effects of caffeic acid phenethyl ester on streptozotocin-induced diabetic liver injury

Date

2016

Author

Taslidere, E.
Gul, M.
Elbe, H.
Cetin, A.
Vardi, N.
Ozyalin, F.
Turkoz, Y.

Metadata

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Abstract

The aim of the present study was to clarify the role of oxidative stress in streptozotocin induced liver injury and the possible protective effect of caffeic acid phenethyl ester (CAPE) using histological and biochemical parameters. 32 male Wistar rats were divided into 4 groups as follows: Group 1: Control animals, Group 2: Control animals given CAPE Group 3: STZ-induced diabetic animals (DM group), Group 4: STZ-induced diabetic rats given CAPE (DM+CAPE group). All the injections started on the same day of single-dose STZ injection and continued for 20 days. At the end of this period, livers were removed and processed for routine histological procedures. Biochemical parameters and morphological changes were examined. In DM group, blood glucose levels were significantly increased compared with the control group. Significant increases in tissue malondialdehyde (MDA) level and decreases in superoxide dismutase (SOD) and total glutathione (GSH) activities were detected in DM group. Administration of CAPE significantly reduced these values. STZ-induced histopathological alterations including inflammatory cell infiltration around portal triad, congestion, loss of glycogen in the hepatocytes. Additionally, degenerative cellular alterations, such as numerous vacuolizations including myelinic figure formation, pyknotic nuclei with peripheral localization of heterochromatin condensation and mitochondria! elongation were observed in cytoplasm of hepatocytes. CAPE significantly reduced these histopathological changes. Our results indicate that CAPE should be considered in the prevention of oxidative stress in diabetic liver (Tab. 3, Fig. 4, Ref. 47). Text in PDF www.elis.sk.

Source

Bratislava Medical Journal-Bratislavske Lekarske Listy

Volume

117

Issue

5

URI

https://doi.org/10.4149/BLL_2016_054
https://hdl.handle.net/20.500.12809/2740

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  • PubMed İndeksli Yayınlar Koleksiyonu [2082]
  • Scopus İndeksli Yayınlar Koleksiyonu [6219]
  • WoS İndeksli Yayınlar Koleksiyonu [6466]



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