Ιατρικά Άρθρα Αλέξανδρος Γ. Σφακιανάκης
Πληροφορίες
Alexandros G. Sfakianakis
Προβολή πλήρους προφίλ
Τρίτη 23 Μαΐου 2017
Curcumin attenuates lipopolysaccharide/d-galactosamine-induced acute liver injury
Curcumin attenuates lipopolysaccharide/d-galactosamine-induced acute liver injury by activating Nrf2 nuclear translocation and inhibiting NF-kB activation
στο Biomedicine & Pharmacotherapy
Μετάφραση άρθρου
Publication date: July 2017
Source:Biomedicine & Pharmacotherapy, Volume 91
Author(s): Yi-Lian Xie, Jin-Guo Chu, Xiao-Min Jian, Jin-Zhong Dong, Li-Ping Wang, Guo-Xiang Li, Nai-Bin Yang
Curcumin, a polyphenol in curry spice isolated from the rhizome of turmeric, has been reported to possess versatile biological properties including anti-inflammatory, anti-oxidant, antifibrotic, and anticancer activities. In this study, the hepatoprotective effect of curcumin was investigated in lipopolysaccharide (LPS)/d-galactosamine (d-GalN)-induced acute liver injury (ALI) in rats. Experimental ALI was induced with an intraperitoneal (ip) injection of sterile 0.9% sodium chloride (NaCl) solution containing 8μg LPS and 800mg/kg d-GalN. Curcumin was administered once daily starting three days prior to LPS/d-GalN treatment. Results indicated that curcumin could attenuate hepatic pathological damage, decrease serum ALT and AST levels, and reduce malondialdehyde (MDA) content in experimental ALI rats. Moreover, higher dosages of curcumin pretreatment inhibited NF-κB activation and reduced serum TNF-α and liver TNF-α levels induced by LPS/d-GalN ip injection. Furthermore, we found that curcumin up-regulated the expression of nuclear Nrf2 and Nrf2-dependent antioxidant defense genes including heme oxygenase-1 (HO-1), glutamate-cysteine ligase (GCLC), NAD(P)H dehydrogenase, and quinone (NQO-1) in a dose-dependent manner. Our results showed that curcumin protected experimental animals against LPS/d-GalN-induced ALI through activation of Nrf2 nuclear translocation and inhibition of NF-κB activation.
Alexandros Sfakianakis
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alsfakia@gmail.com
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