Hepato-preventive and anti-apoptotic role of boric acid against liver injury induced by cyclophosphamide

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Küçük Resim

Tarih

2019

Dergi Başlığı

Dergi ISSN

Cilt Başlığı

Yayıncı

Elsevier GmbH

Erişim Hakkı

info:eu-repo/semantics/closedAccess

Özet

This study aims to examine cyclophosphamide (CP) exsposure associated toxicity on rat livers and the likely defensive effects of boric acid (BA). The rats used in this study were divided into four groups: control group, CP group, BA group, and BA + CP group. The present study was carried out using routine histological H&E stain, immunohistochemical stain caspase-3 as apoptotic marker, serum biochemical analysis for liver function markers (alanine transaminase (ALT), aspartate transaminase (AST) and alkalen phosphatase (ALP)), oxidative stress markers (total oxidant status (TOS), oxidative stress index (OSI) and total antioxidant capacity marker (TAC)). In the CP group, the levels of ALT, AST, ALP, TOS, OSI and caspase-3 increased whereas TAC levels decreased compared with the control group. In the BA + CP group, the levels of ALT, AST, ALP, TOS, OSI and caspase-3 decreased whereas TAC levels increased compared with the CP group. The histopathological evaluation of light microscope images and immunohistochemical caspase-3 activity in the BA + CP group were found to be decrease compared with those in the CP group. In conclusion, BA was successful in defending the liver against apoptosis and histopathological changes that are attributable to CP. © 2019 Elsevier GmbH

Açıklama

Anahtar Kelimeler

Apoptosis, Boric acid, Cyclophosphamide, Liver injury, Oxidative stress

Kaynak

Journal of Trace Elements in Medicine and Biology

WoS Q Değeri

Q2

Scopus Q Değeri

Q1

Cilt

53

Sayı

Künye

Cengiz, M., Cetik Yildiz, S., Demir, C., Şahin, İ. K., Teksoy, Ö., & Ayhanci, A. (2019). Hepato-preventive and anti-apoptotic role of boric acid against liver injury induced by cyclophosphamide. Journal of Trace Elements in Medicine and Biology, 53, 1–7. https://doi.org/10.1016/j.jtemb.2019.01.013